In the acute phase of streptozotocin (STZ)-induced type 1 diabetes, the mechanisms leading to hyperglycemia and a shift toward lipid-dominant metabolism remain unclear. We continuously recorded sympathetic and vagal nerve activity and metabolic parameters in freely moving rats to clarify how insulin deficiency alters substrate utilization and autonomic outflow. Male Wistar rats were chronically implanted with electrodes for cervical vagal nerve activity, renal and lumbar sympathetic nerve activity, arterial pressure telemetry, ECG, and an interstitial glucose sensor. Type 1 diabetes was induced by intraperitoneal STZ (65 mg/kg). STZ administration rapidly decreased plasma insulin, and interstitial glucose stabilized at ~320 mg/dl, producing marked hyperglycemia. The respiratory quotient decreased from ~0.9 to ~0.7, indicating near-complete loss of carbohydrate utilization and a compensatory increase in lipid oxidation. These metabolic changes reflect a forced shift to fat utilization due to impaired cellular glucose uptake caused by insulin deficiency. Continuous autonomic recordings revealed that lumbar sympathetic nerve activity increased persistently by >40%, whereas renal sympathetic nerve activity showed no significant change. Cervical vagal nerve activity exhibited only a transient and minimal response, indicating a lack of active vagal involvement. These findings demonstrate that hyperglycemia and lipid-dominant metabolism after STZ are driven not simply by insulin deficiency itself, but by a compensatory and sustained activation of lumbar sympathetic nerve activity, likely to mobilize alternative fuels. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

BACKGROUND:Excessive salt intake is a major contributor to hypertension; however, the role of sympathetic nerve activity (SNA) remains controversial. Most existing evidence relies on indirect markers or single-time-point measurements. Therefore, we directly and continuously recorded SNA to test the hypothesis that SNA contributes to the initiation, progression, or both phases of salt-induced hypertension. METHODS:We continuously recorded renal and lumbar SNA, arterial pressure, and heart rate for 4 weeks in conscious sham-operated and uninephrectomized rats. After a control period on a normal-salt diet, rats received a subcutaneous deoxycorticosterone acetate (DOCA) pellet with a high-salt diet (4% NaCl) for 17 days, followed by pellet removal and a return to a normal-salt diet for 7 days. RESULTS:DOCA-salt treatment induced a biphasic increase in arterial pressure, with an immediate increase within 24 hours (initiation phase) and a progressive increase after day 6 (developmental phase), which was more pronounced in uninephrectomy rats. In contrast, heart rate and renal SNA decreased from day 1, and lumbar SNA progressively declined in all groups, providing no evidence of sympathetic overactivity during either phase. After DOCA withdrawal, AP declined, whereas renal SNA and lumbar SNA transiently increased. CONCLUSIONS:Continuous recordings demonstrated that neither renal SNA nor lumbar SNA mediated the initiation or development of DOCA-salt hypertension. In the absence of evidence for increased cardiac output, the biphasic rise in AP is attributed to increased peripheral vascular resistance of a nonsympathetic origin, likely driven by DOCA-sodium interactions in the perivascular region.

Long-chain fatty acids (long-chain fatty acids) serve as both metabolic substrates and signaling molecules that modulate autonomic and cardiovascular regulation. However, how different chemical forms and species of long-chain fatty acids influence sympathetic and vagal nerve activity in conscious animals remains unclear. This study examined autonomic responses to intragastric administration of triglyceride oils and individual long-chain fatty acids in freely moving rats. Male Wistar rats were chronically implanted with electrodes for cervical vagal nerve activity (VNA), renal (RSNA) and lumbar sympathetic nerve activity (LSNA), arterial pressure, ECG, and intragastric catheters. After an 18-hour fast, rats received 1 mL of either triglyceride oils (corn or flaxseed oil) or free fatty acids (oleic acid or α-linolenic acid). Autonomic and cardiovascular variables were recorded for 60 min before and 180 min after administration. Triglyceride oils did not alter VNA, whereas LSNA increased immediately and peaked at ~30 min. RSNA increased only after flaxseed oil. Heart rate rose in parallel with LSNA, while arterial pressure remained unchanged. In contrast, free fatty acids markedly increased VNA, with LSNA increasing for both fatty acids and RSNA increasing only after α-linolenic acid. Heart rate increased after oleic acid but showed little change after α-linolenic acid. These findings demonstrate that long-chain fatty acids consistently activate lumbar sympathetic outflow regardless of their chemical form, whereas vagal and renal sympathetic responses vary depending on triglyceride versus free fatty acid structure and on fatty acid species (ω-9 vs. ω-3). The results suggest the involvement of multiple long-chain fatty acid–sensing pathways—including vagal afferents, spinal afferents, and gut hormones (e.g., CCK, GLP-1)—that may underlie the time-dependent and region-specific patterns of sympathetic and vagal activation observed in this study. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Exendin-4 (Ex-4), a long-acting GLP-1 receptor agonist and the native peptide on which the antidiabetic drug exenatide is based, is known to acutely influence energy metabolism and autonomic function. However, the real-time relationship between substrate utilization and coordinated sympathetic–vagal activity has not been fully elucidated. This study aimed to determine how Ex-4 alters metabolic fuel selection and autonomic outputs in freely moving rats. Male Wistar rats were chronically implanted with electrodes for cervical vagal nerve activity (VNA), renal sympathetic nerve activity (RSNA), lumbar sympathetic nerve activity (LSNA), arterial pressure, ECG, and interstitial glucose monitoring, along with intraperitoneal, portal, and intravenous catheters. After recovery, Ex-4 (10 µg/kg) was administered via one of three routes, and oxygen consumption (VO 2 ), energy expenditure (EE), and respiratory quotient (RQ) were continuously recorded. VO 2 and EE remained largely unchanged. In contrast, RQ exhibited a biphasic response—an initial rise followed by a decline to ~0.75. Substrate analysis showed an early increase and subsequent decline in carbohydrate utilization, accompanied by a delayed increase in lipid utilization, indicating a shift from carbohydrate- to fat-dominant metabolism. Blood glucose increased during the fat-utilizing phase. Autonomic recordings revealed route-independent suppression of RSNA (~60%) immediately after Ex-4, whereas LSNA increased 15–40 min after administration. VNA increased promptly across all routes, with sustained elevation after intraperitoneal and intravenous injection. These findings demonstrate that Ex-4 induces a characteristic biphasic shift in metabolic fuel use without altering total energy expenditure. The increase in blood glucose during the fat-dominant phase may reflect enhanced hepatic glucose output driven by increased sympathetic nerve activity, highlighting a sympathetic mechanism that compensates for shifting substrate availability. This abstract was presented at the American Physiology Summit 2026 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

BACKGROUND: Exposure to cold environments is linked to cold-induced hypertension due to activated sympathetic nerve activity (SNA) and arterial baroreceptor reflex dysfunction. However, direct measurement of SNA during cold-induced hypertension and changes in baroreflex control of SNA remain unexplored. METHODS: Chronically instrumented rats were exposed to cold temperatures (10 °C) over 4 days after a control period (24 °C), and renal and lumbar sympathetic nerve activities were simultaneously measured during cold-induced hypertension. Baroreflex curves for renal SNA (RSNA) and lumbar SNA and heart rate were generated by altering arterial pressure via a bolus intravenous infusion of vasoactive drugs. RESULTS: RSNA increased immediately after cold exposure, increased progressively throughout the 4-day period, and remained high after the cold exposure ended. Cold exposure shifted the RSNA baroreflex curve to the right and upward, gradually increasing the upper plateau (maximum capacity of sympathetic drive). The upper plateau remained elevated even after the cold exposure ended. Conversely, cold exposure increased lumbar SNA, heart rate, and arterial pressure, which subsequently returned to control levels after the cold exposure ended. These data indicate that cold exposure increases the maximum capacity to drive renal SNA in a regionally different and time-dependent manner through cumulative effects. CONCLUSIONS: Four days of cold exposure resulted in reversible effects increasing arterial pressure via lumbar SNA and heart rate, alongside time-dependent cumulative effects on RSNA. This study provides direct evidence of a self-activating pathway for RSNA that is activated by cold exposure, thus initiating cold-induced hypertension.

The current study aimed to propose a method to directly measure right cervical vagal nerve activity (cVNA) alongside renal sympathetic nerve activity (RSNA) in conscious rats. The right cervical vagus nerve was surgically exposed and fitted with a bipolar electrode to record cVNA. A microcatheter was used to administer levobupivacaine to selectively block afferent cVNA. Upon levobupivacaine administration, cVNA was reduced by 84%, enabling the exclusive assessment of efferent cVNA. Intravenous and intraperitoneal administration of cholecystokinin-8 (CCK-8) demonstrated that peripherally acting CCK-8 influences the central nervous system through afferent cVNA without affecting the RSNA or efferent cVNA. This technique can be highly applicable for quantifying the dynamic changes in the interaction between vagal and sympathetic nerve activities, thereby shedding light on their roles in maintaining homeostasis and developing autonomic dysfunction, as in obesity and diabetes.NEW & NOTEWORTHY This study proposed a method for directly measuring cervical vagal nerve activity and reversibly blocking afferent cVNA in conscious rats. It demonstrated that CCK-8, when administered intraperitoneally, distinctly influences peripheral afferent vagal nerve activity without affecting renal sympathetic nerve activity, arterial pressure, or heart rate.

Sympathetic nerve activity (SNA) and vagal nerve activity (VNA) play crucial roles in the homeostatic control of plasma glucose concentrations. However, the time course of changes in SNA and VNA during the onset of diabetes remains poorly understood. In this study, we induced type 1 diabetes using streptozotocin (STZ) and continuously monitored renal sympathetic nerve activity (RSNA), lumbar sympathetic nerve activity (LSNA), cervical VNA, heart rate, and heart rate variability before and after the onset of type 1 diabetes. [Methods] Male Wistar rats were chronically implanted with electrodes to measure electroencephalograms, electromyograms, electrocardiograms, RSNA, LSNA, and cervical VNA. Glucose sensors were used to monitor interstitial glucose concentrations. After a 5-day control period, STZ (65 mg/kg) was administered intraperitoneally to induce type 1 diabetes. All parameters were continuously recorded throughout the experiment. [Results] Following STZ administration, blood glucose concentrations rapidly increased within several hours, temporarily decreased, and then rose again, resulting in a sustained hyperglycemic state thereafter. Blood insulin concentrations showed changes mirroring those of blood glucose concentrations. Heart rate was the most sensitive parameter, with a gradual decline immediately after the onset of diabetes. LSNA significantly ( P <0.05) increased by approximately 40% from Day 1 onward compared with the control period. In contrast, cervical VNA, arterial pressure, and RSNA showed no significant changes after STZ administration. [Discussion] A major challenge of this study was the simultaneous and continuous monitoring of cervical vagal nerve activity, RSNA, and LSNA during the transition from a normal state to the onset of type 1 diabetes. The absence of significant changes in cervical VNA suggests that cervical VNA may not be involved in regulating blood glucose concentrations during the transition from normoglycemia to severe hyperglycemia (~350 mg/dL). Similarly, RSNA did not show any notable changes triggered by the onset of type 1 diabetes. However, the increase in LSNA with type 1 diabetes indicated an organ-specific sympathetic drive. These findings suggest that the persistent decline in heart rate after the onset of diabetes cannot be explained by changes in cervical VNA, RSNA, or LSNA. Based on these results, the following causal relationship is hypothesized to explain the decrease in HR and the increase in LSNA: the reduced insulin secretion caused by STZ leads to hyperglycemia, which is associated with decreased glucose availability as a substrate for energy production in muscle cells, including those of the heart. This reduction in energy supply likely contributes to the gradual decrease in HR. The increase in LSNA could be a compensatory mechanism to counteract the reduced glucose uptake by skeletal and cardiac muscles. Moreover, this heightened LSNA may help maintain systemic arterial pressure and ensure adequate tissue perfusion under conditions of impaired metabolic homeostasis caused by type 1 diabetes. JST (JPMJMS2023) This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

GLP-1 (Glucagon-Like Peptide-1) is a type of gastrointestinal hormone that plays an integral role in regulating glucose homeostasis and appetite control. GLP-1 receptors are expressed throughout the body, and it has been suggested that GLP-1 can be detected by vagal afferent nerve activity, leading to changes in sympathetic nerve activity. However, the details of the effects of GLP-1 receptor stimulation on autonomic nerve activity have not been reported. Therefore, this study investigated the effects of different sites of GLP-1 receptor stimulation on autonomic nerve activity by administering GLP-1 receptor agonists via three routes: intravenous (IV), intraportal vein (iport), and intraperitoneal (iperi). Male Wistar rats were chronically implanted with electrodes, catheters for measuring cervical vagal activity, renal and lumbar sympathetic nerve activity, electroencephalogram, electromyogram, electrocardiogram, arterial pressure, sensors for tissue fluid glucose concentration, and catheters for drug administration in the vein, portal vein, and abdominal cavity. Exendin-4, a GLP-1 receptor agonist, was administered to conscious rats via one of the following routes: intravenous, intra-portal vein, or intra-abdominal. Cervical vagal activity was increased in all routes of Exendin-4 administration. Renal sympathetic nerve activity was rapidly decreased by Exendin-4 administration and gradually recovered to pre-administration levels. There were no significant differences in renal sympathetic nerve activity among the different routes of Exendin-4 administration. On the other hand, lumbar sympathetic nerve activity increased slowly after Exendin-4 administration through the iperi and iport routes, while it decreased initially, then gradually increased following administration through the IV route. These results demonstrate that stimulation of GLP-1 receptors by Exendin-4 increases vagal nerve activity, decreases renal sympathetic nerve activity, and produces regionally different responses in lumbar sympathetic nerve activity depending on the site of stimulation. JST (JPMJMS2023). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Vagal nerve activity (VNA) and sympathetic nerve activity (SNA) have been known to influence each other and changes in their activity directly, but details on this remain unknown. This study used an alpha-2 adrenergic receptor agonist (dexmedetomidine) to study how SNA affects VNA in the conscious state. Electroencephalography, electromyography, electrocardiography, cervical VNA, renal SNA, and catheters for arterial pressure measurement and intravenous drug administration were measured after male Wistar rats were anesthetized and implanted with electrodes. Dexmedetomidine (50 micro g/kg) was intravenously administered in conscious rats. Cervical VNA decreased and reached its lowest values about 10 min after intravenous dexmedetomidine administration. However, renal SNA, electromyography, and heart rate decreased immediately after administration, whereas arterial pressure increased immediately. These results show that alpha-2 adrenergic receptor agonists simultaneously inhibit VNA and SNA. Furthermore, the present data suggest that excessive SNA activation increases norepinephrine release, inducing an increase in the concentration of circulating norepinephrine, which in turn inhibits SNA via negative feedback and suppresses VNA. JST (JPMJMS2023) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

In this review, by evaluating the responses during freezing, rapid eye movement (REM) sleep, and treadmill exercise, we discuss how multiple baroreflex loops arranged in parallel act on different organs to modulate sympathetic nerve activity (SNA) in a region-specific and coordinated manner throughout the body. During freezing behaviors, arterial pressure (AP) remains unchanged, heart rate (HR) persistently decreases, renal SNA (RSNA) increases, and lumbar SNA (LSNA) remains unchanged. The baroreflex curve for RSNA shifts upward; that for LSNA remains unchanged; and that for HR shifts to the left. These region-specific changes in baroreflex curves are responsible for the region-specific changes in RSNA, LSNA, and HR during freezing. The decreased HR could allow the heart to conserve energy, which is offset by the increased RSNA caused by decreased vascular conductance, resulting in an unchanged AP. In contrast, the unchanged LSNA leaves the muscles in readiness for fight or flight. During REM sleep, AP increases, RSNA and HR decrease, while LSNA is elevated. The baroreflex curve for RSNA during REM sleep is vertically compressed in comparison with that during non-REM sleep. Cerebral blood flow is elevated while cardiac output is decreased during REM sleep. To address this situation, the brain activates the LSNA selectively, causing muscle vasoconstriction, which overcomes vasodilation of the kidneys as a result of the decreased RSNA and cardiac output. Accordingly, AP can be maintained during REM sleep. During treadmill exercise, AP, HR, and RSNA increase simultaneously. The baroreflex curve for RSNA shifts right-upward with the increased feedback gain, allowing maintenance of a stable AP with significant fluctuations in the vascular conductance of working muscles. Thus, the central nervous system may employ behavior-specific scenarios for modulating baroreflex loops for differential control of SNA, changing the SNA in a region-specific and coordinated manner, and then optimizing circulatory regulation corresponding to different behaviors.

The vagus nerve innervates most of the organs in the thoracic and abdominal cavity and plays a central role in inter-organ networks through afferent and efferent vagal nerve activity. However, few attempts have been made to measure vagal nerve activity in the conscious state; thus, the nature of vagal nerve activity remains unclear. In this study, we attempted to develop a method to measure cervical vagal nerve activity in conscious, freely moving rats. Using male Wistar rats, the right cervical vagus nerve was dissected approximately 1 mm under anesthesia, and a bipolar electrode made of twisted stainless-steel wire was hooked onto the vagus nerve and fixed with silicone gel. A microcatheter for administering a long-acting local anesthetic (levobupivacaine hydrochloride 0.75%) was placed at least 5 mm peripherally from the electrode. Measurements were recorded under conscious and free-living conditions. The right cervical vagal nerve activity (rcVNA) showed continuous activity of approximately 20 μV at peak-to-peak potential. The rcVNA was reduced by approximately 80% after administering 30 μL of levobupivacaine through the microcatheter. This allowed us to block the afferent VNA and selectively measure the efferent VNA. Using this method, we observed that efferent rcVNA decreased during REM sleep compared with NREM sleep. Moreover, we succeeded in measuring rcVNA and renal SNA simultaneously and continuously in conscious rats.

New Findings What is the central question of this study? The functional relationships between central amygdala neuronal activity (CeANA) and sympathetic nerve activity in daily activities remain unclear. We aimed to measure CeANA, renal and lumbar sympathetic nerve activity (RSNA and LSNA, respectively), heart rate (HR) and arterial pressure simultaneously in freely moving rats. What is the main finding and its importance? The CeANA was significantly related to RSNA and LSNA and HR in a behavioural state‐dependent and regionally different manner; meanwhile, CeANA was tightly associated with RSNA and HR across all behavioural states. Thus, it is likely that the amygdala is a component of neural networks generating regional differences in RSNA and LSNA. Abstract The central amygdala (CeA) is involved in generating diverse changes in sympathetic nerve activity (SNA) in response to changes in daily behavioural states. However, the functional relationships between CeA neuronal activity (CeANA) and SNA in daily activities are still unclear. In the present study, we developed a method for simultaneous and continuous measurement of CeANA and SNA in freely moving rats. Wistar rats were chronically instrumented with multiple electrodes (100‐μm‐thick stainless‐steel wire) for the measurement of CeANA, renal SNA (RSNA) and lumbar SNA (LSNA), and electroencephalogram, EMG and ECG electrodes, in addition to catheters for measurement of arterial pressure (AP). During the transition from non‐rapid eye movement sleep to quiet wakefulness, moving and grooming states, a significant linear relationship was observed between CeANA and RSNA ( P < 0.0001), between CeANA and LSNA ( P = 0.0309), between CeANA and heart rate (HR) ( P = 0.0123) and between CeANA and EMG ( P = 0.0089), but no significant correlation was observed between CeANA and AP ( P = 0.5139). During rapid eye movement sleep, the relationships between CeANA and RSNA, LSNA, HR, AP and EMG deviated from the previously observed linear relationships, but the time course of RSNA and HR changes was the mirror image of that of CeANA, whereas the time course of changes in LSNA and AP was not related to that of CeANA. In conclusion, CeANA was related to RSNA, LSNA and HR in a behavioural state‐dependent and regionally different manner, and CeANA was tightly associated with RSNA and HR across all behavioural states.

New Findings What is the central question of this study? Is the arterial baroreflex involved in causing patterned, region-specific changes in sympathetic nerve activity during freezing behaviour in conscious rats? What is the main finding and its importance? Freezing behaviour is accompanied by differential shifts in the baroreflex control of renal and lumbar sympathetic nerve activity and heart rate. It is noteworthy that baroreflex pathways may be discretely separated, allowing differential modification of baroreflex curves that may generate differential changes in sympathetic nerve activity during freezing behaviour. The present study was designed to test whether the baroreflex stimulus-response curves for renal sympathetic nerve activity (RSNA), lumbar sympathetic nerve activity (LSNA) and heart rate (HR) were shifted in a regionally specific manner during freezing behaviour in conscious rats. Male Wistar rats were chronically instrumented with electrodes and arterial and venous catheters for measurement of RSNA, LSNA and electrocardiogram. After a 60-min control period, freezing behaviour in conscious rats was induced by exposure to loud white noise (90 dB) for 10 min. The baroreflex curves for RSNA, LSNA and HR were generated by changing systemic arterial pressure using rapid intravenous infusions of vasoactive drugs and then fitted to an inverse sigmoid function curve. During the freezing behaviour, the baroreflex curve for RSNA was expanded upward with a significant (P < 0.001) increase (by 153% compared with the control level) in the upper plateau (maximum capacity of RSNA drive), whereas the baroreflex curve for LSNA remained unchanged. Conversely, the baroreflex curve for HR was shifted leftward with a significant (P = 0.004) decrease (by 11 mmHg relative to the control level) in the midpoint pressure. Our results indicate that baroreflex curve shifts for RSNA, LSNA and HR occur in a regionally specific manner during freezing behaviour. This indicates that baroreflex pathways may be discretely separated, allowing differential modification of baroreflex curves that may generate differential changes in sympathetic nerve activity during freezing behaviour.

Social defeat stress has been linked to depression, autonomic disorders, and cardiovascular disorders. The hippocampus has been implicated in the pathogenesis of depression, and hippocampal neuronal activity is presumed to be involved in autonomic disorders induced by social defeat stress. Potential linkages among hippocampal neuronal activities, sympathetic nerve activities, and cardiovascular function have received less attention. In the present study, we measured time courses of changes in hippocampal CA1 neuronal activity (CA1NA), renal sympathetic neuronal activity (RSNA), and lumbar sympathetic nerve activity (LSNA), arterial pressure (AP), and heart rate (HR) in response to social defeat stress in rats. Wistar rats were chronically implanted with electrodes for the measurement of CA1NA, RSNA, LSNA; electroencephalography, cervical electromyography, and diaphragm electromyography were performed, and a catheter was used to measure AP. Social defeat was induced by introduction of a Long–Evans rat, which was heavier and more aggressive than a Wistar rat, into the Wistar rat’s home cage for 30 minutes. The intrusion of the Long–Evans rat sometimes resulted in fighting between the Long–Evans and Wistar rats. Following defeat, Wistar rats displayed a submissive posture and exhibited immobilization for several minutes. Fighting caused immediate reduction of CA1NA, which remained suppressed during the period of submissive posture and immobilized behavior. However, the AP, HR, RSNA, and LSNA increased in transient fashion during immobilized behavior. These findings showed that the defeat stress considerably influenced CA1NA, whereas it marginally influenced RSNA, LSNA, AP, and HR. Therefore, it is likely that social defeat stress suppressed hippocampal function in tonic fashion, which could not be measured on the basis of sympathetic nerve activity and cardiovascular function.Support or Funding InformationJSPS Grant

Sympathetic nerve activation is considered an important contributor to mortality following acute myocardial infarction (MI). However, few studies have directly monitored sympathetic nerve activity (SNA) in response to acute MI. Herein, we directly and continuously monitored renal SNA (RSNA) and lumbar SNA (LSNA) before and after MI induced by left anterior descending artery (LAD) ligation. Wistar rats were instrumented with a telemetry transmitter and bipolar electrodes for continuous measurement of mean arterial pressure (MAP), heart rate (HR), RSNA, and LSNA. At 7 days after initial surgery, MAP, HR, RSNA, and LSNA were monitored continuously for 28 days. After 4 days of baseline measurements, rats received either LAD ligation via left thoracotomy (MI group; n=13) or sham surgery (n=11) under inhalation anesthesia. Rats in the MI group were subdivided into those that survived for 24 days (MI‐survivor group) and those that died within 3 days (MI‐3d group) after LAD ligation. Transthoracic echocardiography was performed before and aftJSOn day 1 in the MI‐3d group, LSNA increased by 202% ± 28% and MAP decreased by 38±4 mmHg compared with baseline values, while there were no changes in RSNA and HR. On day 1 in the MI‐survivor group, LSNA showed a trend towards an increase compared with baseline values, while there were no changes in RSNA and HR. In the MI‐survivor group, RSNA increased gradually from day 9, and peaked at day 24 (27%±14%) compared with the sham group, while there were no significant changes in MAP, HR, or LSNA. These data suggest that the RSNA may play an important role in compensating for impaired cardiac performance caused by MI, and that the LSNA and RSNA respond differently and in a region‐specific manner to MI.Support or Funding InformationJSPS Grant.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

To study the contribution of sympathetic nerve activity (SNA) to the development of hypertension, experiments were designed to continuously and simultaneously measure renal (RSNA) and lumbar SNA (LSNA) during the development of hypertension induced by 8% salt loading in Dahl salt-sensitive (DS) rats. Male DS and salt-resistant rats were instrumented with bipolar electrodes to record RSNA and LSNA and a telemeter to record arterial pressure (AP). AP increased during the first 3 days after the onset of salt loading by ≈10 mm Hg in both DS and Dahl salt-resistant rats. AP continued to increase progressively from day 4 to day 14 of salt loading by 33±1 mm Hg in DS rats, while it remained the same in Dahl salt-resistant rats. RSNA and LSNA increased in the initial few days by 6% to 8%, and decreased gradually thereafter, suggesting that increases in neither RSNA nor LSNA are directly linked with the progressive increase in AP induced by salt loading in DS rats. After the cessation of salt loading, AP pressure returned to the presalt loading level in both DS and Dahl salt-resistant rats. RSNA increased significantly by 32±3% after the cessation of salt loading, while LSNA remained the same in DS rats, suggesting that salt-sensitive mechanisms respond to a loss of sodium, not a gain, and selectively activate RSNA in DS rats. In summary, RSNA and LSNA are not likely to be a primary trigger to initiate the progressive increase in AP induced by 8% salt loading in DS rats.

Exercise modulates arterial pressure (AP) regulation over various time spans. AP increases at the onset of exercise and this increase is then sustained during exercise. Once exercise is stopped, AP is suppressed for up to an hour afterwards. Prolonged endurance training is associated with dysfunction of the sympathetic regulation of AP in response to posture changes (orthostatic intolerance). Baroreflex control of sympathetic nerve activity (SNA) has been extensively studied to understand the mechanisms underlying exercise-induced changes in AP. We have previously presented entire baroreflex AP-SNA curves during and after exercise, and during central volume expansion, obtained using direct measurements of renal sympathetic nerve activity (RSNA) in conscious animals. In this review, we describe the modulatory effects of exercise on baroreflex control of AP based on these entire AP-RSNA baroreflex curves. We suggest that both acute and chronic exercise can have modulatory effects on the entire baroreflex curve for SNA, and that these effects differ among time periods.

Acute myocardial infarction (MI) triggers an adverse increase in cardiac sympathetic nerve activity (SNA). Whereas β-adrenergic receptor (β-AR) blockers are routinely used for the management of MI, they may also counter β-AR-mediated vasodilation of coronary vessels. We have reported that ghrelin prevents sympathetic activation following MI. Whether ghrelin modulates coronary vascular tone following MI, either through the modulation of SNA or directly as a vasoactive mediator, has never been addressed. We used synchrotron microangiography to image coronary perfusion and vessel internal diameter (ID) in anesthetized Sprague-Dawley rats, before and then again 30 minutes after induction of an MI (left coronary artery ligation). Rats were injected with either saline or ghrelin (150 µg/kg, subcutaneously), immediately following the MI or sham surgery. Coronary angiograms were also recorded following β-AR blockade (propranolol, 2 mg/kg, intravenously). Finally, wire myography was used to assess the effect of ghrelin on vascular tone in isolated human internal mammary arteries (IMAs). Acute MI enhanced coronary perfusion to nonischemicregions through dilation of small arterioles (ID 50 to 250 µm) and microvessel recruitment, irrespective of ghrelin treatment. In ghrelin-treated rats, β-AR blockade did not alter the ischemia-induced vasodilation, yet in saline-treated rats, β-AR blockade abolished the vasodilation of small arterioles. Finally, ghrelin caused a dose-dependent vasodilation of IMA rings (preconstricted with phenylephrine). In summary, this study highlights ghrelin as a promising adjunct therapy that can be used in combination with routine β-AR blockade treatment for preserving coronary blood flow and cardiac performance in patients who suffer an acute MI.

The hippocampus has been suggested to play a significant role in adaptation to chronic stress. However, there has been lack of direct evidence for responses of hippocampal neuronal activity to chronic stress. The present study was aimed to record hippocampal CA1 neuronal and sympathetic nerve activities during chronic stress. Wistar rats were instrumented chronically with a combined probe made with multiple electrodes (100 micrometer stainless steel wires) for measurement of hippocampal CA1 neuronal activity and glass fiber for measurement of hippocampal cerebral blood flow (CBF), electrodes for measurements of renal (RSNA) and lumbar (LSNA) sympathetic nerve activity, and electroencephalogram, electromyogram, and electrocardiogram and with catheter for measurement of systemic arterial pressure (AP). Rats were exposed repeatedly to restraint water‐immersion stress (RWIS) for 90 min/day over 5 days. Hippocampal CA1 neuronal activity, RSNA, and LSNA were measured continuously and simultaneously before, during, and after RWIS. Hippocampal CA1 neuronal activity decreased immediately after onset of RWIS and the decreased level was maintained throughout the 90 min of RWIS on the first day of stress exposure. On day 5 of RWIS, hippocampal CA1 neuronal activity decreased immediately after onset of RWIS, however it gradually recovered to the control level during the RWIS period. Thus, hippocampal CA1 neurons gradually adapted to the repeated RWIS exposure while RSNA and LSNA increased immediately after the onset of RWIS and showed no adaptive response during repeated exposure to RWIS. Support or Funding Information JSPS Grant This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .