Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal and vascular responsiveness to graded doses of angiotensin II (A II) were recorded for seven normal subjects and 12 patients with essential hypertension while in balance on an intake of 200 mEq sodium/100 mEq potassium. Patients with essential hypertension had been previously studied and known to have normal responses of plasma renin activity to sodium restriction and upright posture. A II was administered for 30 minutes at rates of 0.1, 0.3, 1, and 3 ng/kg per minute and plasma aldosterone responses were assessed 20 and 30 minutes later; blood pressure was monitored at intervals of 1 minute during infusion of A II at each rate. A significant increment in plasma aldosterone occurred at an infusion rate of 0.3 ng/kg per minute in patients with hypertension. This change was not seen until the infusion rate reached 1.0 ng/kg per minute in the normotensive control subjects. Even at an A II infusion rate of 1 ng/kg per minute, the increment in plasma aldosterone levels in normotensive subjects (4.2 +/- 0.6 ng/dl) was significantly less (P less than 0.001) than that in patients with essential hypertension (19 +/- 3 ng/dl). In both groups, a significant rise in mean arterial blood pressure occurred at an A II dose of 0.3 ng/kg per minute, but the pressor response of the hypertensive group was significantly greater at the highest infusion rate (3 ng/kg per minute) (P less than 0.05). Thus, enhanced adrenal and pressor responsiveness to infused A II was observed in the hypertensive subjects, suggesting a change in A II receptor affinity.
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PMID:Enhanced aldosterone response to angiotensin II in human hypertension. 17 61

Adrenal steroid secretion rates and the renin-angiotensin-aldosterone (RAA) system were studied in the normothermic marmot. Adrenal secretion by the anesthetized, laparotomized marmot was (mean +/- SEM); aldosterone 1.2 +/- 0.3 ng/min, deoxycorticosterone 16.7 +/- 11.5 ng/min, corticosterone 15.2 +/- 7.8 ng/min, and cortisol 554 +/- 108 ng/min. Four forcings were investigated that affect feedback control at different sites: adrenocorticotropic hormone (ACTH) and angiotensin II (AII) infusion, sodium (Na) depletion, and Na loading. Plasma aldosterone, cortisol, Na, and potassium (K) concentrations as well as plasma renin activity (PRA) hematocrit (Hct), and in some studies, blood pressure were measured. ACTH infusion increased the plasma concentrations of aldosterone and cortisol. AII infusion increased aldosterone concentration, blood pressure, and Hct. Na depletion increased aldosterone, Hct, and PRA; plasma Na and K were decreased. Aldosterone concentration, Hct, and PRA decreased after salt loading. Normothermic, salt-depleted marmots demonstrated a pronounced fall in blood pressure following infusion of the AII analog, 1-sarcosine-8-alanine AII. The average plasma values for aldosterone, PRA, and cortisol found in 44 control animals were: aldosterone 3.8 +/- 0.3 ng/100 ml, PRA 1.9 +/- 0.2 ng AI-ml-1-h-1, and cortisol 54 +/- 4 ng/ml. It was concluded that normothermic marmots have a RAA system comparable to other mammalian species.
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PMID:Renin-angiotensin-aldosterone system of the normothermic marmot. 19 79

Restraint causes an increase in plasma renin activity (PRA) which is not affected by pretreatment with dl-propranolo (1 mg/kg IP) or sotalol (15 mg/kg IP). These doses of beta-adrenergic blocking agents are effective in suppressing the stimulation of PRA by isoproterenol. Large doses of dl-propranolol (10 mg/kg IP) and d-propranolol (5 mg/kg IP) attenuate the restraint-induced PRA increase. Adrenal demedullectomy does not affect the PRA response to restraint. Renal denervation blunts the PRA rise due to restraint, but not to direct stimulation by the beta-adrenergic agonist, isoproterenol. It is concluded that the increase in PRA during restraint stress in rats is not solely dependent on an intact renal sympathetic innervation. A significant portion of this stress-induced PRA increase appears to involve a non-adrenergic mechanism.
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PMID:On the mechanism of renin release by restraint stress in rats. 20 48

Plasma renin activity (PRA) was measured in 14 control subjects and 27 patients with essential hypertension (EH) (low renin group: 9, normal renin group: 11, and high renin group: 7) before and after the following stimulation tests. Test procedures: 1) Circadian rhythm (0600, 1600 and 2400h). 2) Adrenal stimulation test (ACTH: 12.5 I.U.). 3) Adrenal suppression test (Dexamethasone: 1.0 mg). 4) Metopirone test (1.5 g). 5) Angiotensin II infusion test (8 ng/kg/min). 6) Saline infusion test (1000 ml/hr). Patients with low PRA showed significantly lower levels of PRA than those of other two groups in circadian rhythm, after 2 hours of ACTH infusion and after angiotensin II infusion. Furthermore, these patients showed significantly higher responses of PRA than other two groups after furosemide test under dexamethasone and after metopirone test. In case of saline infusion test, patients with low and normal PRA did not show significantly decreased levels of PRA after the infusion, though all patients with high PRA and all control subjects showed significantly decreased levels of PRA. From the present studies, it might be concluded that patients with low PRA has an unknown mineralocorticoid excess which is ACTH dependent and 11 hydroxylated and some of hypertensive patients have an abnormality in their renin-angiotensin-aldosterone volume feed back loop as a factor for hypertension.
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PMID:Pathogenesis of essential hypertension with low renin: responses of plasma renin activity to various stimulation tests in essential hypertension. 21 18

Glucocorticoid stimulation and suppression tests are essential to the definitive diagnosis of diseases of the hypothalamic-pituitary-adrenal axis, because they document abnormal physiologic control of hormonal secretion. Similarly, diseases of the renin-angiotensin-aldosterone axis are diagnosed by mineralocorticoid stimulation and suppression testing. [Ed. Note: See Moore TJ, Williams GH: Adrenal causes of hypertension, in this issue.] Unlike tests of glucocorticoid function, testing of the renin-angiotension-aldosterone system is more complicated, because knowledge of posture and dietary sodium are necessary to interpret the results. However, measurement of the tropic hormone renin and plasma levels of aldosterone can be accurately made, allowing precise definition of this system. Errors are most commonly encountered when dynamic tests of cortisol output are performed in patients taking medications that may interfere with the assays or with the metabolism of the administered compounds, such as dexamethasone or metyrapone. Abnormal, spurious values may also be obtained in some individuals who do not have adrenocortical hyperfunction if they are very obese or if testing is performed in a setting of clinical stress. Careful attention to these pitfalls will avoid errors and allow the clinician to arrive at the correct diagnosis.
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PMID:Adrenal function testing. 21 24

Angiotensin II and its C-terminal heptapeptide fragment, [des-Asp1]angiotensin II, influence a variety of angiotensin receptors in a qualitatively similar manner. On the basis of potency studies, angiotensin II appears to be the important mediator of the renin-angiotensin system at the peripheral arteriolar receptors to maintain arterial blood pressure. However, both angiotensin II and the heptapeptide are approximately equally potent at receptor sites in the adrenal cortex, the renal arterioles, and the juxtaglomerular cells of the kidneys. Adrenal cortical receptor affinity appears to be greater for the heptapeptide than for angiotensin II. Analogues of the heptapeptide are better antagonists than analogues of the octapeptide in blocking the steroidogenic responses to both angiotensin II and heptapeptide. Circulating plasma levels of [des-Asp1]angiotensin II appear to be low in most species; there is strong evidence, however, that local generation of heptapeptide can occur under certain conditions. It seems likely that both peptides act at common receptor sites to mediate the response to the renin-angiotensin system but more data are needed before a definite physiologic role can be assigned to the heptapeptide.
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PMID:[Des-Asp1] angiotensin II: mediator of the renin-angiotensin system? 32 Dec 57

In submaxillary sialoadenectomized and nephrectomized mice aggressive behaviour provoked 5 to 40-fold increases in plasma renin concentration. The changes in renin concentration with time were different in different groups of confronted mice with only partial correlation between the pattern and the observable degree of fight. The changes were similar in sialoadenectomized mice with untouched kidneys as in sialoadenectomized and nephrectomized, indicating that aggression causes no measurable, if any, renal renin release. Repeated aggression with 2 hourly intervals provoked repeated renin release from extrarenal and extrasubmaxillary sources. The renin concentrations of different organs showed the same mutual relationship as in other mammals, but were about 10-fold higher. Splenectomy was without effect on the aggression-provoked renin release. Antibodies against pure mouse renin neutralized the renin in plasma and organs, which contained only insignificant, if any, pepsin activatable inactive renin. Adrenaline, apomorphine, carbachol and dihydralazine were as isoprenaline and noradrenaline without effect on renin release in sialoadenectomized and nephrectomized mice.
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PMID:Aggression-provoked renin release from extrarenal and extrasubmaxillary sources in mice. 39 25

Adrenal incompetence developed in rats 6 weeks after adrenalectomy without any salt and hormonal compensation. In individual fragments of the isolated glomeruli containing juxtaglomerular cells (JGC) renin activity increased 1.2 times on the average, and there was revealed renin-like activity (RLA) in the fragments containing mesangial cells (MC). Signs of intensified renin secretion (expressed in reduction of granule count, marked development of granular endoplasmic reticulum, Golgi complex and microtubules) were noted in the JGC. In MC such organoids were well developed, but no granules were revealed. The following occurred in 8 to 12 weeks with the restoration of the 11-OCS and sodium level in the plasma: renin JGC activity became normal, RLA activity in MC disappeared, and the initial ultrastructure of both of these cells was restored. The reserve role of MC as the source of renin-like substances was confirmed.
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PMID:[Dynamics of renin production by the juxtaglomerular and mesangial cells of individual rat kidney glomeruli following adrenalectomy]. 42 Sep 31

Participation of the renin-angiotensin system in the potentiation of responses to adrenergic nerve stimulation in the pump-perfused dog paw was studied during suprarenal aortic constriction. Vasoconstrictor responses in the paw were elicited by norepinephrine injected intra-arterially and by sympathetic nerve stimulation in a control session and during suprarenal aortic constriction (cephalad to the origin of one or two renal arteries). Aortic constriction decreased renal blood flow by approximately 50% and increased systemic blood pressure and plasma renin activity. The vasoconstrictor responses to norepinephrine and nerve stimulation were not significantly affected when the constriction was cephalad to only one renal artery, but there was a 31% increase in the response to stimulation at 5 Hz during aortic constriction above two renal arteries. There was an approximate 2-fold greater increase in plasma renin activity during the latter than in the former case. Saralasin administered intra-arterially to the paw reversed the adrenergic potentiating effect of aortic constriction. These results indicate that when the renin-angiotensin system is activated by restricting renal blood flow, sufficient circulating endogenous angiotensin is formed to cause a moderate adrenergic potentiating effect in the canine cutaneous circulation of the paw.
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PMID:Blockade by saralasin of adrenergic potentiation induced by renin-angiotensin system. 44 37

Adrenal steroids and compenents of the renin-angiotensin system were measured before and after adrenalectomy in a woman with Cushing's syndrome and hypertension from a functioning adrenocortical adenoma. Aldosterone, deoxycorticosterone and cortisol were produced in excess by the adenoma, and were measured in tumor tissue. High plasma renin substrate concentrations, and normal basal and furosemide-stimulated plasma renin activities and plasma renin concentrations which were present before surgery, decreased after adrenalectomy, and the hypertension diminished. The inappropriately normal levels of renin and potassium in this patient, despite autonomous aldosterone overproduction, suggest an ineffective mineralocorticoid action of aldosterone, possibly from interaction with her other adenoma-produced steroids. The decrease in components of the renin-angiotensin system suggests a partial renin-dependence of her hypertension.
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PMID:Hypertension and aldosterone overproduction without renin suppression in Cushing's syndrome from an adrenal adenoma. 47 1


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