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)

Types of beta-adrenoceptors mediating renin release induced by isoproterenol were investigated in conscious dogs. The nonselective beta-adrenoceptor blocking drugs propranolol, D-32, and pindolol significantly inhibited increases in heart rate and plasma renin activity and a fall of blood pressure produced by intravenous infusion of isoproterenol (10 microgram . kg-1 . 20 min-1). d-Propranolol and d-D-32 did not inhibit these three responses to isoproterenol. The selective beta 1-adrenoceptor blocking drug atenolol, at the oral dose of 6 mg/kg, which selectively suppressed isoproterenol-induced tachycardia, significantly inhibited the renin release caused by isoproterenol. By contrast, the renin release induced by isoproterenol was not modified by the selective beta 2-adrenoceptor blocking drug IPS-339 at an oral dose of 3 mg/kg, which fully and selectively antagonized the fall of blood pressure in response to isoproterenol. There was good correlation between suppression of isoproterenol-induced renin release and that of isoproterenol-induced tachycardia after various beta-adrenoceptor blocking drugs. These results lead to the conclusion that in conscious dogs the beta-adrenoceptors mediating release are mainly of the beta 1 type.
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PMID:Analysis of beta-adrenoceptors mediating renin release produced by isoproterenol in conscious dogs. 610 74

In healthy volunteers, the effects of prenalterol, a new beta 1-adrenoceptor agonist, on renal hemodynamics, excretory function, plasma-renin-activity, plasma cAMP concentration, and plasma and urinary norepinephrine were studied. Besides an increase in blood pressure, which was adjusted to about 20 mmHg above the resting values, and an increase of heart rate, prenalterol induced only transient decreases of urinary volume and free water clearance and in increase of sodium excretion. The other parameters measured did not change. Thus prenalterol mainly exerts positive inotropic and chronotropic effects and does not affect renal circulation.
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PMID:Effects of a beta 1-selective adrenergic agonist in normal human volunteers. 610 43

alpha-, beta 1- and beta 2-adrenergic receptors in the kidney mediate vasoconstriction, renin secretion and vasodilatation, respectively. Blockade of beta-receptors may therefore be expected to influence renal blood flow and possibly glomerular filtration rate by intrarenal effects as well as by reducing cardiac output and blood pressure. Since the various beta-adrenergic blocking drugs available differ in the degree to which they block beta 2-receptors (cardioselectivity) and also in their intrinsic sympathomimetic activity, they would be expected to have different effects on renal function. The acute administration of beta-blockers usually results in a reduction in effective renal plasma flow and glomerular filtration rate, whether or not the drug is cardioselective or has intrinsic sympathomimetic activity, with the exceptions of nadolol, which has actually increased effective renal plasma flow in some studies and of tolamolol. With chronic oral administration, the non-cardioselective beta-blockers reduced glomerular filtration rate and effective renal plasma flow. The cardioselective drugs do not usually produce significant reductions in glomerular filtration rate or effective renal plasma flow, although small increases in serum urea during treatment do occur. Interestingly, in contrast to findings with intravenous administration, orally administered nadolol produced a slight reduction in glomerular filtration rate in 1 study, so the effect of this agent on renal function under clinical conditions remains uncertain. It seems likely that beta-blockers reduce renal function predominantly by blocking beta 2-receptors in the kidney. To keep area of discussion in perspective, it is important to realise that although there have been isolated reports of serious deterioration in renal function coinciding with beta-blocker treatment, the great majority of reports are of reduction in glomerular filtration rate which are not of clinical significance, even in patients with pre-existing impairment of renal function. The beta-blockers with low lipid solubility-i.e. atenolol, nadolol and sotalol-are not metabolised, and their dose must be reduced in renal failure. Propranolol has active metabolites and its dose must also be reduced slightly in uraemia.
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PMID:Beta-blockers and renal function. 612 52

Exposure of rats to air at 5 C for 1-12 days is accompanied by a relative dehydration in spite of the continued presence of water. Dehydration during exposure to cold was manifested by: 1) a reduction in the ratio of water/food ingested; 2) an increase in the ratio of urine excreted/water ingested; 3) an increased evaporative water loss; 4) an increased serum osmolality and chloride concentration; and 5) a striking thirst and ingestion of water after transfer from cold to air at 26 C. Drinking began within 15 min and lasted approximately 1 h. Thermogenic drinking persisted for at least 120 days of exposure to cold. It was not thwarted by preventing access to water for either 1 or 2 h after transfer to warm air, but either intragastric or intraperitoneal administration of a water load equal to 3% of body weight inhibited water intake after transfer. These characteristics of thermogenic drinking are similar to those observed after 24 h of dehydration at 26 C; they also suggest that the cold-exposed rat is dehydrated relative to controls. These results suggest that osmoreceptors may play a role in the induction of thermogenic drinking. However, angiotensin II receptors may also play a role. Thermogenic drinking was inhibited by a beta 2-adrenergic, but not a beta 1-adrenergic, antagonist as well as by captopril, an inhibitor of the conversion of angiotensin I to angiotensin II. Further, plasma renin activity increased fourfold within 15 min after removal from cold. This suggests that an additional component involved in thermogenic drinking is the angiotensin II receptor. The extent to which thermogenic drinking is mediated by each pathway is unknown and will require additional studies.
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PMID:Thermogenic drinking: mediation by osmoreceptor and angiotensin II pathways. 612 48

The purpose of this study was to evaluate the acute hemodynamic and hormonal effects induced by short-term exposure to loud noise in man. Loud noise (95 dBA or 100 dBA) caused an increase in blood-pressure in healthy normotensive subjects as well as in patients with essential hypertension. The blood pressure elevation was caused by vasoconstriction in patients with essential hypertension and in normotensive subjects with a positive family history of hypertension, while the blood pressure response in normotensive subjects without a family history of hypertension was due mainly to an increase in cardiac output. This might indicate that there are genetically determined differences in the cardiovascular response to noise. Stimulation with noise did not increase plasma levels of catecholamines, prolactin, cortisol or growth in normotensive subjects. In patients with essential hypertension plasma noradrenalin increased, while plasma adrenalin and plasma renin activity did not change. The increase in diastolic blood pressure caused by loud noise was not affected by beta 1-selective or non-selective beta-adrenoceptor blockade, nor was it changed by alpha 1-or combined alpha 1-and non-selective beta-adrenoceptor blockade. The elevation in blood pressure induced by noise is usually mediated by vasoconstriction, i.e. an alpha 1-effect. When alpha 1-adrenoceptors are blocked, the blood pressure response to noise is mediated by an increase in cardiac output, i.e. a beta-adrenoceptor mediated effect. It thus seems as if an increased pressure is essential during exposure to loud noise. If one part of the sympathetic nervous system is blocked, other parts can be activated in order to preserve the blood pressure on an elevated level. This indicates a temporary resetting of the baroreceptors during exposure to noise, which probably is mediated from the hypothalamus.
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PMID:Cardiovascular effects of noise. 612 83

Haemodialysis hypotension occurs with particular frequency in bilateral nephrectomised patients. This reflects the importance of the renin-angiotensin-aldosterone system for maintaining normal blood pressure. Failure of vascular access (due to clotting and thrombosis of shunts) and ischaemic necrosis of transplanted kidneys in hypotensive patients prompted us to treat them orally with a new beta 1-adrenergic agent (prenalterol). Blood pressure was normalised in 4 out of 5 patients. Because of delayed renal elimination of the drug, daily dosage must be reduced to prevent symptoms of adrenergic stimulation. A study of the pharmacokinetics of prenalterol in uraemia is in preparation.
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PMID:Haemodynamic effects of prenalterol in patients on dialysis. 612 86

To determine the beta-adrenoceptor subtype controlling renin release from the kidneys, several beta-adrenoceptor subtype selective agonists and antagonists were administered to 15 healthy volunteers. While isoprenaline infusion (1, 2 and 4 micrograms/min for 5 min each) markedly increased plasma renin activity (PRA), the beta 2-selective agonist fenoterol failed to change PRA. The isoprenaline induced rise in PRA could be completely prevented by the beta 1-selective antagonists metoprolol (10 mg i.v. 45 min prior to isoprenaline infusion) and betaxolol (5 mg i.v. 45 min prior to infusion) indicating that renin release is mediated by beta 1-adrenoceptors. Binding studies with the highly specific beta-adrenoceptor radioligand (+/-)-125iodocyanopindolol demonstrated that membranes from human kidney cortical slices contain predominantly, if not exclusively, beta 1-adrenoceptors. These in vivo and in vitro results support the view that the beta-adrenoceptor mediating renin release from the human kidney is of the beta 1-subtype.
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PMID:Subclassification of human beta-adrenergic receptors mediating renin release. 613 58

This survey discloses the main mechanisms regulating renin release from the kidneys. Stimulation or inhibition of renin at least during a normal sodium intake seems to depend mostly on the sympathetic nervous system and be mediated through beta 1-adrenoceptors. The suppression of renin release is maintained during long-term treatment with both selective (beta 1) and non-selective (beta 1 + beta 2)-adrenoceptor blocking drugs. The role of alpha-adrenoceptors on renin release is less clear, both stimulating and suppressive effects having been described after treatment with alpha 1-adrenoceptor blocking therapy (i.e. prazosin). In certain conditions, i.e. when renal vascular resistance is increased or renal perfusion pressure augmented, renal prostaglandins (PG) especially PGE2, may play an important part in renin release. Angiotensin II (A II) and aldosterone generally follow the shifts in renin release. Thus, a decrease in both A II and plasma aldosterone is seen during long-term treatment with beta-adrenoceptor-blockade and may contribute to the blood-pressure lowering effect of these drugs.
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PMID:Adrenergic regulation of renin release and effects on angiotensin and aldosterone. 613 31

The contribution of beta 1-adrenoceptors to the regulation of plasma renin activity was investigated in nine healthy sodium-replete volunteers: seven subjects received a cumulative intravenous dose of 75 micrograms/kg prenalterol, a predominant beta 1-adrenoceptor agonist, and two subjects only vehiculum. In the seven actively treated subjects beta 1-adrenoceptor agonism increased (P less than 0.001) systolic intra-arterial pressure by an average of 16 +/- 4 mm Hg and heart rate by 19 +/- 3 beats min. These increases were significantly (P less than 0.04) different from the changes observed in the two control subjects (+ 3 +/- 4 mm Hg and -1 +/- 4 beats/min, respectively). Plasma renin activity, however, tended to decrease in both the actively (-38%) and saline (-28%) treated subjects. Predominant beta 1-adrenoceptor agonism, powerful enough to increase systolic pressure and heart rate does not increase plasma renin activity in supine sodium-replete normal man.
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PMID:Effects of beta 1-adrenoceptor agonism on plasma renin activity in normal men. 613 22

The effects of prenalterol, a selective beta 1-adrenoreceptor agonist, were studied in a patient with the Shy-Drager syndrome, presenting with incapacitating orthostatic hypotension. The main haemodynamic defect was an impressive postural fall in stroke volume and cardiac output pointing to denervation of the capacitance vessels. Prenalterol 4 X 30 mg orally produced a marked increase in supine and standing blood pressure, along with substantial symptomatic improvement. Notable positive chronotropic and inotropic effects were observed. Association of fludrocortisone 0.5 mg/day resulted in further haemodynamic and symptomatic improvement, presumably due to plasma volume expansion. Haemodynamically, prenalterol and fludrocortisone resulted in a substantial increase in standing cardiac output, primarily due to the chronotropic effects of prenalterol. In addition to the haemodynamic effects, prenalterol stimulated the renin-aldosterone system and restored the normal diurnal pattern of water and sodium excretion, the latter may have contributed to the improvement of orthostatic tolerance. Prenalterol could be a valuable adjunct to the existing treatment schedules of neurogenic orthostatic hypotension.
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PMID:Prenalterol in the treatment of orthostatic hypotension in Shy-Drager syndrome. 614 74


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