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)

Plasma ions and cortisol levels were measured sequentially during the adaptation of European eels (Anguilla anguilla) from fresh water (FW) to sea water (SW). The importance of the renin-angiotensin system in the regulation of this adaptation was assessed using captopril (SQ14225, an inhibitor of angiotensin I-converting enzyme). The effects of captopril on renal function in FW- and SW-adapted trout were also examined. During the first 5 hr in sea water, plasma levels of cortisol in eels increased threefold, plasma sodium rose steadily from 137 to 156 mmol/l and plasma potassium fell from 2.1 to 1.6 mmol/l. In contrast, captopril-treated eels when adapted to sea water had plasma cortisol levels twice those of controls. Captopril treatment did not affect the electrolyte responses to seawater adaptation. Captopril injected into eels which were fully adapted to and wholly maintained in sea water had no effect on plasma levels of cortisol, sodium, and potassium. Plasma cortisol was 30% lower in freshwater eels 2 hr after an injection of captopril but plasma sodium and potassium levels were unchanged. In both FW- and SW-adapted trout, captopril infusions doubled the glomerular filtration and urine production rates and the tubular transport maxima for glucose without changes in plasma composition.
Gen Comp Endocrinol 1985 Apr
PMID:Control of renal and adrenocortical function by the renin-angiotensin system in two euryhaline teleost fishes. 388 78

In isolated aortic rings and in vitro perfused mesenteric arteries of Wistar rats the vasoconstrictor responses to norepinephrine (NE) were not affected by captopril (2 X 10(-4) M). However, captopril (1 mg/kg i.v.) in pithed Wistar rats attenuated significantly the increases in diastolic blood pressure induced by NE. In pithed rats the effect of captopril on NE diastolic blood pressure responses disappeared either in the presence of an angiotensin II (5 ng X kg-1 X min) infusion or when the rats were previously nephrectomized. These findings suggest that the effect of captopril on vascular responses to norepinephrine is mediated by an inhibition of the renin-angiotensin system and not by an antagonistic effect on alpha-adrenergic receptors.
Gen Pharmacol 1985
PMID:Effect of captopril on norepinephrine vascular contractility. 389 54

The ultrastructural localization of renin in the juxtaglomerular apparatus of the kidney of the toad Bufo bufo has been examined using an immunogold staining method for electron microscopic immunocytochemistry and an antiserum to renin isolated from the submandibular gland of the mouse. Renin immunoreactivity was confined to lamellated granules in the cytoplasm of epitheloid or juxtaglomerular cells in the glomerular afferent arterioles and also in the media cells of larger arteries. Mouse kidney tissue, examined for purposes of comparison, showed immunolabeling limited to the granules of the juxtaglomerular cells. The presence of renin or a renin-like substance in the juxtaglomerular granules of the toad kidney is discussed in relation to the lysosomal nature of these granules. A model is presented linking the lysosomal function of the juxtaglomerular granules and the release of renin mediated by beta-adrenergic receptors present on the surface of the juxtaglomerular cells.
Gen Comp Endocrinol 1985 Dec
PMID:Immunoelectron microscopic localization of renin in the juxtaglomerular cells of the amphibian Bufo bufo. 393 11

Drinking behaviour and its possible regulation by the renin-angiotensin system (RAS) has been examined in the euryhaline flounder. Fluid intake was greater in seawater (SW)-adapted than freshwater (FW)-adapted fish, the latter having significantly lower plasma sodium, chloride, and osmotic concentrations. Oesophageal cannulation in SW-adapted fish resulted in further elevation of drinking rates, which increased proportionally with progressive body water loss as measured by the fall in body weight and rise in plasma tonicity. The influence of the RAS on drinking in SW-adapted fish was examined in animals with an intact gastrointestinal tract. Fluid intake fell markedly following administration of the converting enzyme inhibitor, Captopril. Infusions of angiotensin I (AI) and angiotensin II (AII) induced dose-related increments in the rate of drinking. The increased drinking in response to AI was inhibited, however, by the simultaneous administration of Captopril. The results are consistent with the presence in the flounder of the major elements of the RAS, including AI, AII, and a converting enzyme-like substance. The RAS appears to play an important regulatory role in the adaptative drinking behaviour associated with migration of euryhaline teleosts between FW and SW.
Gen Comp Endocrinol 1983 Sep
PMID:The renin-angiotensin system and drinking in the euryhaline flounder, Platichthys flesus. 635 35

Marsupial mice, Antechinus stuartii, were given intraperitoneal (ip) injections of 1-30 micrograms of Val5-angiotensin II amide to determine whether it had any effect on thirst. Drinking in the first hour after injection and measured water intake over 2 and 24 hr were not substantially increased compared with controls. Intraperitoneal injection of sheep renin had no effect on water intake. Water deprivation increased 2- and 24-hr water intake. Sheep renin and Val5-angiotensin II amide elicited pressor responses after ip injection. By comparison, rats given 100 micrograms of Val5-angiotensin II amide ip increased water intake in the first 2 hr after injection compared with saline-injected and noninjected controls. The results suggest that the thirst mechanism in Antechinus is insensitive to exogenous and to low levels of endogenous circulating angiotensin II. The explanation of this difference from other mammals may be found in evidence that the thirst mechanism in species which do not normally drink water in nature is relatively insensitive to exogenous angiotensin.
Gen Comp Endocrinol 1983 Dec
PMID:Water drinking and the effect of angiotensin and renin in a dasyurid marsupial (Antechinus stuartii). 636 83

The pressor actions of homologous kidney extract and human angiotensins I and II were studied in the conscious rat snake, Ptyas korros. A converting enzyme inhibitor (captopril), an angiotensin II analogue [( Sar1,Ala8]ANG II), an alpha-adrenergic receptor antagonist (phentolamine), and a catecholamine releaser (reserpine) were used to elucidate their actions. It was found that captopril attenuated the pressor effects of the kidney extract and angiotensin I but not that of angiotensin II. [Sar1,Ala8]ANG II and phentolamine both significantly attenuated, but did not completely inhibit the vasopressor actions of the kidney extract and angiotensins I and II. However, reserpine administration did not reduce the action of angiotensin II. These findings suggest that the renin-angiotensin system in snakes is similar to those present in mammals and other nonmammalian species, except for the mechanism of angiotensin II action. In the present study, angiotensin II was found to act partly through the alpha-adrenergic receptor which is not as specific as that in mammals and thus may respond to an agonist other than its usual ones, and partly through the vascular angiotensin II receptor.
Gen Comp Endocrinol 1984 Nov
PMID:The vasopressor action of the renin-angiotensin system in the rat snake, Ptyas korros. 639 11

Dorsal aortic blood pressure (PSYS, systolic; PDIAS, diastolic; and PDA, mean) and heart rate (HR) were measured in resting freshwater bowfins (n = 6), Amia calva L., before and after i.v. injections of 50, 100, 200, 500, and 1000 ng.kg-1 of synthetic [Asn1, Val5]-angiotensin II (ANG II). Baseline PSYS, PDIAS, and PDA were 27.7 +/- 2.8, 22.4 +/- 1.8, and 24.5 +/- 2 mm Hg, respectively. Bowfins were only moderately responsive to ANG II in a stepwise manner and the increase in blood pressure became significant only at the two highest doses; lower doses tended only to increase arterial pressure. Pressor responses due to 200 and 500 ng.kg-1 decayed over a greater time period compared with other doses. alpha-Adrenergic blockade abolished 70% of the ANG II-mediated pressor responses. Eel, salmon, and goosefish angiotensin I (ANG I; 500 ng.kg-1) elicited similar vasopressor responses (magnitude and time course) which were eliminated by prior angiotensin converting enzyme inhibition (captopril; 2-10 mg.kg-1). Bullfrog ANG I evoked a pressor effect, only at a higher dose (5000 ng.kg-1). Consecutive norepinephrine (NE) injections (100, 200, 500, and 1000 ng.kg-1) increased PSYS, PDIAS, and PDA in a dose-dependent manner which was dependent on alpha-adrenoceptors since phentolamine (1-3 mg.kg-1) abolished 80% of the pressor action of NE. PSYS was elevated by 100 ng.kg-1 of NE but PDIAS and PDA were significantly increased only at 200 ng.kg-1 ANG II and NE had no measurable chronotropic effect and resting HR (27.2 +/- 0.8 beats.min-1) was unchanged. Captopril and phentolamine treatments produced rapid hypotension and bradycardia (25-30%) which lasted from 15 to 30 and 20 to 40 min, respectively. The rising and decreasing phases of the NE-mediated pressor responses had shorter durations than ANG II effects. Tachyphylaxis occurred with the high doses of ANG II and NE. The data show that in the ancient bowfin, which evidently lacks renal juxtaglomerular cells, the cardiovascular system can be regulated by the renin-angiotensin system and NE.
Gen Comp Endocrinol 1995 Jun
PMID:Angiotensin I- and II- and norepinephrine-mediated pressor responses in an ancient holostean fish, the bowfin (Amia calva). 762 88

1. We investigated the renal protective effect of efonidipine hydrochloride (NZ-105) in spontaneously hypertensive rats (SHR). SHR were given a diet containing 0.075% NZ-105 from 8 weeks old for 20 weeks. 2. 24-hr urinary protein excretion in the control SHR (drug-free diet) increased with age (from 77.3 mg/kg/day at 8 weeks old to 385.4 mg/kg/day at 28 weeks old), while that in NZ-105-treated SHR was maintained at almost the same level as that in Wistar-Kyoto rats (WKY), matched control animals throughout the experimental period. 3. The histological changes of the kidney were examined by light microscopy at the end of the treatment period. In control SHR, swelling and hyalinization of glomeruli, dilatation of renal tubules containing hyaline casts and arteriolosclerosis were revealed. The long-term administration of NZ-105 markedly suppressed these changes. 4. The kidney weights and plasma creatinine concentration in control SHR were higher than those in WKY, while they were significantly reduced in NZ-105-treated SHR. The long-term administration of NZ-105 also suppressed the elevation of systolic blood pressure and the increases of plasma renin activity and aldosterone concentration. 5. These findings suggest that NZ-105 inhibits the development of proteinuria and progressive kidney damage in SHR and may become a useful antihypertensive drug with the renal protective effect.
Gen Pharmacol 1994 Dec
PMID:Renal protective effect of efonidipine hydrochloride (NZ-105), a new calcium antagonist, in spontaneously hypertensive rats. 772 Oct 30

To determine if acute or chronic (21 days) losartan (10 mg/kg, s.c.) regulates the renin-angiotensin system in interscapular brown adipose tissue, angiotensin II (AII) content and [3H]overflow from slices preloaded with [3H]norepinephrine were examined. Acute or chronic losartan administration had no effect on AII content. AII increased evoked [3H] overflow from slices from control rats. Losartan administration did not alter basal [3H]outflow or evoked [3H]overflow. Acute losartan administration inhibited AII-induced enhancement of evoked [3H]overflow. Tolerance developed to the inhibitory effect of losartan following chronic administration.
J Neural Transm Gen Sect 1994
PMID:Acute and chronic losartan administration: effect on angiotensin II content and modulation of [3H]norepinephrine release from rat interscapular brown adipose tissue. 773 13

1. Isolated aortic segments from transgenic rats for the mouse renin gene Ren-2 were more sensitive than those from control Sprague-Dawley ones to the vasoconstrictions induced by angiotensin II and to the potentiation of norepinephrine contractions by this peptide. 2. In transgenic, but not in control aorta, pretreatment with angiotensinogen potentiated norepinephrine-induced vasoconstrictions, this effect being abolished by captopril. 3. These results suggest that in the aorta of transgenic rats there is a higher functional tissue renin-angiotensin system that potentiates the vascular reactivity to norepinephrine.
Gen Pharmacol 1994 Oct
PMID:Functional vascular renin-angiotensin system in hypertensive transgenic rats for the mouse renin gene Ren-2. 787 40


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