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)

1 The regulation of renin secretion is mediated by way of adrenoceptors. The role of alpha-adrenoceptors remains controversial, whereas it is generally accepted that activation of beta-adrenoceptors stimulates renin and their blockade suppresses renin. 2 Although experimental renin regulation appears to be a beta 2-receptor function, clinical studies suggest that in man it is a beta 1 effect. 3 beta-Adrenoceptor-blocking agents are effective antihypertensive agents, but have variable effects on renin secretion; this variability may be attributable to different degrees of instrinsic partial beta-agonistic activity and/or different receptor or organ selectivity of various compounds. 4 Antihypertensive effectiveness seems unrelated in magnitude or timing to the baseline levels or the changes of plasma renin activity for the majority of beta-adrenoceptor-blocking drugs.
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PMID:Antihypertensive action of beta-adrenoceptor blockade and the renin-angiotensin system. 3 76

Plasma renin activity (PRA), aldosterone and cortisol's variations are studied in normal salt repleted voluntary men (120 mEq/24 h sodium) before and after furosemide infusion and/or constant infusion of ACTH (beta 1-24 corticotrophin). PRA is determined by angiotensin I radioimmunoassay, plasma aldosterone by specific radioimmunoassay and plasma cortisol by competitive transcortine binding radioassay. 1) PRA and plasma aldosterone increase clearly after acute sodium depletion secundary to furosemide infusion; plasma cortisol increases a little. PRA and aldosterone's variations are identical after endogenous ACTH suppression by dexamethazone administration before study. 2) PRA is not influenced by constant infusion (16 ng/kg/mn) after acute infusion (0.3 mg intravenously) of ACTH (beta 1-24); plasma aldosterone and plasma cortisol increase dramatically and remain constant along the experience. 3) If acute sodium depletion is realized 120 mn after ACTH infusion, PRA still raises; on the other hand plasma aldosterone remains constant. These results confirm that acute sodium depletion stimulates aldosterone secretion by the way of renin angiotensin system then ACTH acts directly on the adrenal cortex. Nevertheless the stimulative action of acute sodium depletion on aldosterone secretion is suppressed by previous acute ACTH stimulation.
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PMID:[Effect of furosemide and ACTH on plasma renin, aldosterone and cortisol levels in normal man]. 17 5

The effect of the primarily beta 2 type adrenergic receptor stimulating terbutaline (10(-7)--10(-5) M) and of the beta 1 and beta 2 type adrenergic receptor stimulating isoproterenol (10(-7)--10(-5) M) was studied on renin release from incubated slices of renal cortex. Renin release and cAMP content of the slices were significantly higher in the presence of both terbutaline and isoproterenol. A logarithmic dose--response relationship was shown to be present between the beta mimetics and the renin concentration in the medium, and the cAMP content of tissue slices. In equal doses isoproterenol was about 1.5 times more potent than terbutaline. No change was seen in the renin content of the tissue slices. The results supports the view that beside the beta 1 type adrenergic receptors of the renal cortex--even if to a lesser extent--the beta 2 type adrenergic receptors, too, are involved in the regulation of renin release.
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PMID:The role of beta receptors in the regulation of renin release. 23 5

The antihypertensive effect of atenolol, a new beta 1 receptor blocking agent, was studied in a double blind non cross-over trial in 40 patients (pts) affected by mild to moderately severe essential hypertension with normal plasma renin activity. After a run-in period (15 days) of placebo treatment pts were assigned to two groups. The first (group A) continued placebo treatment for 30 days, the second (Group B) were given atenolol (ICI 66082) 100 mg daily for 30 days also. Atenolol significantly reduced systolic and diastolic blood pressure in recumbent and standing position and heart rate at rest. No significantly changes of the same parameters were observed in group A. Body weight and plasma renin activity was unchanged in both groups. Atenolol treatment never was discharged in order to side effects. These results seem to suggest that atenolol can be an useful drug in the treatment of systemic blood hypertension.
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PMID:[Efficacy and tolerability of a cardioselective beta-blocking drug (atenolol) in the treatment of essential hypertension. A double blind study (author's transl)]. 35 98

The antihypertensive action of beta-blocking agents has been suggested to be associated with the decrease in plasma renin activity (PRA) and can be antagonized by indomethacin, a prostaglandin (PG) synthesis inhibitor. We studied the acute and long-term effects of a beta 1-blocking agent, atenolol (50 mg b.i.d.), on blood pressure (BP), PRA and urinary PGF2 alpha excretion in 12 male patients (40 years old) with essential hypertension. BP was measured by means of a brachial cuff. PRA and PGF2 alpha were estimated radioimmunologically. One day after the initiation of atenolol treatment, BP fell significantly, the supine values from 159/114 to 143/104 mmHg and the erect from 158/118 to 140/106 mmHg. In six weeks BP decreased further to 135/94 and 134/96 mmHg, respectively. After the cessation of atenolol for three weeks BP rose to the pre-atenolol level. When the dose was readjusted (25-150 mg daily for 26 weeks), diastolic BP remained at 100 mmHg or higher in only two patients. During the atenolol treatment PRA declined to one-third of the pre-atenolol level in one day and to one-half in six weeks. The urinary excretion of PGF2 alpha was not affected by atenolol. Our results suggest that 1) the antihypertensive action of atenolol and the reduction of PRA are substantial already in one day, and 2) the decrease in BP or PRA is not associated with PGF2 alpha production.
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PMID:The effects of a beta 1-blocking agent, atenolol, on blood pressure, plasma renin activity and prostaglandin F2 alpha excretion in patients with essential hypertension. 48 51

Transforming growth factors-beta (TFG beta s) are multifunctional peptides that affect proliferation, differentiation, and many other functions in a variety of cell types. In this study we examined the effect of TGF beta 1 on aldosterone and adrenal renin production using cultured bovine adrenal zona glomerulosa cells. Collagenase-dispersed zona glomerulosa cells were incubated in PFMR-4 medium containing 10% fetal calf serum for 72 h, and the medium was replaced with serum-free medium for the next 24 h. The cells during this 24-h period were exposed to TGF beta 1, ACTH, and (Bu)2cAMP (dbcAMP). It was observed that TGF beta 1 at 1 nM 1) inhibited basal aldosterone secretion from 680.0 +/- 40.0 to 270.0 +/- 10.0 pg/10(6) cells.h, 2) inhibited ACTH- and dbcAMP-stimulated aldosterone production, 3) increased levels of active renin in the cells from 17.8 +/- 2.5 to 70.7 +/- 4.4 pg angiotensin-I/10(6) cells.h and prorenin from 270.0 +/- 5.0 to 970.0 +/- 90 pg angiotensin-I/10(6) cells.h, 4) stimulated prorenin in the medium synergistically in combination with ACTH and dbcAMP, and 5) had no significant effect on basal cAMP production, but significantly inhibited the ACTH-stimulated production of cAMP. These observations show that TGF beta 1 is a potent inhibitor of basal and ACTH- and cAMP-stimulated aldosterone production and inhibits ACTH-stimulated cAMP production. Contrary to its effect on aldosterone, TGF beta 1 stimulates the synthesis and release of adrenal renin and prorenin. TGF beta 1 may act as an autocrine or paracrine regulator of aldosterone production.
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PMID:Transforming growth factor-beta 1 inhibits aldosterone and stimulates adrenal renin in cultured bovine zona glomerulosa cells. 132 77

Treatment of male rabbits with adriamycin at a cardiotoxic dose (1 mg/kg intravenously, i.v., twice a week for 9 weeks) caused cardiovascular disturbances characteristic of chronic heart failure. The severity of symptoms varied, indicating differences in the individual sensitivity of the animals to adriamycin. Thus, cardiac output (CO) was decreased by greater than 40% in only 4 of the 7 animals in which it was measurable at 9 weeks. Elevated levels of atrial natriuretic factor (ANF) and plasma renin activity (PRA), as well as pulmonary congestion, hydrothorax, and ascites were also evident. The baroreflex response to sodium nitroprusside (NPS) was blunted. The response to the inotropic drug dobutamine was depressed by 50% as compared with the control animals. Right ventricular beta-adrenoceptor density was significantly reduced in these animals (22.9 +/- 3.1 as compared with 31.8 +/- 1.0 fmol/mg protein in control animals) owing to a selective downregulation of the beta 1-adrenoceptor population. The loss of beta-adrenoceptors was highly correlated with severity of heart failure symptoms: i.e., baroreflex dysfunction as indicated by the NPS slope (r = 0.91), decrease in CO during the previous weeks (r = 0.88), and plasma norepinephrine (NE) levels (r = 0.96). However, when all adriamycin-treated animals were compared collectively regardless of the severity of heart failure, with the controls, no difference in the beta-adrenoceptor density was detectable, a finding in agreement with previous observations in this model. Chronic treatment of rabbits with adriamycin thus causes low-output failure, reflecting some of the findings reported for the human disease; however, individual sensitivity to adriamycin varies considerably between rabbits.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic adriamycin treatment and its effect on the cardiac beta-adrenergic system in the rabbit. 138 76

The renin-angiotensin-aldosterone system is mainly involved in the regulation of arterial blood pressure and fluid balance. One of the main stimuli for the secretion of renin present in the renal juxtamedullary cells, but also in some other tissues, is provided by the sympathetic nervous system via the action of norepinephrine on beta 1-adrenoceptors. There is good evidence in animal experiments that angiotensin II (Ang II) facilitates sympathetic neurotransmission by several mechanisms, all of which seem to involve distinct, but perhaps heterogeneous, Ang II receptors. Acting within the central nervous system, angiotensin augments sympathetic nerve outflow directly, but probably also by inhibiting the reflex decrease in sympathetic nerve activity following an increase in arterial pressure. Ang II also stimulates adrenomedullary and ganglionic transmission as well as enhances the release of sympathetic transmitter by a presynaptic action. In addition, there is some evidence that angiotensin can inhibit norepinephrine reuptake and augment its biosynthesis and responses mediated via both extrasynaptic alpha 2- and intrasynaptic alpha 1-adrenoceptors. Angiotensin-converting enzyme inhibitors, particularly when the endogenous renin-angiotensin activity is high, attenuate sympathetic neurotransmission. Despite a clear demonstration that the renin-angiotensin system augments the activity of the sympathetic nervous system in animals, evidence for such a role in humans is tenuous. This is probably mainly due to the difficulty in quantitatively monitoring and assessing the autonomic function in humans. It is possible that in congestive heart failure, where the renin-angiotensin system can be highly activated, sympathetic facilitation by angiotensin as well as its attenuation by converting enzyme inhibitors may be important.
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PMID:Interaction between the renin-angiotensin-aldosterone and sympathetic nervous systems. 138 70

Circulating plasma concentrations of norepinephrine, renin, angiotensin and vasopressin are increased in congestive heart failure. By increasing ventricular afterload, heart failure is further worsened, which in turn--in a vicious cycle--stimulates neurohumoral vasoconstrictor mechanisms. Furthermore, because of the compensatory but excessive stimulation of the sympathomimetic system, a down-regulation and desensitization particularly of the myocardial beta 1 receptors and depletion of myocardial catecholamine occurs in chronic heart failure. These defects may be restored toward normal by interventions that attenuate the activity of the sympathetic nervous system. A direct approach to modify the excessive vasoconstriction is to administer systemic vasodilator drugs, but despite favorable short-term effects, tolerance developed to most of these drugs during long-term treatment. One reason for the loss of effectiveness is the reflex activation of the sympathetic system, which increases vasoconstrictor hormone concentrations. Activation of the renin-angiotensin system can be modified effectively by angiotensin-converting enzyme inhibitors that have shown favorable responses in patients with chronic heart failure. Beta-blocking agents interfere with endogenous sympathetic activation and have produced beneficial effects in patients with congestive cardiomyopathy. Long-term treatment is associated with up-regulation of the number of beta receptors and an improved responsiveness to catecholamines. Owing to the negative inotropic effects of beta-blocking agents, some of the patients with severe heart failure deteriorated hemodynamically and clinically. Theoretically, it should be advantageous to have a substance that combines protection against excessive beta stimulation with a mild inotropic support to prevent cardiac decompensation. This may be achieved by a selective beta 1-partial agonist like xamoterol.
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PMID:Interrupting the adaptive changes in congestive heart failure. 167 86

1. The effects of sustained moderate exercise in the sitting position on renal haemodynamics and glomerular filtration were measured in six normotensive patients with moderately impaired renal function and seven age-matched normal volunteers. 2. The changes in the effects of exercise on renal function induced by chronic cardioselective beta-adrenoceptor blockade by drugs with (epanolol) and without intrinsic sympathomimetic activity (atenolol) were examined. 3. Both beta-adrenoceptor blockers attenuated the heart rate increase with exercise, but only atenolol lowered blood pressure significantly. In resting volunteers on atenolol, associated with the fall in blood pressure there was a significant reduction in glomerular filtration rate. 4. Glomerular filtration fell significantly in all groups with exercise, and renal blood flow also fell in parallel. These changes were not influenced by drug treatment. 5. The exercise-induced rise in PRA was suppressed by atenolol but not by epanolol. 6. The renal function and haemodynamic responses to moderate exercise does not appear to be mediated by the systemic renin-angiotensin system or by beta 1-adrenoceptors.
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PMID:The effects of selective beta-adrenoceptor antagonists and partial agonist activity on renal function during exercise in normal subjects and those with moderate renal impairment. 168 67


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