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 effect of labetalol, a new alpha and beta adrenergic blocker, on blood pressure, heart rate, plasma renin activity (PRA), and urinary aldosterone excretion was assessed in 23 essential hypertensive patients, divided in 2 subgroups: 11 with normal electrocardiogram and 12 with left ventricular hypertrophy (LVH). In the first subgroup significant differences were found in the arithmethyc mean for sistolic blood pressure in sitting position (control: 166.1 +/- 17.2 mm of Hg treatment: 153.9 +/- 13.8, p less than or equal to 0.005) and in standing position (control: 165.3 +/- 17.3, treatment: 152.8 +/- 13.8, p less than or equal to 0.005) and for diastolic blood pressure (control: 102.7 +/- 12.6 to 89.9 +/- 10.1, p less than or equal to 0.001 and 103.2 +/- 11.8 to 91.2 +/- 10.8, p less than or equal to 0.001; in sitting and orthostatic positions, respectively.). No significant differences were found in the group with LVH. Heart rate decreased in the total population during treatment (- 6.0 +/- 7.5, p less than or equal to 0.05 and - 5.4 +/- 7.5 beats per minute, p less than or equal to 0.05 in sitting and orthostatic positions, respectively. PRA diminished in 12 of 15 cases studied (- 2.5 +/- 4.65 ng/ml/hr., p greater than 0.5). Correlation coefficient between decrements of diastolic blood pressure (sitting position) and ARP was 0.637. Aldosterone decreased in a non significant way during treatment. These data support the thesis of an important role of the adrenergic system in the pathogenesis of non complicated essential hypertension and, therefore, simultaneous alpha and beta receptor blockade in these cases has a better therapeutic effect. The good correlation between the decrements of ARP and blood pressure suggests an intervention of the inhibition of renin angiotensine system, brought about by the blocker property of labetalol, in the antihypertensive mechanism of the drug.
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PMID:[Effect of alpha, beta blocker, labetol on the angiotensin renin system in arterial hypertension]. 35 32

The effects of changes in brain serotonin content after injections of p-chlorophenylalanine (p-CPA), L-5-hydroxytryptophan (L-5HTP) and 5-6-dihydroxytryptamine (5-6DHT) on the mean arterial pressure (MAP), plasma renin activity (PRA) and peripheral levels of atrial natriuretic peptide (ANP) have been studied in normal and hypertensive (2K:1C model) male Wistar rats. The p-CPA (250 mg/kg) and L-5HTP (200 mg/kg) were injected i.p., while 5-6 DHT (15 micrograms/animal in 10 mu/animal vehicle) was injected into lateral brain ventricles. The effects were studied 24 h after the p-CPA injection, 2 h after L-5HTP and 10 or 20 days after 5-6DHT administration. The fall in brain serotonin produced by p-CPA and 5-6DHT did not modify the MAP values in the normal and hypertensive rat model, whereas the increase induced after L-5HTP injection only caused a slight decrease in arterial pressure in normotensive animals. The ARP experimented remarkable rises in the normal and hypertensive rats, these values increasing after L-5HTP and falling after p-CPA and 5-6 DHT injections. Similar changes are detected in the normal group after administration of these substances related to serotoninergic brain activity. The ANP levels rose after renal artery constriction, and they are not affected by the above mentioned substances. Only p-CPA and 5-6DHT reduced a low decrease in the ANP levels 10 days after their administration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of brain serotonin on the arterial pressure and plasma renin in normal and hypertensive rats]. 143 79

A study was made of the activity of plasma renin (APR), and the blood levels of ACTH, 17-hydroxyprogesterone (17-OHP) and aldosterone (A) in 50 children suffering from congenital adrenocortical hyperplasia as a result of 21-hydroxylase deficiency; 38 girls and 12 boys aged 1.5 mos. to 14 years were divided into 2 groups: (1) 35 with a salt losing type of disease; (2) 15 with a common virile type of disease. ARP in the 1st group did not exceed the control values and was unaccompanied by adequate secretion of A. Moderate ARP in parallel with a high level of A was noted in the 2nd group. Mineral corticoid therapy resulted in reduced ARP and A concentration, and a tendency to a decrease in the levels of ACTH and 17-OHP was noted. Variations in ARP and in the level of A did not manifest themselves clinically and were unaccompanied by electrolytic disorders. In the authors' opinion, a choice of adequate therapy for both types of disease must be based on the results of investigation of the above hormonal parameters.
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PMID:[Renin-angiotensin and hypophyseo-adrenal systems in children suffering from congenital adrenocortical hyperplasia resulting from 21-hydroxylase deficiency]. 166 52

Plasma active renin (PAR), plasma inactive renin (PIR), and plasma renin activity (PRA) were determined after intravenous bolus injection of the renin inhibitor SR 42128, in sodium repleted and sodium depleted macacas. The kit renin of Pasteur Diagnostics allows determination of PAR after renin inhibition by SR 42128. PAR and total plasmatic renin (TPR) were determined before and after treatment of plasma using trypsin. IR = TPR-PAR. ARP was measured by RIA of angiotensin I. Sodium depletion induced a dramatic increase of PAR (1,678 + 11.5 pg/ml compared to 94.4 + 11.5, n = 6). PIR rose from 322.1 + 34.3 pg/ml to 1,137 + 206 (n = 6). In sodium repleted macacas, SR 42128 (3 mg/kg and 9 mg/kg) induced a PRA inhibition of 90 to 100 p. 100, for 4 h post-injection. PAR increased to reach maximal level after 90 min and remained constant up to 4 h post-injection (increase of 420 p. 100 at 3 mg/kg and 620 p. 100 at 9 mg/kg). PIR increased more slowly for 4 h (maximum increase of 250 p. 100). PRA was also inhibited in sodium depleted macacas by SR 42128 at the doses of 3 mg/kg and 9 mg/kg ARP was inhibited. PIR increased more slowly, but significantly at 9 mg/kg. We conclude that the activity of SR 42128 on PAR and PIR levels is the sole consequence of the inhibition of the Renin Angiotensin system.
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PMID:[Increase in plasma levels of active and inactive renin after inhibition of renin activity by SR 42128 in conscious Macaca monkeys]. 311 88

Primary hyperaldosteronism (HA1) represent a rare etiology of arterial hypertension (less than 1%). It concerns, most of the time, aldosterone-producing adenomas or bilateral adrenal hyperplasias although intermediate forms have been reported. The diagnosis of HA1 is based on simple examinations, especially systematic measurement of kaliemia in every hypertensive patient with a normal sodium diet before treatment. The elevation of aldosterone blood levels associated with a low plasma renin activity confirms the autonomous nature of the hormonal secretion which is dissociated from the renin-angiotensin system. Study of the ratio aldosterone blood level/ARP and the captopril test are particularly useful in borderline cases. Once the diagnosis of HA1 is made, a topographic analysis may be undertaken; tomodensitometry and adrenal scintigraphy are currently the examinations of choice in the diagnosis of adrenal tumors. Due to biological, morphological and topographic factors, aldosterone-producing adenomas may be identified with a great deal of certainty: surgical excision ensures a cure in a large majority of cases. The treatment of bilateral hyperplasias remains medical.
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PMID:[Diagnosis of primary hyperaldosteronism. Apropos of 3 cases]. 342 22