Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Acute oral administration of metoprolol and propranolol to ten normal males resulted in equal reduction in heart rate both supine and after passive tilting to 60 degrees. 2. Tilted systolic blood pressure was reduced by both agents but metoprolol alone reduced supine systolic blood pressure. 3. Tilted but not supine diastolic blood pressure was reduced by both agents. 4. Metoprolol and propranolol both reduced the rise in plasma renin activity induced by tilting. 5. No effect of tilting was observed on plasma aldosterone.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Comparison of metoprolol and propranolol in modification of haemodynamic and renin-aldosterone responses to tilting in humans. 107 76

1. In eighteen subjects with mild to moderate hypertension the effectiveness of the new vasodilator drug L6150 (Lepetit) was studied. Its mechanism of action was identified by systemic and renal blood flow measurements and by estimating changes in plasma renin and aldosterone concentration and plasma volume. The reflexly induced hyperkinetic circulatory state could be completely corrected by adding propranolol or prevented by pretreatment with the latter drug. 2. Sodium retention was an invariable phenomenon. It was not due to a stimulation of the reninangiotensin-aldosterone axis since plasma aldosterone was significantly decreased, presumably as a consequence of plasma volume expansion.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Haemodynamic and endocrinological changes during anti-hypertensive treatment with a new vasodilator substance (L6150) and propranolol. 107 88

1. The cardio-renal haemodynamic and endocrine effects of the anti-hypertensive agents 2-(2,6-dichlorophenylamine)-2-imidazoline hydrochloride (clonidine, St 155) and 2-(5-fluor-o-toluidine)-2-imidazoline hydrochloride (St 600) were investigated in twelve patients with essential hypertension. 2. The anti-hypertensive action of both compounds was similar and was accompanied by a reduction in heart rate and in cardiac output, total peripheral resistance being unchanged. There was no alteration in renal blood flow and glomerular filtration rate, and renal vascular resistance showed a significant decrease. Blood volume and plasma renin concentration did not change significantly. An inverse relation changes in plasma volume and plasma aldosterone concentration was observed. In the face of similar reductions in blood pressure, no differences were observed between systemic and renal haemodynamic and endocrine responses after clonidine and St 600.
Clin Sci Mol Med Suppl 1976 Dec
PMID:Haemodynamic and endocrine changes during anti-hypertensive treatment with clonidine and its derivative St 600. 107 97

1. Competitive or non-competitive inhibition of the myotropic and pressor response of angiotensin II is dependent on the nature of the substituent in position 8 of the antagonist peptide analogue. Substituents in other positions of the molecule, particularly position 1, contribute greatly to the potency of these antagonists. 2. As is evidenced after adrenalectomy or after blockade with phentolamine and phenoxybenzamine, the initial pressor activity observed with all the antagonistic peptides is partially due to the release of catecholamines and partially to a direct myotropic effect. 3. [Sar1, Thr8]angiotensin II has been found to possess the lowest agonist to antagonist ratio of all antagonists tested. 4. [Des-Asp1, Ile8]angiotensin II selectively and specifically inhibits the release of aldosterone from adrenal cortex. Thus, unlike angiotensin II, this heptapeptide has pronounced organ specificity, suggesting that the heptapeptide (angiotensin III) is the aldosterone-releasing hormone.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Inhibition of the pressor and aldosterone-releasing effects of angiotensin II. 107 65

1. The effect of infusions of equimolar doses of angiotensin II (AII) and of the angiotensin analogue Sar1-Ile8-angiotensin II on arterial blood pressure, plasma aldosterone and plasma renin activity were compared in normal anaesthetized dexamethasone suppressed dogs. 2. Angiotensin II induced a significant increase of blood pressure and of plasma aldosterone whereas plasma renin activity decreased. The blood pressure was only slightly affected by large doses of the analogue. Plasma aldosterone, however, increased and plasma renin activity decreased. These changes were significant but less pronounced than after the infusions of angiotensin II. Plasma aldosterone remained high and renin activity low for 40 min after the infusions of the analogue. 3. The results suggest a strong agonistic potency of Sar1-Ile8-angiotensin II at the adrenal and renal angiotensin receptors, and that it is almost ineffective at the vascular receptors. The inhibition of renin secretion by angiotensin seems not be related to its vasoconstrictive activity.
Clin Sci Mol Med Suppl 1975 Jun
PMID:Effect of angiotensin II and of an angiotensin II analogue (Sar1-Ile8-angiotensin II) on blood pressure, plasma aldosterone and plasma renin activity in the dog. 107 88

1. To examine the role of angiotensin II in the maintenance of blood pressure and control of aldosterone secretion, eight normal human subjects were studied on a tilt table in sodium-replete and sodium-depleted states, before and after the administration of an angiotensin converting-enzyme inhibitor (CEI). 2. Administration of CEI was followed by a marked fall in blood pressure on tilting in sodium-depleted, but not in sodium-replete, subjects. CEI administration also resulted in a rise in plasma renin activity in the supine position, in the absence of haemodynamic change. The rise in plasma aldosterone observed both in response to tilting and sodium depletion did not occur after CEI, even though plasma renin activities were higher. 3. These results indicate that: (a) angiotensin II is essential for blood pressure control in the sodium-depleted individual; (b) angiotensin II exerts direct feedback control on renin secretion; (c) angiotensin II is the primary stimulus to aldosterone secretion in response to both sodium depletion and posture.
Clin Sci Mol Med Suppl 1975 Jun
PMID:The role of the renin--angiotensin--aldosterone system in cardiovascular homeostasis in normal man. 107 90

1. The anti-hypertensive effect of converting enzyme inhibition was evaluated in twenty-three hypertensive patients (seven renovascular, four essential, four malignant, one scleroderma, three chronic renal failure, four primary or idiopathic aldosteronism). 2. In sixteen patients a single injection (1--4 mg/kg) of the inhibitor produced an immediate anti-hypertensive effect, which lasted up to 16 h. In six patients the anti-hypertensive effect of the inhibitor was significantly improved after sodium depletion. 3. Plasma renin activities increased and plasma aldosterone concentrations decreased consistently except in idiopathic aldosteronism. 4. Converting enzyme inhibition provides a direct way of defining the degree of renin-dependency of the hypertension. Accordingly, it can be used diagnostically and for planning appropriate therapy. Therapeutically, it could be advantageous in hypertensive emergencies because of its safety, specificity and capacity to reduce aldosterone secretion.
Clin Sci Mol Med Suppl 1975 Jun
PMID:The use of angiotensin-converting enzyme inhibitor in the diagnosis and treatment of hypertension. 107 92

1. 24 h aldosterone secretion rates (ASR) have been measured in six normal volunteers while recumbent all day and while standing for 12 h, on 200 and 10 mmol/day sodium diets and after salt-poor albumin infusions (75 g in 150 ml), which significantly expanded plasma volume. 2. The mean ASR on the 10 mmol/day sodium diet, both without and with the salt-poor albumin infusion, was highly significantly increased above the mean ASR on the 200 mmol/day sodium diet, both in the recumbent and in the upright posture. 3. There was no significant difference between the mean ASR values on the 10 mmol/day sodium diet alone and after the infusion of albumin either in the recumbent or in the upright posture. 4. The above abservations su;gest that sodium deprivation raises ASR by a mechanism or mechanisms unrelated to plasma volume.
Clin Sci Mol Med 1975 Mar
PMID:The role of plasma volume in the increase of aldosterone secretion rate during sodium deprivation. 111 36

1. Healthy subjects, given a long-acting preparation of vasopressin intramuscularly, excreted a significantly less concentrated urine than when subjected to fluid deprivation for 28 h. 2. When fludrocortisone, a potent mineralocorticoid, was given in addition to vasopressin the urine was not significantly less concentrated than after fluid deprivation. 3. Oral urea-loading also enhanced the urine-concentrating power of vasopressin but its effect was less marked than that of fludrocortisone. Oral urea did not increase further the urine concentration achieved by combined fludrocortisone and vasopressin. 4. Renal concentrating power was assessed in fourteen patients with renal disease and impaired concentrating ability. Fludrocortisone significantly enhanced the urine concentration achieved by vasopressin alone and the resultant urine was not significantly less concentrated than that achieved by fluid deprivation. 5. The action of fludrocortisone in enhancing the urine-concentrating effect of vasopressin is similar to that of aldosterone and is probably due to the increased sequestration of solute in the renal medulla, caused by increased reabsorption of sodium chloride in the ascending limb of the loop of Henle. 6. In the clinical assessment of renal concentrating power, the combined use of fludrocortisone and vasopressin has potential advantages over established methods.
Clin Sci Mol Med 1975 Apr
PMID:Assessment of urine-concentrating ability in man: effect of fludrocortisone and urea in enhancing response to vasopressin. 112 20

1. Rabbits were actively immunized aganist angiotensin II (AII). 2. Basal plasma aldosterone concentration was 0-058 plus or minus 0-027 pmol/ml (20-7 plus or minus 9-6 pg/ml) (mean plus or minus SD) in immunized and 0-056 plus or minus 0-021 pmol/ml (20-2 plus or minus 7-5 pe. When the endogenous formation of AII was stimulated by frusemide, by haemorrhage or by feeding with low sodium diet, a significant increase of plasma aldosterone was observed with no difference between immunized and non-immunized animals. 3. In non-immune rabbits, the average mean arterial blood pressure rose 13 mmgHg during the infusion of AII (5 pmol min--1 kg-1) and 27 mmHg during the infusion of 50 pmol min-1 kg-1. In contrast, there was no clear increase in blood pressure in the immunized animals. The blood pressure rose in immune animals (15 mmHg) and in non-immune animals (36 mmHg) during the infusion of 200 pmol min-1 kg-1 ALL. Plasma aldosterone rose in all animals in response to each of the three infusions with no significant difference between the two groups. 4. It is concluded that the immunization against ALL blocked only the pressor effect of the peptide but had no clear influence on the response of plasma aldosterone to increased ALL. Differences between the affinities of the adrenal and vascular AII receptors may explain these findings.
Clin Sci Mol Med 1975 May
PMID:Effect of immunization against angiotensin II on blood pressure and on plasma aldosterone in the rabbit. 112 32


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