Cyclical secretion of prorenin during the menstrual cycle: synchronization with luteinizing hormone and progesterone.

Sealey, Jean E.; Atlas, Steven A.; Glorioso, Nicola; Manapat, Henrietta; Laragh, John H.

doi:10.1073/pnas.82.24.8705

Cited by 103 publications

(46 citation statements)

References 27 publications

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“…Sealey and her group have also demonstrated that plasma prorenin peaks shortly after the luteinizing hormone peak during the normal menstrual cycle (24). These data strongly suggest gonadotropins may regulate theca cell renin production, as they appear to regulate Leydig cell renin production (25).…”

Section: Discussionmentioning

confidence: 66%

Human ovarian theca cells are a source of renin.

Yung

Sherrod

Løbo

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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Human ovarian follicular fluid contains renin-like activity. In normal women, circulating levels of prorenin, the biosynthetic precursor of renin (EC 3.4.23.15), change in parallel with changes in progesterone during the menstrual cycle. Therefore, the ovary has been implicated as a source of plasma prorenin. In the present studies, we report the finding of high concentrations of prorenin in human ovarian follicular fluid (3000 ng-ml-P'hr-vs. 10-40 ngml1X hrXC in normal human plasma) obtained from follicles of women prepared for in vitro fertilization. The inactive reninlike enzyme was identified as prorenin by its activation characteristics, its molecular weight of 47,000, which is the same as that for recombinant prorenin, and its cross-reactivity with human renal renin antibodies. Culture of isolated human theca cells and isolated granulosa cells indicated that prorenin is secreted by theca cells but not by granulosa cells. Prorenin production by theca cells peaked during the first 10 days of culture and gradually decreased by 17 days. Active renin levels were 10% or less of the prorenin levels. Prorenin was barely detectable in medium from granulosa cells cultured for 24 days. Immunohistochemical staining of human ovaries (n = 5) with anti-human renin antibody demonstrated the presence of renin primarily in theca cells. These studies suggest that the theca cell is the source of the large quantities of prorenin in human ovarian follicular fluid.

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Section: Discussionmentioning

confidence: 66%

Human ovarian theca cells are a source of renin.

Yung

Sherrod

Løbo

et al. 1988

Proc. Natl. Acad. Sci. U.S.A.

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“…Studies of the regulation of active renin and prorenin secretion were performed in 32 normal human volunteers who ranged in age from 21 to 56 yr. Only male subjects were used to avoid the potential confounding effects of variation in prorenin levels throughout the menstrual cycle (20 was the same on both diets. Samples for plasma renin measurements were obtained at the end of the period of equilibration.…”

Section: Subjectsmentioning

confidence: 99%

Response of plasma prorenin and active renin to chronic and acute alterations of renin secretion in normal humans. Studies using a direct immunoradiometric assay.

Toffelmire¹,

Slater²,

Corvol³

et al. 1989

J. Clin. Invest.

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We employed a novel immunoradiometric assay to measure plasma levels of active renin and prorenin in physiologic and pharmacologic studies designed to characterize renin biosynthesis and processing in response to both chronic and acute stimuli of renin secretion in normal human subjects. Stimulation of renin secretion with prolonged dietary sodium restriction or amiloride resulted in marked increases in the plasma levels of prorenin, active renin, and plasma renin activity (PRA); suppression of renin secretion with indomethacin resulted in parallel decreases in prorenin, active renin, and PRA. In contrast, acute stimulation with upright activity or administration of an angiotensin-converting enzyme inhibitor, which increased active renin and PRA from 2-to 15-fold, had no effect on prorenin levels. Based on studies in cultured human juxtaglomerular tumor cells, it has been proposed that prorenin is secreted constitutively whereas active renin is stored in and released from secretory granules through a regulated pathway. Our studies are consistent with such a model: the parallel changes in active renin and prorenin with experimental maneuvers of long duration suggest that both the constitutive and regulated pathways are altered under these conditions. The increase in active renin levels in the absence of a change in prorenin that occurs in response to acute stimuli presumably represents the release of preformed active enzyme that is stored in secretory granules.

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“…The process, apparently via the ovarian follicle, doubles the concentration of plasma prorenin. 70 - 71 There appears to be no renin secretion from the ovary, and there is no increase in plasma renin during the surge of ovarian prorenin secretion, suggesting that the ovarian prorenin system functions independently of plasma renin.…”

Section: -65mentioning

confidence: 99%

Lewis K. Dahl Memorial Lecture. The renin system and four lines fo hypertension research. Nephron heterogeneity, the calcium connection, the prorenin vasodilator limb, and plasma renin and heart attack.

Laragh

1992

Hypertension

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As the major regulator of arterial blood pressure and sodium balance, the renin axis supports normotension or hypertension via angiotensin-mediated vasoconstriction and angiotensin plus aldosterone-induced renal sodium retention. In this endocrine servo control, renal renin is released by hypotension or salt depletion; conversely, with hypertension or volume excess, plasma renin activity falls to zero. Accordingly, any renal renin secretion is abnormal in the face of arterial hypertension. Human hypertensive disorders comprise a spectrum of abnormal vasoconstriction-volume products (renin-sodium profiles). Excess plasma renin activity for the sodium balance is created by nephron heterogeneity in which a subpopulation of ischemic nephrons hypersecretes renin and retains sodium. This excess renin impairs adaptive natriuresis of neighboring normal nephrons. Research defining the pivotal role of vascular cytosolic calcium for transducing sodium or renin-mediated vasoconstriction explains the selective value of calcium antagonists for correcting the sodium-volume-mediated, and beta-blockers or angiotensin converting enzyme inhibitors for correcting renin-mediated, arteriolar vasoconstriction. The renin precursor prorenin appears to be physiologically active, causing selective vasodilation that offsets renin-mediated vasoconstriction. Overactivity of prorenin may be involved in the hyperperfusion vascular injuries of diabetes mellitus and toxemias. Prorenin underactivity may facilitate renin-mediated ischemic vascular injury. In essential hypertension, undue plasma renin activity is powerfully and independently associated with heart attack risk. Conversely, patients with low renin activity are protected from heart attack despite higher blood pressures and greater age. Also, renin or angiotensin administration consistently causes vascular injury in the heart, brain, and kidneys of animals. These data suggest new potentials for the prevention of cardiovascular sequelae (heart attack and stroke) by using explicit strategies to curtail plasma renin activity.

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Cyclical secretion of prorenin during the menstrual cycle: synchronization with luteinizing hormone and progesterone.

Cited by 103 publications

References 27 publications

Human ovarian theca cells are a source of renin.

Human ovarian theca cells are a source of renin.

Response of plasma prorenin and active renin to chronic and acute alterations of renin secretion in normal humans. Studies using a direct immunoradiometric assay.

Lewis K. Dahl Memorial Lecture. The renin system and four lines fo hypertension research. Nephron heterogeneity, the calcium connection, the prorenin vasodilator limb, and plasma renin and heart attack.

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