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.) Total renin, active renin, prorenin, angiotensin II, estradiol and progesterone were measured in maternal, placental and fetal blood and in trophoblastic and uterine tissues of the guinea pig. Furthermore, membrane angiotensin II receptors were measured in trophoblastic tissues. 2.) Blood and tissue concentrations of total renin, active renin, angiotensin II and steroids are shown to increase with gestational age. At the full term of pregnancy (70th post-coital day), tissue concentrations of total renin in chorion (23,900 +/- 2,752 ng/g of tissue/h), maternal placenta (14,210 +/- 1,131), fetal placenta (12,475 +/- 927) and uterus (7,677 +/- 798) are 100 time higher than those observed in placental, fetal and maternal blood. Distribution of blood and tissue prorenin (inactive renin) is similar to that found for total renin. Active renin/Total renin ratio reaches 1% in uterine, placental and chorion tissues and 9.3 +/- 1.0% in maternal, placental and fetal blood. 3.) Angiotensin II levels in systemic maternal blood (690 +/- 99 pg/ml) and in uterine blood (467 +/- 84) are higher than those found in placental blood (266 +/- 39) and in different trophoblastic tissues (between 200 and 400 pg/g). Angiotensin II receptor concentrations are highest in chorion. 4.) Regarding the steroid hormones, it is noted that placental and maternal blood contain more progesterone than trophoblastic tissues. The highest concentrations of estradiol are found in chorion tissue and uterine blood. 5.) A positive correlation is observed between angiotensin II and estradiol in uterine blood (r = 0.69, P less than 0.01) and in chorion (r = 0.71, P less than 0.01). These findings indicate that angiotensin II and estradiol could, by their interactions, play an important role in the physiology of pregnancy.
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PMID:[Study of the fetal and maternal renin-angiotensin system and chorio-placental steroids in the guinea pig]. 182 Apr 54

Angiotensin converting enzyme (ACE) inhibitors have been shown to improve morbidity and mortality in patients with heart failure. However, despite the demonstrated clinical benefits many physicians are reluctant to prescribe ACE-inhibitors to the mostly elderly heart failure patients due to concern for side effects which may be related to ACE-inhibitor-induced bradykinin accumulation. Angiotensin II receptor antagonists may provide more effective blockade of the renin-angiotensin-aldosterone system without causing bradykinin accumulation and thus associated side effects. The potential benefits of treating heart failure patients with an angiotensin II receptor antagonist instead of or in addition to an ACE-inhibitor are discussed.
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PMID:Theoretical basis for the use of angiotensin II antagonists in the treatment of heart failure. 763 6

Angiotensin II may act as an angiogenic and growth promoting factor on different cell types. To assess the role of angiotensin II on the compensatory renal response of the remnant kidney to unilateral nephrectomy (UNX), we measured renin, angiotensinogen, and angiotensin II type 1 receptor (AT1) mRNA levels as well as angiotensin II receptor density in 2 groups of 7 Sprague-Dawley rats 7 days after either shamp operation or UNX, Following UNX, the ratio of kidney weight to body weight (KW/BW) increased from 0.38 +/- 0.01 to 0.46 +/- 0.01% (p < 0.01). Neither renin (kidney) or angiotensiongen (kidney and liver) mRNA levels, determined by slot blot hybridization, changed after UNX. Angiotensin II receptor density was determined using an 125I-Sar1-Ile8 Ang II in situ receptor binding assay on fixed kidney sections. Binding specificity was verified using unlabeled Sar1-Ang II. Glomerular angiotensin II receptor density did not change significantly after UNX, nor did AT1 receptor mRNA. Thus, these data do not support a critical role for angiotensin II in the compensatory renal growth following uninephrectomy.
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PMID:[Gene expression of the renin-angiotensin system in compensatory renal hypertrophy secondary to contralateral nephrectomy]. 775 71

Recent developments in the techniques of molecular biology and the availability of inhibitors of the renin-angiotensin system have provided new insight into renin-angiotensin research. The control mechanism of renin release and the metabolism of circulating renin have been well characterized on the molecular level. Angiotensin II has been shown to play an important role not only in the regulation of blood pressure but also in cell growth and hypertrophy. ACE inhibitors are effective for the treatments of hypertension and heart failure. Furthermore, recent studies suggest that ACE inhibitors may prevent atherosclerosis and glomerulosclerosis. Angiotensin II receptor antagonists have similar beneficial effects. These effects of ACE inhibitors and angiotensin II-receptor antagonists may be mediated by growth factors and the extracellular matrix.
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PMID:[Pharmacology of the renin-angiotensin system]. 795 18

A genetically growth hormone (GH)-deficient strain of Lewis rats was used to test the hypothesis that the actions of GH on electrolyte and fluid homeostasis are mediated by the renin-angiotensin-aldosterone system (RAAS). Dwarf rats injected with recombinant bGH (2 mg.kg-1 x day-1) for 7 days (group GH1+) and 28 days (group GH4+), respectively, were compared with saline-injected dwarf (group GH-) and normal (group N) Lewis rats. GH decreased Na+ excretion and increased renal glomerular filtration rate in dwarf rats. The dietary intake and plasma concentrations of Na+ and K+ remained unchanged. GH increased plasma insulin-like growth factor I (IGF-I) concentrations in dwarf rats (GH - = 109 +/- 9, GH1+ = 184 +/- 5, GH4+ = 189 +/- 28, N = 477 +/- 29 ng/ml plasma). Plasma angiotensinogen increased towards the levels found in normal Lewis rats (GH- = 859 +/- 38, GH1+ = 906 +/- 18, GH4+ = 1,027 +/- 19, N = 1497 +/- 80 ng angiotensin I/ml plasma); plasma renin activity increased above that of the normal Lewis (GH- = 10.2 +/- 0.6, GH1+ = 11.7 +/- 0.7, GH4+ = 16.7 +/- 2.4, N = 10.6 +/- 0.8 ng angiotensin I.ml plasma-1 x h-1). Plasma aldosterone, corticosterone, and triodothyronine concentrations were unchanged by GH treatment. Angiotensin II receptor densities in GH- rats (liver = 356 +/- 23, kidney = 228 +/- 28, adrenal = 478 +/- 58 fmol/mg protein) were upregulated by GH (GH4+ rats; liver = 573 +/- 27, kidney = 360 +/- 86, adrenal = 721 +/- 78 fmol/mg protein).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Stimulation of the renin-angiotensin system by growth hormone in Lewis dwarf rats. 836 3

We evaluated the properties of glomerular angiotensin II receptors in renal glomeruli isolated from control rats and from rats with gentamicin-induced renal failure. There were no differences in the affinity of angiotensin II for its receptor between glomeruli from control and those from rats treated with gentamicin. Angiotensin II receptor density was lower in glomeruli from rats with renal failure than in those from control rats (985 +/- 71 in gentamicin treated rats vs. 1602 +/- 213 fmol/mg prot in controls). No significant differences were observed in renin activity in the supernatant from glomeruli isolated from control rats (3.74 +/- 0.29 ng angiotensin l/mL h) and those isolated from rats with gentamicin-induced renal failure (2.99 +/- 0.29 ng angiotensin l/mL h, p > 0.1). These findings do not support the contention of a role of angiotensin II in the development and maintenance of gentamicin-induced ARF.
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PMID:Glomerular angiotensin II receptors in gentamicin-induced renal failure in the rat. 877 Dec 41

As an antihypertensive regimen, angiotensin I-converting enzyme (ACE) inhibition appears to have an antiproliferative cardiovascular effect that is not caused by blood pressure reduction alone. On the other hand, ACE inhibition has been shown to induce neocapillarization in hypertrophied myocardium. The possible mechanisms behind these beneficial cardiovascular effects of ACE inhibition are the suppression of angiotensin II formation and the potentiation of bradykinin. Angiotensin II receptor antagonism appears to have a similar antiproliferative effect on myocardium and vascular smooth muscle as ACE inhibition. This suggests that the antiproliferative action of both regimens is due only to the reduction of the pressor and growth effects of angiotensin II, or that both regimens have an additional, similarly effective antiproliferative action. Recently, knowledge about angiotensin II receptors has almost exponentially expanded. The two main classes of angiotensin II receptors, type 1 and 2 (AT1 and AT2), have been shown to belong to the same receptor family. However, their signal transduction and function seem to differ totally. The function and signal transduction of AT1 are to a large extent known. All the well-known physiological and pathophysiological effects of angiotensin II have been attributed to AT1. On the other hand, AT2 has quite recently been shown to mediate antiproliferation and differentiation at least in some tissues and cells, e.g. in vascular endothelial cells and some cells of neuronal origin. This review highlights the recent findings on angiotensin II receptors, and discusses the mechanisms behind the beneficial cardiovascular effects of interfering with the renin-angiotensin system.
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PMID:The role of angiotensin receptors in cardiovascular diseases. 907 21

The renin-angiotensin-aldosterone system (RAAS) plays an important role in blood pressure regulation and fluid and electrolyte homeostasis. Angiotensin converting enzyme inhibitors (ACEI) were the first of the RAAS blocking agents to be widely used in the treatment of hypertension and congestive heart failure. Angiotensin II receptor antagonists, another class of pharmacological blockers of the RAAS, have more recently been shown to be safe and useful in hypertension and perhaps also in heart failure. This review deals with the similarities and differences between these two classes of drugs with particular emphasis on the effects of the drugs on the heart, the blood vessels, the kidney (role of the drugs as nephroprotective), the brain, the hormonal profile and finally the potential adverse effects. The place of angiotensin II antagonists in congestive heart failure remains to be more precisely defined.
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PMID:[Comparison between the effects of angiotensin-converting enzyme inhibitors and angiotensin II antagonists]. 977 25

Angiotensin II receptor antagonists lower blood pressure by blocking the final step in the renin pathway, whereas ACE inhibitors reduce angiotensin II production. ACE inhibitors also block kinin degradation, which may alter both efficacy and side-effects. Irbesartan, one of the newer receptor antagonists, has confirmed their tolerability and shown similar dose-related efficacy to other major classes.
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PMID:Irbesartan treatment in hypertension. 985 Mar 1

Pharmacological blockade of the renin-angiotensin system has been found to be a safe and efficacious way to treat hypertension and congestive heart failure. The success of the angiotensin converting enzyme inhibitors has led to interest in alternative ways to block the renin-angiotensin system. Angiotensin II receptor antagonists are a new class of anti-hypertensive drugs that provide a specific blockade of the effects of angiotensin II. Losartan potassium, the first compound of this class, has recently been approved in Japan. It seems likely that the angiotensin receptor antagonists will be suitable to first-line therapy and use of this class for treatment of hypertension will dramatically increase in Japan because of the excellent clinical and laboratory safety profiles.
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PMID:[Angiotensin II receptor antagonists: a review of the development and future perspective]. 1036 27


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