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 benefits and potential risks of estrogen use in post menopausal women were discussed at the 61st Annual Meeting of the Endocrine Society. The proven benefits of estrogen treatment include: 1) relief of symptoms such as hot flashes and atrophic changes in the vagina and breast due to a postmenopausal decrease in estrogen; and 2) a diminution of the degree of menapausal osteoporosis, a major health problem in aged 65 and older. Studies have shown a consistant improvement in the maintenance of skeletal mass when estrogen therapy is given. Adverse reactions to estrogen include an increase hepatic secretion of renin substrate resulting in increased blood pressure. Also, studies show both an increased coagulability of blood and cholesterol supersaturation of bile. Prime concern to women treated with the hormone therapy is the two to eight fold increase in risk of developing uterine cancer which increases with duration of estrogen use. Estrogen, although itself not a carcinogen appears to maintain the uterus in a condition that allows it to more readily respond to a carcinogenic stimuli. The relationship of estrogen use to lipoprotein metabolism and coronary heart disease is yet another area to be further studied.
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PMID:Postmenopausal estrogen therapy. 47 81

1 The characteristics of renin-like activity in rat uterus were studied. The optimum temperature was 50 degrees C and optimum pH 4.0. Potassium (100 mM) enhanced this activity but sodium or calcium had no effect. 2 Uterine renin-like activity was unchanged 24 h after bilateral nephrectomy. 3 Renin-like activity in the uterus increased slowly from birth to 4 weeks of age and faster between the 4th and 8th week. 4 Ovariectomy caused a considerable fall in uterine renin-like activity. 5 The following factors, known to affect renin secretion in the kidney, i.e., hypovolaemia, sodium loading, adrenalectomy, administration of desoxycorticosterone acetate and injection of isoprenaline, had no effect on uterine renin-like activity. 6 Stilboestrol, an oestrogen, caused a significant increase of uterine renin-like activity. Progesterone and testosterone had no significant effect on this activity but blocked the increase caused by stilboestrol. 7 During pregnancy there was a small but significant fall of renin-like activity in the uterus in the first week and a continuous increase throughout the later period of pregnancy. 8 It is concluded that uterine renin-like activity is independent of kidney renin and does not respond to stimuli affecting kidney renin. Uterine renin activity is hormone-dependent and may be governed by the ratio, oestrogen : progesterone.
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PMID:Rat uterus renin-like activity: effect of stimuli and hormones. 126 Jan 72

Diethylstilbestrol (DES) treatment of a male Syrian hamster resulted in the development of a renal tumor and its widely scattered serosal metastases. Cells in both the primary tumor and metastatic nodules contained secretory granules. The tumors were transplanted serially into DES-supported and non-DES-supported host hamsters until DES-independent tumors developed. Rabbit antiserum to mouse salivary renin and rabbit antiserum to rat kidney resin were reacted with sections of the primary tumor, metastatic nodules, and all transport tumors. The sections were stained by the PAP and Vector-ABC-AP procedures. Renin-positive material was observed in all tumors. Plasma renin activity (PRA) was determined for the host hamsters carrying the renal tumor transplants and compared to the PRA values that had been determined for normal non-DES-treated male and female hamsters. It was found that the average PRA values of host hamsters carrying the tumor transplants were significantly higher than the normal PRA values.
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PMID:Immunohistochemical renin study of DES-induced renal tumor in the Syrian hamster. 305 27

This article reviews the effects of estrogens on protein production by the liver, lipid metabolism, bone maturation and structure, and mineral metabolism. Also presented is a comparison of natural steroidal estrogens (estradiol, estrone, conjugated estrogens, and equine estrogens), synthetic steroidal estrogens (esters and 17-alpha-ethinyl estradiol), and nonsteroidal estrogens (diethylstilbestrol, dienestrol, and chlorotrianisene). Delivery of estrogens by different routes produces different effects. However, the metabolic changes that occur from enzyme induction within hepatic tissue are probably related to the type and dosage of estrogen rather than to the route of administration. Preparations containing estrogens that occur naturally in humans have the least exaggerated potency in the hepatic system relative to their estrogenicity, while conjugated estrogens that contain a mixture of equine estrogens are 2-3 times more potent in the hepatic system and ethinyl estradiol and diethylstilbestrol demonstrate a hepatic potency that is 4-18 fold greater than their estrogen potency. Estrogen is believed to induce a hypercoagulation state associated with both oral contraceptive (OC) use and pregnancy, but the clinical significance of increased levels of clotting factors remains undetermined. Estrogen appears to inhibit bone resorption in postmenopausal women and improve calcium balance. Although estrogen receptors are present in the kidney, their physiologic significance remains unknown. Estrogen does cause an increase in levels of plasma renin substrate, plasma renin activity, and angiotensin. Estrogen-induced increases in angiotensin, leading to renal sodium retention, appear to be the mechanism underlying the association of OCs with hypertension.
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PMID:Pharmacology of estrogens and estrogen-induced effects on nonreproductive organs and systems. 377 5

A prospective study examined the sequential effects of diethylstilboestrol (stilboestrol) on sodium balance, cardiac state, and renin-angiotensin-aldosterone activity in six patients with metastatic carcinoma of the prostate. Whereas metabolic balance studies did not show evidence of sodium retention during the first seven days of treatment, there was a significant and progressive increase in plasma volume after three months (mean increase 541 ml; p less than 0.01). Stilboestrol increased supine plasma renin and angiotensin II values but the response of renin-angiotensin-aldosterone activity to erect posture was progressively reduced during treatment. No significant changes in blood pressure or indices of cardiac function occurred during the three months of observation. The findings of increased basal renin-angiotensin-aldosterone activity and an increase in plasma volume suggest an important mechanism of the cardiac complications associated with oestrogen treatment.
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PMID:Effect of stilboestrol on sodium balance, cardiac state, and renin-angiotensin-aldosterone activity in prostatic carcinoma. 393 10

Estrogen may be important in the hemodynamic changes that develop during pregnancy; its role in the development of vascular refractoriness to the pressor effects of infused angiotensin II is unknown. We, therefore, examined the pressor responses to six doses of angiotensin II (0.115 to 5.73 micrograms/min) in unanesthetized, nonpregnant sheep both before and after treatment with either high-dose or low-dose 17 beta-estradiol (E2) and constructed dose-response curves. Although mean arterial pressure was unchanged after the infusion of E2, cardiac output rose 28% and systemic vascular resistance fell 19% (p less than 0.001). Infused angiotensin II resulted in dose-dependent rises in mean arterial pressure before and after E2; however, the pressor response after E2 was decreased 30% to 50%. Plasma renin activity rose from 1.15 +/- 0.09 ng/ml X hr to 2.57 +/- 0.39 and 3.21 +/- 0.61 ng/ml X hr with low-dose and high-dose E2, respectively (p less than 0.05). Acutely estrogenized nonpregnant sheep develop significant alterations in both the cardiovascular and the renin-angiotensin systems in addition to decreased pressor responsiveness to infused angiotensin II. Although our findings suggest that estrogen may be important in the development of the vascular refractoriness to angiotensin II seen in pregnancy, additional studies are needed to clarify the role of each E2-induced change.
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PMID:Estrogen-induced refractoriness to the pressor effects of infused angiotensin II. 636 12

Oral therapy with natural or synthetic estrogens, like ethinylestradiol, suffers from low, suboptimally defined bioavailability and excess hepatic estrogen actions. N,N-alkylated and non-alkylated sulfamates of ethinylestradiol, estradiol and estrone overcome these deficiencies. Ovariectomized Wistar rats (n = 6-7/group) were orally treated for 7 days, and killed on day 8, plasma was gained on days 0, 4, and 8. Systemic estrogenicity was quantified by assessment of uterine weight, vaginal cornification, and measurement of gonadotropins by homologous RIA. Estrogenicity in the liver was analysed. Angiotensinogen was estimated by RIA of angiotensin-1 after incubation of EDTA-plasma with porcine renin. Total and high-density cholesterol were measured by enzymatic methods. Preliminary biotransformation studies were performed after oral administration of 10 micrograms, 5 microCi [2,4,6,7-3H]estradiol sulfamate. Ethinylestradiol led to distinct elevation of angiotensin-1 and dramatic depression of cholesterol fractions, reflecting hepatic estrogen effects, already at doses with marginal systemic effects. Estradiol and estrone had systemic and hepatic estrogenic activity at much higher doses only. Estrogen sulfamates had systemic estrogen activity 10-90-fold above that of their parent estrogen. Non-alkylated sulfamates of given estrogens were more active than N-alkylated ones. Elevation of systemic estrogen activity was always combined with a dramatic reduction of hepatic estrogenicity. Estradiol sulfamate had a 90-fold elevated systemic estrogen activity vs estradiol, but lacked hepatic activity including the 30-fold dose inducing vaginal response. Three hours after administration no unchanged estradiol sulfamate was detectable in plasma. Rather peaks, probably representing estradiol and estrone, were found. Estrogen sulfamates are considered prodrugs of their parent estrogen, which do not interact with any liver function during the first-pass. They represent a new strategy of oral hormone administration. Their main potential seems to be the systemic generation of natural estrogens when used in oral contraceptives.
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PMID:Sulfamates of various estrogens are prodrugs with increased systemic and reduced hepatic estrogenicity at oral application. 854 Dec 36

Eight angiotensin peptides [angiotensin-(1-7), angiotensin II, angiotensin-(1-9), angiotensin I, angiotensin-(2-7), angiotensin-(2-8), angiotensin-(2-9), and angiotensin-(2-10)] were measured in plasma and kidney of adrenalectomized rats and estrogen-treated rats. In comparison with sham-operated rats, adrenalectomy increased plasma renin levels by 50-fold and reduced plasma angiotensinogen levels by 67%. Adrenalectomy increased plasma angiotensin peptide levels by 9- to 30-fold, but the increases in renal angiotensin peptide levels were much less than those seen for plasma. In comparison with vehicle-treated rats, estrogen treatment increased plasma angiotensinogen levels by 3-fold and reduced plasma renin levels by 41%. Estrogen treatment decreased plasma angiotensin peptide levels, whereas renal angiotensin peptide levels increased by as much as 2- to 3-fold. These results confirm the differential regulation of angiotensin peptide levels in plasma and kidney, and provide further support for the essential role of angiotensinogen in modulating plasma and tissue angiotensin peptide levels.
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PMID:Differential regulation of angiotensin peptides in plasma and kidney: effects of adrenalectomy and estrogen treatment. 924 48

In pursuit of the hypothesis that estrogen shifts the vasoconstrictor-vasodilator balance of the renin-angiotensin system, we investigated the cardiovascular responses to administration of angiotensin-(1-7) [ANG-(1-7)] and angiotensin II (ANG II) in female transgenic (mRen2)27-positive [Tg(+)] and -negative [Tg(-)] rats in the presence and absence of 3 wk of estrogen replacement therapy. Fifty-three female Tg(-) and Tg(+) rats were oophorectomized and received either 17 beta-estradiol (1.5 mg/rat s.c. for 3 wk) or vehicle. At the end of 3 wk of estrogen treatment, mean blood pressure was lowered in freely moving chronically cannulated Tg(+) (159 +/- 4 vs. 145 +/- 5 mmHg, P < 0.05) and Tg(-) (119 +/- 4 vs. 108 +/- 2 mmHg, P < 0.05) rats. Moreover, the magnitude of the depressor component of the biphasic response to ANG-(1-7) was significantly enhanced in estrogen-treated Tg(+) rats, whereas the pressor component to ANG-(1-7) was attenuated in both Tg(+) and Tg(-) rats. Estrogen replacement significantly attenuated the pressor response to ANG II in both Tg(+) and Tg(-) rats. In addition, estrogen replacement therapy significantly reduced plasma ANG-converting enzyme activity in association with a reduction in circulating levels of ANG II. Tissue levels (kidney and aorta) of ANG-converting enzyme were also reduced with chronic estrogen replacement therapy. On the other hand, estrogen augmented the levels of plasma ANG-(1-7) in Tg(+) animals. Plasma renin activity was unchanged with estrogen treatment. These findings provide the first evidence demonstrating that estrogen is protective against hypertension, possibly by amplifying the vasodilator contributions of ANG-(1-7), while reducing the formation and vasoconstrictor actions of ANG II.
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PMID:Estrogen protects transgenic hypertensive rats by shifting the vasoconstrictor-vasodilator balance of RAS. 943 44

Estrogen stimulates the renin-angiotensin system by augmenting both tissue and circulating levels of angiotensinogen and renin. We show, however, that angiotensin converting enzyme (ACE) activity in the circulation and in tissues is reduced in two animal models of postmenopausal chronic hormone replacement. We observed a reduction of ACE activity in association with a significant increase in plasma angiotensin I (Ang I) and hyperreninemia in ovariectomized monkeys treated with Premarin (conjugated equine estrogen) replacement for 30 months. Plasma angiotensin II (Ang II) levels were not increased in monkeys treated with estrogen, suggesting that the decrease in ACE curtailed the formation of the peptide. The Ang II/Ang I ratio, an in vivo index of ACE activity, was significantly reduced by estrogen treatment, further supporting the biochemical significance of estrogen's inhibition of ACE. In ovariectomized transgenic hypertensive (mRen2)27 rats submitted to estrogen replacement treatment for 3 weeks, ACE activity in plasma and tissue (aorta and kidney) and circulating Ang II levels were reduced, whereas circulating levels of angiotensin-(1-7) (Ang-(1-7)) were increased. Ang-(1-7), the N-terminal fragment of Ang II, is a novel vasodilator and antihypertensive peptide. Thus, the net balance of these effects of estrogen on the reninangiotensin vasoconstrictor/vasodilator system is to promote the anti-hypertensive effect.
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PMID:Bi-directional actions of estrogen on the renin-angiotensin system. 1034 98


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