1. The protease inhibitors Trasylol and soyabean trypsin inhibitor prevented the activation of plasma inactive renin by acid. 2. N-Ethylmaleimide inhibited acid-activation to some extent but o-phenathroline had no effect. 3. Acid-activation of the inactive renin in human plasma is mediated by a serine protease.
1. One major subprogramme of the North Karelia Project was the hypertension programme which aimed at lowering of the high blood pressure among the whole population, and expecially among middle-aged men. The hypertension programme consisted of intervention integrated with the existing health care structure of the county of North Karelia. 2. The hypertension register, which was the major tool of the programme, aimed to maintain patients in treatment and to get information about the development of the programme. Registration of hypertensive subjects was continuous between 1972 and 1977 and registered patients had annual follow-up examinations. 3. After 5 years of the programme, there were approximately 17 000 registered patients which is 9.7% of the total population. 4. Proportion of drop-outs at the annual follow-up examinations was less than 10%. 83% of the registered hypertensive subjects were under drug treatment after 3 years intervention. The percentage of normotensive subjects increased significantly year by year. 5. Preliminary results from the stroke register of the North Karelia Project indicate that the incidence of stroke decreased as hypertension control was improved.
1. 20 subjects with uncomplicated essential hypertension were studied, 10 of whom were on propranolol treatment. Several blood samples for determination of total and active renin were drawn simultaneously from the renal artery and vein after angiographic studies. 2. In all patients renal blood flow was measured by Hippuran-clearance at the time of blood sampling. Intrarenal blood flow was assessed by xenon-washout. 3. The results indicate that under basal conditions renin is secreted mainly in the active form, although secretion of inactive renin does occur. During propranolol treatment there is a tendency for secretion of active renin to be reduced.
Other| December 01 1978 The Isolated Perfused Rat Kidney B. D. Ross B. D. Ross 1Nuffield Department of Clinical Biochemistry, The Radcliffe Infirmary, Oxford, U.K. Search for other works by this author on: This Site PubMed Google Scholar Clin Sci Mol Med (1978) 55 (6): 513–521. https://doi.org/10.1042/cs0550513 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Cite Icon Cite Get Permissions Citation B. D. Ross; The Isolated Perfused Rat Kidney. Clin Sci Mol Med 1 December 1978; 55 (6): 513–521. doi: https://doi.org/10.1042/cs0550513 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search © 1978 The Biochemical Society and the Medical Research Society1978 Article PDF first page preview Close Modal You do not currently have access to this content.
1. 10,294 hypertensive patients were treated and followed by 2200 general practitioners under the supervision of 130 cardiologists and nephrologists. 2. The treatment groups, randomly allocated, were designated to use three distinct antihypertensive drugs, administered alone, and combined two-by-two. 3. Some 75% of patients had a supine diastolic blood pressure of less than 95 mmHg after 4 months treatment. 4. A total of 12% of patients had dropped out by 4 months from entry; no clear relationship was established between side effects and drop out.
1. Data have been combined from three previous series to provide revised standards for the prediction of physiological dead-space volume (VD), arterial oxygen tension (Pa,O2), alveolar-to-arterial oxygen-tension difference (PAO2--Pa,O2) and venous admixture fraction (QVa/Qt) in the sitting position. 2. These standards, based on measurements in 96 healthy men and women aged from 20 to 74 years, largely confirm conclusions drawn from the first series of 48 subjects. 3. VD is best predicted on age, height, tidal volume and the reciprocal of respiratory frequency. Pa,O2,(PA,O2--Pa,O2) and Qva/Qt are adequately predicted on age alone.
1. Captopril or SQ 14 225, administered orally twice a day, reduced the blood pressure of hypertensive patients whatever their clinical diagnosis and even when their plasma renin activity was 'normal' or low. 2. Long-term administration of captopril, either alone or together with diuretics, provides a powerful new tool with which to treat ambulatory hypertensive patients. 3. The renin system may play an important role in maintaining blood pressure in a majority of hypertensive patients.
1. Blood pressure, height, weight and 24 h urinary output of sodium, potassium and creatinine were measured in over 500 adults of each sex during a health survey of the population of a small town. 2. Both systolic and diastolic pressure were significantly related to Quetelet's index (weight/height2) and heart rate. 3. There was no significant relationship between blood pressure and output of sodium or potassium, sodium/potassium ratio or sodium/creatinine ratio.
1. The response of active and inactive plasma renin to orthostasis and frusemide and to inhibition of prostaglandin synthesis by indomethacin was tested in normal human volunteers. 2. Active renin increased by orthostasis and frusemide and decreased by indomethacin. The latter also blunted the increase of active renin after stimuli. 3. Inactive renin was slightly increased by orthostasis, but was not significantly influenced by acute administration of frusemide or inhibition of prostaglandin synthesis by indomethacin. 4. The results show differences in the response of active and inactive renin to stimuli and suppression. Opposite changes of active and inactive renin were not observed in the experimental conditions studied.
1. In normally hydrated rats prostaglandin F2α (PGF2α) in doses of 5 μg/100 g body weight given subcutaneously every 2 h (three times) induced a significant increase in urinary kallikrein activity, and in sodium, potassium and water excretion for 8 h after the first injection. In moderately hyperhydrated rats loaded 2·5% of body wt. with 0·5% NaCl solution, PGF2α produced similar changes in kallikrein activity and electrolyte excretion. 2. In normally hydrated rats prostaglandin E2 (PGE2) in the same conditions and doses as in 1 had no effect on kallikrein activity, showing a tendency to decrease potassium and water excretion. 3. PGE2 in doses of 5, 12·5 and 25 μg/100 g body wt. in overhydrated rats given 2·5% and 0·5% NaCl and 5% of tap water/100 g body wt. 1 h later, significantly increased kallikrein activity in the urine collected for 120 min after the injections. A significant decrease in potassium and water excretion was observed with the highest dose. 4. PGF2α, had no effect on kallikrein activity in overhydrated rats, but an increase in sodium and a decrease in potassium excretion was seen at the highest dose. 5. The different actions of PGE2 and PGF2α may be part of a regulatory mechanism associated with the kallikrein—kinin system which contributes maintainance of extracellular fluid homeostasis.
Conference Abstract| December 01 1978 Nomenclature of Experimental Renal Hypertension: Report of the Nomenclature Committee of the International Society of Hypertension Dr D. Ganten Dr D. Ganten Search for other works by this author on: This Site PubMed Google Scholar Clin Sci Mol Med (1978) 55 (s4): 211s. https://doi.org/10.1042/cs055211s Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation Dr D. Ganten; Nomenclature of Experimental Renal Hypertension: Report of the Nomenclature Committee of the International Society of Hypertension. Clin Sci Mol Med 1 December 1978; 55 (s4): 211s. doi: https://doi.org/10.1042/cs055211s Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsClinical Science Search Advanced Search Keywords: Nomenclature Committee Report, renal hypertension This content is only available as a PDF. © 1978 The Biochemical Society and the Medical Research Society1978 Article PDF first page preview Close Modal You do not currently have access to this content.
1. Twenty-five patients with mild essential hypertension, identified during a survey of a population born in 1936, were investigated. 2. Basal and post-frusemide values for plasma renin concentration and plasma angiotensin II concentration did not differ markedly from reference values in 25 40-year-old control subjects. In the untreated, sodium replete state saralasin infusion (5·4 nmol min−1 kg−1) produced an increase in mean arterial pressure in the patient group as a whole. 3. Twenty-one patients were treated with hydrochlorothiazide, mean dose 75 mg/day for 3 months. Pre-treatment, frusemide-stimulated plasma renin concentration and plasma angiotensin II, and values during thiazide treatment were higher in ‘non-responders’ (n = 10) to hydrochlorothiazide treatment than in ‘thiazide-responders’ (n = 11). During thiazide therapy, angiotensin II blockade induced a clear-cut decrease in mean arterial pressure in all ‘thiazide-nonresponders’ whereas only four out of 11 ‘thiazide-responders’ showed a borderline decline in mean arterial pressure. 4. The functional significance of the renin—angiotensin system in mild essential hypertension emerges only after thiazide treatment. Thiazide-induced stimulation of the renin—angiotensin system counter-balanced the hypotensive effect of thiazide in some 40% of the treated patients. Thus the responsiveness of the renin—angiotensin system determined the blood pressure response to thiazide treatment.
1. Ouabain-sensitive uptake of 86Rb, a measure of the Na+-K+ pump activity, was studied in tail arteries of rats made hypertensive with deoxycorticosterone and saline. 2. Decreased activity of the ouabain-sensitive Na+-K+ pump supports the hypothesis that the activity of Na+-K+ pump is suppressed in volume expanded hypertension.
1. The serum concentrations of cholesterol and triglycerides were measured before and during the treatment of hypertension. Thirty-six patients were treated with hydrochlorothiazide and 29 with spironolactone. 2. Serum cholesterol increased from 214 to 227 mg/100 ml (P less than 0.005) and triglyceride did not change during treatment with hydrochlorothiazide. Serum triglyceride increased from 112 to 133 mg/100 ml (P less than 0.05) and cholesterol did not change during treatment with spironolactone. 3. Serum lipid responses to diuretics varied among patients. To identify patients susceptible to larger increases, subgroup analysis was carried out. Patients who were younger and had lower pretreatment serum cholesterol and systolic blood pressure had larger increments in cholesterol during treatment. In these subgroups coronary risk status did not improve during therapy. 4. The incidence of myocardial infarction may not be reduced so long as diuretics serve as first-line drugs in the treatment of mild hypertension.
1. Serial venous blood samples were obtained from 45 patients with acute myocardial infarction. Ten of these patients were receiving beta-adreno-receptor-blocking drugs at the time of onset of chest pain and continued on these drugs during their stay in the coronary care unit. The activities of creatine kinase and its MB-isoenzyme (CK-MB) were assayed in the plasma. A lysosomal enzyme, beta-N-acetylglucosaminidase, was also assayed. 2. In the 35 untreated patients it was found that creatine kinase activity was maximal at a mean time of 21.3 +/- 1.3 h after the onset of chest pain, whereas in the patients receiving beta-adrenoreceptor-blocking drugs peak activity of the enzyme occurred at 24.4 +/- 0.7 h. 3. Peak CK-MB acitivity was also delayed from 18.1 +/- 1.6 h in the control group to 22.4 +/- 1.2 h in the treated patients. 4. The lysosomal enzyme showed a similar pattern of changes to that of CK-MB. Maximum activity in plasma occurred at 18.0 +/- 1.0 h after the onset of chest pain in the control group of patients. In the treated patients peak lysosomal enzyme activity was not found until 24.2 +/- 1.2 h. 5. These alterations in the time-course of plasma enzyme changes after acute myocardial infarction are consistent with the suggestion that beta-receptor antagonists may delay tissue damage during myocardial ischaemia.
1. Almost all the factors that may cause a rise in blood pressure are, in turn, influenced by the increase in blood pressure per se. Thus any primary involvement of one or more of these factors in the pathogenesis of essential hypertension must be evaluated before or during the development of hypertension. 2. Young normotensive subjects both of whose parents are hypertensive have a much higher probability of developing hypertension than those whose parents are both normotensive. 3. The following measurements were made in 56 subjects of the first group (both parents hypertensive) and 35 of the second group (both parents normotensive), matched for age, sex and body surface area: renal plasma flow and glomerular filtration rate, using p-aminohippurate and inulin clearance; 24 h urinary excretion of aldosterone, protein and electrolytes; plasma renin activity; plasma volume. Plasma catecholamines and cardiac index were also measured in 26 subjects of the first group and 25 subjects of the second group using a radioenzymic method and echocardiography. 4. All these factors were similar in the two groups except that renal plasma flow was higher in the first group (767·2 ± 30 versus 650·7 ± 17 ml/min, P < 0·01). Plasma renin activity tended to be lower in subjects with a higher renal plasma flow, but there was no significant negative correlation between the two factors. 5. The possibility that the higher renal plasma flow in subjects with a high probability of developing hypertension is a compensatory mechanism for a primary intrarenal defect is discussed.
1. Vitamin B12 absorption was measured in 18 patients with tropical malabsorption. 2. Absorption was particularly impaired in patients with severe mucosal lesions. 3. Sequential measurements with 57Co- and 58Co-labelled vitamin B12 were made before and 48 h after the start of tetracycline therapy. A rapid improvement (on average 22% increase in absorption) occurred in four of six patients with marked mucosal lesions. Further improvement occurred in four of five patients measured after 4 weeks' tetracycline, including the two who failed to improve initially. 4. These rapid changes in vitamin B12 absorption after antibiotics occur too early to be due to mucosal recovery and suggest that bacterial metabolism is an important factor in the malabsorption in these patients.
1. The properties of inactive and active renin in human plasma and amniotic fluid were studied chromatographically. Activation was achieved at pH 3.3 with and without added pepsin. 2. Acid activation of renin was time- and temperature-dependent but was inhibited by dilution of the sample. The dilution effect was corrected by adding pepsin. Such characteristics indicate that activation at low pH is catalysed by intrinsic enzymes. 3. Separation and/or dilution of the activating enzyme during ion-exchange chromatography concealed the eluted position of inactive renin and reduced the amount recovered. Only after full activation of the eluted renin was achieved with added pepsin was a distinct peak of inactive renin exposed. 4. At pH 7.5 inactive renin carried a lower negative charge than the active enzyme. This charge difference was lost after activation. 5. No molecular-weight differences between active, inactive renin or the International Renin Standard were detected by gel filtration. No renin of larger molecular weight was present. 6. These findings will be helpful in purification studies of human inactive renin.
1. Human alpha1-antitrypsin was isolated with preserved microheterogeneity from subjects of Pi types M, S and MMalton. The M-protein was partially (20%) and completely desialylated. The proteins were labelled with either 125I or 131I. 2. The disappearance rate of these alpha1-antitrypsins was studied after simultaneous injection of the two types of labelled protein into Pi M subjects. The fractional catabolic rates of S- and MMalton-protein were 0.36 and 0.34 day(-1) respectively compared with 0.28 day(-1) for M-protein. The ratio of extravascular to plasma pools was 1.4 for S- protein and 1.6 for MMalton-protein. The 20% desialylated M-protein showed an increase of about 100% in its fractional catabolic rate. The disappearance rate of completely desialylated alpha1-antitrypsin was extremely rapid. 3. The slightly higher fractional catabolic rate of S- than of M-protein can only partly explain the 40% lower plasma concentration in subjects of Pi type S. Similarly the slight increase in catabolic rate of Pi MMalton- protein is too small to explain why the alpha1-antitrypsin content of the blood in Pi MMalton subjects is only 15% of that normally found. A low hepatic secretion seems to be the major cause of the low alpha1-antitrypsin concentration found in subjects of types Pi S and MMalton, as in Pi type Z.
1. Plasma adrenaline and noradrenaline were measured in supine and upright positions in 27 essential hypertensive patients and in 12 age-matched control subjects. 2. Plasma adrenaline was markedly increased in a large proportion of patients, compared with control subjects, either in supine or in upright positions, whereas no significant differences were found in plasma noradrenaline. 3. Six hypertensive patients were chronically treated with beta-adrenoreceptor-blocking agents (five with propranolol and one with pindolol). Plasma noradrenaline was not significantly changed in the supine position but was markedly increased on standing in four out of six patients. Plasma adrenaline was decreased in five out of six patients either in suprine or upright positions. 4. These findings support the view that the adrenergic system participates in the mechanism of essential hypertension.
