Continuous electrical stimulation of the cut synpathetic innervation to perfused gracilis muscles restored vasoconstrictor tone and active dilatation resulted when stimulation was terminated. This dilatation was unaffected by cholinergic blockade but was blocked by the antihistamine tripelennamine. Prior vasoconstriction was not required to produce active dilatation since sympathetic stimulation applied during infusion of xylocholine (betaTM10) produced no vasoconstrictor response yet an antihistamine-sensitive vasodilatation appeared when stimulation ceased. This dilatation was also blocked by the alpha-adrenergic receptor blocker phentolamine even though adrenergic vasoconstrictor tone was absent. These results suggest that the release of histamine from its storage site is mediated by an alpha-receptor mechanism. Since betaTM10 abolished adrenergic vasoconstriction but preserved histamine-mediated vasodilatation that could be prevented by alpha-adrenergic blockade, it is proposed that histamine release may be under the control of separate adrenergic fibers without a vasoconstrictor function. This mechanism may underlie the process of active reflex vasodilatation since upon reflex withdrawal of tonic sympathetic activity an antihistamine-sensitive vasodilatation occurs.

The effect of metabolic inhibitors on myogenic tone, norepinephrine and barium chlorideinduced contractions, adenosine triphosphate (ATP) content, 45 Ca uptake and efflux and the total calcium content of tibial arteries were evaluated with the technique of superfusion in the absence and presence of ruthenium red, dinitrophenol, cyanide, azide and fluoroacetate. Ruthenium red did not affect myogenic tone despite a decrease in passive 45 Ca influx. Each of the remaining metabolic inhibitors decreased myogenic tone and ATP despite an increase in 45 Ca influx and total tibial artery calcium content. Dinitrophenol reduced slightly the contractile responses of tibial arteries to norepinephrine and almost abolished the contractile response to barium chloride. Cyanide, azide and fluoroacetic acid did not significantly alter the contractile responses of tibial arteries to norepinephrine or barium chloride. These data are consistent with the conclusions that myogenic tone and norepinephrine-induced contraction can be differentially inhibited by inhibition of metabolism and calcium uptake. Inhibitors of oxidative metabolism decreased myogenic tone with little inhibition of the responses to vasoactive stimuli. These data suggest that myogenic tone is in some manner dependent on a functional tricarboxylic acid cycle and oxidative phosphorylation. Inhibition of resting calcium influx did not affect myogenic tone. Therefore, myogenic tone does not appear to be primarily dependent on the fraction of passive calcium influx inhibited by ruthenium red. In addition, the ability of ATP-deficient, metabolically inhibited tibial arteries to contract to norepinephrine and barium chloride suggests that energy for norepinephrine and barium chloride-induced contractions do not appear to be dependent on preformed existing stores of ATP generated via the tricarboxylic acid cycle and oxidative phosphorylation or that a large safety factor exists for maintaining contractile integrity of this preparation.

The effect of metabolic inhibitors on norepinephrine (NE), epinephrine (E), tyramine (T), serotonin (5-HT), potassium chloride (KCl), and barium chloride (BaCl2) induced contraction was evaluated with the superfused canine dorsal metatarsal veins. ATP content was evaluated in the absence and presence of dinitrophenol, cyanide, azide, fluoroacetate, and iodoacetate. Contractile responses to vasoactive stimuli were measured before and during continuous superfusion with these inhibitors. Each of the metabolic inhibitors decreased tone and ATP. Dinitrophenol reduced the contractile responses of tibial arteries to NE, E, 5-HT, and KCl but abolished the contractile response to T and BaCl2. Cyanide and fluoroacetic acid did not significantly alter the contractile responses of tibial arteries to KCl or E but reduced the contractile responses to T, 5-HT, NE, and BaCl2. Azide reduced the responses to KCl, 5-HT, and T but not to NE, E, or BaCl2. Fluoroacetic acid reduced the responses to tyramine and serotonin but not to NE, E, KCl, or BaCl2. These findings are consistent with the conclusions that (1) vasoactive stimuli utilized different metabolic pathways to sustain their contractile response, (2) the adrenergic neuronal uptake mechanism or release process for catecholamines is more sensitive to metabolic inhibition than the contractile process, and (3) myogenic tone is more dependent on a functional oxidative metabolic pathway than the contractile responses to vasoactive stimuli.

Superfused helical strips of canine anterior mesenteric arteries relaxed in approximately 12% of the preparations when challenged with vasoconstrictor agents such as serotonin, norepinephrine, barium chloride and KCl. The muscle fibers in most of these preparations were longitudinally oriented.

The aortic depressor reflex cannot be elicited in anesthetized dogs during continuous carotid sinus nerve stimulation. It is postulated that the blockade of the aortic reflex is due to excitation of unidentified afferent fibers contained in the carotid sinus nerve, which probably do not arise from chemoreceptors and which are apparently not of the classical baroreceptor type since the selective stimulus of increased sinus pressure failed to block the aortic reflex.

ARTICLESActive vasodilatation evoked by stimulation of sinus nerves in the conscious dogDC Heitz, RA Shaffer, and MJ BrodyDC Heitz, RA Shaffer, and MJ BrodyPublished Online:01 May 1970https://doi.org/10.1152/ajplegacy.1970.218.5.1296MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAutonomic control of skeletal muscle blood flow at the onset of exerciseJohn B. Buckwalter, and Philip S. Clifford1 November 1999 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 277, No. 5Locomotor System: Skeletal MuscleCirculation to Skeletal Muscle1 January 2011Reflex cardiovascular responses induced by electrical stimulation of glossopharyngeal nerves in the ratJournal of Pharmacological Methods, Vol. 5, No. 1Baroreceptor and chemoreceptor reflexes in postganglionic neurones supplying skeletal muscle and hairy skinJournal of the Autonomic Nervous System, Vol. 2, No. 3Effects on the General Hemodynamics and Peripheral CirculationNeurogenic vasodilatationGeneral Pharmacology: The Vascular System, Vol. 9, No. 4EFFECTS OF GUANETHIDINE ON HISTAMINE RELEASE DURING REFLEX VASODILATATION IN THE DOG19 July 2012 | British Journal of Pharmacology, Vol. 60, No. 3Studies on the hemodynamic changes in the perfused hindlimb induced by the electrostimulation of the sinus nerve in the dogLife Sciences, Vol. 19, No. 9 More from this issue > Volume 218Issue 5May 1970Pages 1296-1300 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.218.5.1296PubMed4985607History Published online 1 May 1970 Published in print 1 May 1970 Metrics

The effect of furosemide on renal hemodynamics has been studied quite extensively. However, the possibility that the hemodynamic effects of furosemide are not limited to renal vessels and that this drug also affects other vascular beds has not been examined. In the present study the effect of furosemide on limb blood flow was assessed in unanesthetized dogs containing chronically implanted flow transducers and pressure cannulas. The results showed that the effect of flurosemide on limb blood flow differs quite markedly from the effect of this drug on renal blood flow. Furosemide increases renal blood flow but was found to produce a decrease in limb blood flow. Renal blood flow rose rapidly after drug administration, was elevated maximally by 10 minutes and had returned to the control level of flow by 30 minutes after drug administration. Limb blood flow, in contrast, decreased much less rapidly and remained below the control level of flow after reqal blood flow had returned to the control level of flow. Intraiiac infusions of furosemide failed to alter limb blood flow; whereas, intrarenal infusions of the drug produced almost immediate changes in renal blood flow. Changes in renal blood flow and limb blood flow produced by furosemide were not altered by prior treatment with the ganghionic blocking agent pentolinium. Thus, furosemide does not appear to act directly on limb vascular smooth muscle nor does it appear to decrease limb blood flow by an indirect neurogenic or reflex mechanism. However, when furosemide was given to nephrectomized dogs, it was found that bilateral nephrectomy abolished the decrease in limb blood flow produced by furosemide. It therefore appears that the sustained decrease in limb blood flow produced by furosemide administration may result from the action of a circulating vasoconstrictor substance elaborated by the kidney.

ARTICLESA device for chronic exteriorization of indwelling vascular cathetersD. C. Heitz, R. A. Shaffer, and M. J. BrodyD. C. Heitz, R. A. Shaffer, and M. J. BrodyPublished Online:01 May 1969https://doi.org/10.1152/jappl.1969.26.5.664MoreSectionsPDF (533 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByA hypertensive response to infusion of prostaglandin F2α into the vertebral artery of the conscious dogEuropean Journal of Pharmacology, Vol. 16, No. 2 More from this issue > Volume 26Issue 5May 1969Pages 664-666 Copyright & PermissionsCopyright © 1969 the American Physiological Societyhttps://doi.org/10.1152/jappl.1969.26.5.664PubMed5781624History Published online 1 May 1969 Published in print 1 May 1969 Metrics