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)

The renin-angiotensin-aldosterone system in patients with acromegaly was evaluated by infusing [sarcosine1, isoleucine8]angiotensin II, a competitive angiotensin II antagonist, into five acromegalic patients with hypertension and three normotensive acromegalics. The drug was infused at a rate of 600 ng/kg . min for 30 min, 1 h after iv injection of 40 mg furosemide. In addition, before the infusion, plasma samples were obtained for determination of PRA and plasma aldosterone concentration. A significant pressor response to [sarcosine1, isoleucine8]angiotensin II was observed in all eight patients. Preinfusion PRA and plasma aldosterone concentration were significantly lower than in normal controls. It is concluded that in acromegaly, the renin-angiotensin-aldosterone system is suppressed and that this system is probably not involved in maintenance of the high blood pressure observed in some acromegalic patients.
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PMID:Blood pressure response to an angiotensin II antagonist in patients with acromegaly. 42 97

The behaviour of the renin-angiotensin-aldosterone system was evaluated in 16 acromegalic patients, of whom 7 were hypertensive. The patients were studied in basal conditions, after suppression with 9alpha-fluorohydrocortisone, and after stimulation with furosemide. Baseline and after furosemide PRA were significantly lower in acromegalic hypertensive patients than in the normotensive group. Mean urinary aldosterone excretion was found at the upper limits of the normal range; it was occasionally elevated, but the values were not satistically different in the two groups. There was a suppression after 9 alpha fluorohydrocortisone in both groups, though it did not reached the 50%. These data show that there is a disorder of the renin-angiotensin-aldosterone system in acromegalic subjects. This defective regulation is sometimes similar to that present in primary aldosteronism. In fact in two patients a typical phlebographic and scintigraphic picture of primary aldosteronism has been found; surgery, performed in both patients, revealed a large cortical adenoma in one case and a macronodular hyperplasia in the second case. However, the relationship between this adrenal abnormalities and hypertension in acromegaly are not yet completely clarified.
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PMID:Plasma renin activity and urinary aldosterone in acromegaly. 48 12

1. In 29 patients with acromegaly, plasma renin activity and growth hormone were measured during fasting and recumbency on free diet. Exchangeable sodium was measured in all cases and expressed as a percentage of the expected value on the basis of lean body mass. 2. Twenty-two control subjects without evidence of cardiovascular, renal or endocrine disease were studied in the same way. 3. There was a significant increase in exchangeable sodium and suppression of plasma renin activity in the acromegalic patients in comparison with control subjects. 4. There was a significant positive correlation between exchangeable sodium and plasma growth hormone. 5. Hypertensive acromegalic patients (diastolic blood pressure larger than or equal to 100 mmHg) tend to have a lower (although not significantly so) exchangeable sodium than normotensive subjects. 6. We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly.
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PMID:An investigation into the pathogenesis of hypertension in acromegaly. 87 24

The diurnal rhythm of plasma aldosterone concentration (PA), plasma renin activity (PRA), plasma cortisol (PC) and serum growth hormone (GH) were examined in 5 cases of normotensive acromegaly and the results were compared with the observations in normal subjects. Moreover, the response of PA to angiotensin-II infusion was studied in 6 cases of normotensive acromegaly. A normal diurnal rhythm with the lowest values in the evening or midnight and the highest values in the morning was observed in 3 of 5 cases in PA and 3 of 4 cases in PC. On the other hand, no apparent rhythm of GH was observed in any cases and that of PRA in 4 of 5 cases. Although there was a significant positive correlation between PA and PC, no significant correlation was demonstrated between PA and PRA. The response of PA to angiotensin-II fusion was significantly suppressed in normotensive acromegaly as compared to the normal subjects in spite of normal levels of PRA except for 1 case. The above observations were interpreted to suggest that the aldosterone regulation system is slightly altered in a certain number of patients with normotensive acromegaly in contrast to the normal subjects in which PRA is the main contributing factor. The low PA and suppressed response of PA toangiotensin-II infusion may suggest the defective action of angiotensin-II infusion on the adrenal gland.
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PMID:The diurnal rhythm of plasma aldosterone, plasma renin activity, plasma cortisol and serum growth hormone and subnormal responsiveness of aldosterone to angiotensin-II in the patients with normotensive acromegaly. 94 56

The effect of acute administration of 2 preparations of growth hormone (hGH) on plasma renin activity (PRA) was studied in normal volunteers. 4 IU of standard, commercially available hGH II, Kabi, Sweden) were injected im into each of four normal subjects, and the PRA was determined in the basal state and at 30, 60, 120, 180, and 240 min after injection. Free fatty acid (FFA) was determined basally and at 15 and 210 min post-injection. The study was repeated on a different day in the same group using highly purified hGH (hGH I, 4 IU) virtually free of arginine-vasopressin. Four other normal subjects received 12 IU standard hGH (hGH II, Kabi, Sweden). There was no significant difference in PRA values with 4 IU of either preparation or with 12 IU of hGH II in any of the groups, although mean PRA was elevated in two of the patients receiving 12 IU hGH II. A rise in FFA occurred in all subjects, indicating the biological activity of hGH preparations. The possible significance of these findings to the renin-angiotensin system found in acromegaly is considered.
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PMID:The effect of different preparations of human growth hormone on plasma renin activity in normal males. 126 36

Growth hormone (GH) hypersecretion is associated with an increased incidence of hypertension and cardiac hypertrophy, resulting in excess cardiovascular morbidity and mortality. Abnormalities in the renin-angiotensin-aldosterone (RAA) system have been reported in acromegaly and in normal adults treated with recombinant human GH. The RAA system was investigated in prepubertal children with idiopathic short stature during treatment with recombinant human GH in doses up to 40 IU/m2/week. In addition, left ventricular size and function were assessed by serial echocardiography over an initial 12-month period. Modest and transient increases in blood pressure and body weight were observed during the first 7 days of GH treatment, but this was not accompanied by activation of the RAA system. Echocardiographic parameters of left ventricular size and function remained within the normal range for age and body size. Short-term GH treatment of idiopathic short stature was thus not associated with an increase in risk factors known to be associated with later cardiovascular morbidity. Longer follow-up studies will be required to confirm the safety of high-dose GH in this respect.
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PMID:Growth hormone treatment in idiopathic short stature: a preliminary analysis of cardiovascular effects. 130 8

Primarily hypervolaemic, high output forms of hypertension, with features indicating or strongly suggesting fluid overload as the cause of elevated cardiac output, resulting from renal disease with reduced glomerular filtration rate causing sodium retention, renal tubular causes of sodium retention, greatly excessive sodium intake and low renin hypertension, can be treated by reduction of sodium intake and potentiation of its excretion by diuretic therapy, removal of the cause (e.g. aldosteronoma), and calcium antagonists. Excessive vasoconstriction resulting from noradrenaline (norepinephrine) in neurogenic hypertension, phaeochromocytoma, orthostatic hypertension and alpha-adrenergic drug administration; angiotensin excess due to renal ischaemia brought about by aortic coarctation, renal arterial and arteriolar stenosis, intraluminal obstruction, external renal compression, renin-producing tumours, intrinsic kidney diseases and excessive renin substrate; and vascular structural disorders such as atherosclerosis, arteriolitides and fibrosis with or without calcification of major arteries may also induce hypertension. Secondary hypertension of uncertain mechanism may occur in hyperparathyroidism, hyper-or hypothyroidism, or acromegaly. All are best treated by appropriate correction of the endocrine excess or deficiency. It may also occur in pregnancy, where the mechanism may involve prostaglandin-thromboxane imbalance or calcium deficiency; calcium deficiency with some evidence of benefit from calcium supplements; and the recumbent hypertension paradoxically associated with autonomic failure. Excellent responses to specific correction of the underlying cause or pathogenetic mechanism is usual in young individuals but less frequent in older patients.
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PMID:Secondary hypertension. An overview of its causes and management. 137 54

Six patients with chronic congestive cardiac failure, who had never received any drug treatment, were studied before and after one month of therapy with frusemide alone at a dose of 40 mg a day. Measurements were made at rest of plasma epinephrine, norepinephrine, renin activity, aldosterone, atrial natriuretic peptide, cortisol, growth hormone and prolactin, together with central hemodynamics, body fluid volumes and renal function. The initial measurements of hemodynamics, body fluid compartments and renal function confirmed the presence of the physiopathology typical of congestive cardiac failure. Plasma concentrations of norepinephrine, atrial natriuretic peptide, aldosterone and growth hormone were significantly increased. The mean value of plasma renin activity, although high, was not significantly different from normal. After one month of treatment, body weight, body fluid volumes and exchangeable sodium were reduced. Hemodynamics and renal plasma flow and glomerular filtration were not significantly affected. Plasma norepinephrine fell to within normal limits; atrial natriuretic peptide increased significantly; plasma renin activity and cortisol increased to levels which were abnormally high; growth hormone increased to levels similar to those associated with acromegaly. Increased circulating concentrations of atrial natriuretic peptide during treatment by frusemide may have an important influence on the kidney, blood vessels and neuro-endocrine response.
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PMID:Diuretics as initial and sole treatment in chronic cardiac failure. 176 May 18

Administration of human growth hormone (GH) is associated with clinically significant sodium retention. There is evidence that the antinatriuretic properties of GH are mediated by activation of the renin-angiotensin system, as well as a direct action on the kidney. The antinatriuretic properties of GH may be of pathophysiological significance in acromegaly, where increased body sodium and plasma volume occur, and may contribute to the development of hypertension in this condition.
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PMID:Role of growth hormone in fluid homeostasis. 180 84

Atrial natriuretic hormone is involved in the control of blood pressure and water-electrolyte balance. In order to assess the relationship between atrial natriuretic hormone and hypertension in acromegaly, 34 subjects were studied, 18 with acromegaly (10 normotensive and 8 hypertensive) and 16 healthy controls. Plasma atrial natriuretic hormone levels, as well as plasma renin activity, aldosterone and growth hormone levels were measured in basal conditions in all subjects. Additionally, plasma renin activity and aldosterone levels were determined after standard stimulation. In hypertensive acromegalic patients, atrial natriuretic hormone plasma concentrations (39.8 +/- 3.5 ng/l) were significantly higher than in patients without hypertension (27.9 +/- 4.1 ng/l), and in controls (28.6 +/- 1.3 ng/l) (p less than 0.01 in both comparisons). Stimulated plasma renin activity values were decreased in hypertensive acromegalic patients when compared with those in normotensive patients (1.14 +/- 0.29 vs 4.03 +/- 0.66 micrograms.l-1.h-1, p less than 0.01). In acromegaly, atrial natriuretic hormone levels correlated with mean arterial pressure (r = 0.58, p = 0.01). These results suggest that atrial natriuretic hormone plasma levels are slightly increased in patients with acromegaly and hypertension.
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PMID:Plasma concentrations of atrial natriuretic hormone in acromegaly: relationship to hypertension. 183 35


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