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Biomedical subjects

J E Sealey

Publications and source records attributed to J E Sealey.

At least 73 records · Page 4Linked to original sources
PubMed1990

Infusion of recombinant human prorenin into rhesus monkeys. Effects on hemodynamics, renin-angiotensin-aldosterone axis and plasma testosterone.

Prorenin, the biosynthetic precursor of active renin, is present in high concentrations in the kidney and reproductive organs. We have proposed that prorenin may be the vehicle of local renin systems, separating the functions of circulating and tissue renin. In the present study, we investigated the effect of increasing plasma prorenin 3- to 4-fold by infusing recombinant prorenin, 400 ng/min for 40 min, into male rhesus monkeys. The prorenin was first warmed to 37 degrees C to reduce the endogenous renin activity to a minimum. The study included a 20 min baseline and a 40 min recovery period. Plasma prorenin increased from 72 +/- 14 ng/mL/h to a maximum of 246 +/- 18 ng/mL/h during the infusion (P less than .001) and fell to 169 +/- 23 ng/mL/h 40 min after the infusion was stopped. Active renin did not change significantly. Plasma aldosterone increased slightly during the prorenin infusion (by 13%) and returned to baseline during the recovery period (P less than .05 compared to the infusion period). Plasma testosterone fell significantly from 1.9 +/- 0.1 ng/mL to 1.6 +/- 0.1 ng/mL during the infusion and further to 1.4 +/- 0.1 ng/mL during the post-infusion period (P less than .05). Blood pressure fell slightly but not significantly. Heart rate, glomerular filtration rate and renal blood flow, as well as urine flow and urine sodium and potassium excretion showed no significant change. These results demonstrate that human recombinant prorenin is not converted to active renin in the circulation of rhesus monkeys.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensinogen↗
PubMed1990

Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats.

We studied the effects of regular diet (0.35% NaCl/1.1% potassium), high sodium diet (4% NaCl/0.75% potassium), or high sodium and high potassium diet (4% NaCl/2.11% potassium) on blood pressure, plasma renin activity, renal and cerebrovascular lesions, and incidence of stroke and mortality in male stroke-prone spontaneously hypertensive rats (SHRSP). In the first 4 weeks, the rise in blood pressure was higher in high NaCl than in high NaCl/high potassium or regular diet groups. However, by 8 and 12 weeks, the blood pressure in all three groups was similar. After 4 weeks of diet, plasma renin activity was similar in the three groups (3.4 +/- 0.8, 4.1 +/- 0.9, and 5.2 +/- 1.6 ng/ml/hr, in high NaCl, high NaCl/high potassium, and regular diet groups, respectively) and were not related to sodium excretion. After 8 weeks, plasma renin activity was significantly increased only in the high NaCl group (13.7 +/- 3.7 ng/ml/hr), and by 12 weeks plasma renin activity was significantly higher in the high NaCl group (25.3 +/- 3.6 ng/ml/hr) than in the high NaCl/high potassium (11.1 +/- 2.9 ng/ml/hr) or in the regular diet (7.8 +/- 4.6 ng/ml/hr) groups. Moderate to severe renal vascular lesions were first detected in the high NaCl group by 8 weeks of diet. At 12 weeks, renal vascular damage index (RVDI), estimated histologically, was significantly higher in the high NaCl group (RVDI = 79 +/- 14) than in the high NaCl/high potassium (RVDI = 40 +/- 11) and regular diet (RVDI = 7.8 +/- 4.6) groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Angiotensin II-induced atrial natriuretic factor release in dogs is not related to hemodynamic responses.

Angiotensin II (Ang II) and atrial natriuretic factor (ANF) appear to act as functional antagonists in the regulation of fluid and electrolyte homeostasis and blood pressure. To further define the relations between these hormones in vivo, we investigated the effect of low doses of Ang II (1-10 ng/kg/min) on plasma ANF levels. We also evaluated the influence of ANF release on the renal and hormonal responses to ANG II. Studies were performed in anesthetized and conscious instrumented dogs during sustained saline load and converting enzyme inhibition. In the anesthetized dogs, Ang II significantly increased plasma ANF levels and ANF arteriovenous difference without changing either atrial pressures or hematocrit. In both conscious and anesthetized dogs, ANF increases were not correlated with blood pressure responses to Ang II and did not occur in control groups when Ang II was replaced by vehicle. Ang II-induced sodium retention and stimulation of aldosterone production were attenuated, and renin suppression was enhanced in dogs having the largest changes in plasma ANF in response to converting enzyme inhibition or Ang II. These results demonstrate that in volume-replete dogs Ang II can promote ANF release independently of changes in atrial pressures or systemic hemodynamics, suggesting that Ang II may exert a significant modulatory effect on ANF secretion. The results also show significant relations between ANF and renal and adrenal responses to Ang II, which may suggest that, in turn, endogenous ANF modulates the effects of Ang II.

Adrenal Glands↗
PubMed1989

Atrial natriuretic factor in normal and hypertensive pregnancy.

Atrial natriuretic factor may play a role in the regulation of blood pressure, renal function, and volume homeostasis in normal and pathologic states. Atrial natriuretic factor and plasma renin activity were measured by radioimmunoassay in pregnant women with normal blood pressure (n = 29), chronic hypertension (n = 17), and preeclampsia (n = 18) during the first, second, and third trimesters and in the postpartum period. Serial data were obtained in 11 patients. Nonpregnant age-matched women were used as controls (n = 14). In normal gestation and in chronic hypertension, atrial natriuretic factor levels were in the same range as that in the control group. Mean atrial natriuretic factor was significantly higher in the antepartum and postpartum periods in severe preeclampsia. There was an inverse relationship between atrial natriuretic factor and plasma renin activity in pregnancies complicated by chronic hypertension or preeclampsia. Although fluctuations in atrial natriuretic factor levels did not predict preeclampsia, atrial natriuretic factor did correlate with the severity of the disease.

Atrial Natriuretic Factor↗
PubMed1989

Increased plasma atrial natriuretic factor and reduced plasma renin in patients with poorly controlled diabetes mellitus.

1. To investigate atrial natriuretic factor (ANF) and its relationship to the renin system in diabetes, we measured plasma immunoreactive ANF and plasma renin activity (PRA) in 27 non-ketotic diabetic patients without evidence of cardiac or overt renal disease, and compared them with 26 age- and sex-matched normal subjects. 2. Diabetic patients were divided prospectively into poor (PGC, n = 14) or moderate (MGC, n = 13) glycaemic control depending on their concurrent plasma glycohaemoglobin (HbA1) levels (greater than 9% or less than 9%, respectively). Plasma ANF was elevated in PGC diabetic patients (15.7 +/- 1.8 fmol/ml, mean +/- SEM) compared with MGC diabetics (9.9 +/- 0.8 fmol/ml, P less than 0.001) and normal subjects (10.1 +/- 1.3 fmol/ml, P less than 0.05). 3. In contrast, PRA was lower in the PGC diabetic patients (1.3 +/- 0.3 pmol of angiotensin 1 h-1 ml-1) compared with the other groups (2.5 +/- 0.5 and 2.1 +/- 0.2 pmol of angiotensin I h-1 ml-1, P less than 0.05). Diabetic groups had proportionally more patients with high prorenin values (over 30 ng h-1 ml-1) than the normal group, but there was no difference between the diabetic groups. 4. Among the diabetic patients, ANF was directly related to HbA1 (r = 0.49, P less than 0.005) and urinary albumin excretion (r = 0.40, P less than 0.02), and was inversely related to PRA (r = 0.36, P less than 0.04) and plasma creatinine (r = -0.42, P less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1989

Prorenin and renin as separate mediators of tissue and circulating systems.

The renin gene is expressed in extrarenal tissues. High concentrations of renin occur in female reproductive organs: the adrenals of rats and mice have intermediate levels. The testis also synthesizes renin, as does the anterior pituitary. In contrast, very low levels of renin (ie, below plasma levels) are found in the heart and extrarenal vascular tissues. The predominant form of renin in the human ovary, placenta, and uterus is prorenin and the human ovary, testis, and adrenals have been shown to secrete prorenin into the circulation. The kidney is the only organ that secretes active renin and it is also the major source of plasma prorenin. We have used the ovary as a model to study extrarenal renin. Ovarian prorenin secretion changes dynamically during the menstrual cycle and during gestation. Secretion occurs during the LH surge and when hCG is present in the blood during pregnancy. Plasma active renin does not change concurrently and only low levels of active renin are found in association with very high concentrations of prorenin in ovarian follicular fluid after gonadotropin stimulation. To explain the preponderance of prorenin, and the virtual absence of renin in the ovary we hypothesize that prorenin need not be converted to active renin to have effect. In vitro, when prorenin is acidified to pH 3.3 or cooled to 0 degrees C, it develops intrinsic catalytic activity without cleavage of the prosegment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Hemodynamic responses to converting enzyme inhibition in patients with renal disease.

We studied the effects of lisinopril on mean arterial blood pressure (MAP), plasma renin activity (PRA), and renal hemodynamics in nine patients with chronic renal disease and hypertension, before, and after three months of therapy. Lisinopril normalized blood pressure in five of nine patients (responders) and did not in the remaining four (nonresponders). PRA rose after lisinopril (4.8 +/- 2.6 ng/mL/h to 25 +/- 15 ng/mL/h, P less than 0.05) in responders, but not in nonresponders (2.0 +/- 1.4 ng/mL/h to 3.4 +/- 2.9 ng/mL/h). Glomerular filtration rate remained stable in both groups (responders: 43 +/- 11 mL/min to 43 +/- 22 mL/min; nonresponders: 39 +/- 25 mL/min to 32 +/- 21 mL/min). In the responders renal hemodynamics remained stable after lisinopril (renal plasma flow: 223 +/- 80 mL/min to 216 +/- 91 mL/min; filtration fraction: .20 +/- .04 to .20 +/- .05; renal vascular resistance: 386 +/- 179 to 326 +/- 209 units). In the nonresponders, renal plasma flow decreased (228 +/- 141 mL/min to 162 +/- 117 mL/min, P less than 0.005), filtration fraction increased (.19 +/- .08 to .24 +/- .12, P less than 0.05), and renal vascular resistance increased (695 +/- 747 to 1265 +/- 1574 units, P less than 0.05) after chronic lisinopril therapy. We conclude (1) there is a heterogeneous response to lisinopril in patients with chronic renal disease and hypertension, (2) lisinopril monotherapy may result in effective blood pressure control without renal hemodynamic compromise, and (3) an increase in PRA following converting enzyme inhibition may identify those in whom the circulating renin angiotensin system is participating in systemic hypertension and intrarenal hemodynamic changes.

Adult↗
PubMed1989

Dexamethasone-inhibitable stimulation of plasma prorenin by ketamine in cats.

Plasma prorenin in humans is derived from both renal and extrarenal sources, but in the cat most plasma prorenin is normally of renal origin. Sodium depletion and beta-adrenergic blockade can increase plasma prorenin in cats, but the effects of sedatives and glucocorticoids are unknown. We examined the effect of ketamine, a centrally acting nonbarbiturate anesthetic, and of the glucocorticoid dexamethasone on plasma prorenin and renin. Intramuscular injection of ketamine (20 mg/kg, three times a day) for 4 days increased plasma prorenin slowly and consistently, from 7.4 +/- 1.4 (+/- SEM) to 11.4 +/- 2.2, 17.1 +/- 2.5, 20.2 +/- 3.0, and 29.2 +/- 3.4 ng/ml.h (P less than 0.001) on days 1, 2, 3, and 4, respectively, without any effect on plasma active renin. Plasma renin substrate and cortisol were also unchanged. Bilateral nephrectomy reduced both baseline and stimulated plasma prorenin to undetectable levels. Treatment with alpha 1-blocker, beta 1-blocker, angiotensin-converting enzyme inhibitor, or Ca2+ antagonist did not affect the rise in prorenin induced by ketamine, but dexamethasone completely blocked the response. In contrast, dexamethasone alone had little effect on plasma prorenin. These results demonstrate that repetitive ketamine administration selectively increases plasma prorenin, suggesting that renal prorenin secretion may be regulated independently of active renin. Blockade of stimulated, but not baseline, plasma prorenin by dexamethasone is consistent with a negative effect of glucocorticoids on the regulatory elements of the renin gene.

Animals↗
PubMed1989

Tissue levels of active and total renin, angiotensinogen, human chorionic gonadotropin, estradiol, and progesterone in human placentas from different methods of delivery.

The components of the renin system are present in placental tissue, but their function in this tissue is not known. We investigated the relative distribution of the various components throughout the placenta to determine whether the distribution is consistent with a role for them in parturition or in stimulation or inhibition of placental hormone biosynthesis. Thus, active and total renin were measured in fetal membranes (chorion laeve and amnion) and in discoid placenta (chorion frondosum and chorion plate) of women who were delivered vaginally (n = 12) or by cesarean section with (n = 6) or without labor (n = 9). The interrelationships between active and total renin and angiotensinogen, progesterone, hCG, and estradiol concentrations were investigated. Labor had no significant effect on the concentration of active or total renin, angiotensinogen, hCG, or estradiol in any part of the placenta. Tissue progesterone concentrations were higher in placentas from women who underwent vaginal deliveries than in those who had cesarean sections with or without labor (P less than 0.02). The chorion laeve had 20 times more total renin per g than the discoid placenta and 3 times more than the amnion. In contrast the discoid placenta had 5 times more hCG per g and 3 times more progesterone per g than the fetal membranes. The concentration of estradiol was lower in amnion, while that of angiotensinogen was lower in the chorion frondosum than in all other regions. The tissue concentrations of active renin, prorenin, or total renin were not related to those of any of the other hormones. Altogether these data do not provide evidence of a role for the placental renin system in parturition or placental hormone biosynthesis.

Angiotensinogen↗
PubMed1988

Regulation of glomerular filtration rate in chronic congestive heart failure patients.

The purpose of this study was to identify the factor(s) that characterize impaired glomerular filtration rate (GFR) in congestive heart failure (CHF) patients. We studied 34 patients, measuring systemic hemodynamics, vasoactive hormones, and sodium and volume status. Renal plasma flow (para-aminohippurate) and GFR (inulin) were assessed by steady-state clearance techniques. Both linear and multiple regression analyses were performed. Impaired GFR was characterized by reduction of renal blood flow and renal fraction of cardiac output, and by an increase of renal vascular resistance. The correlation between GFR and filtration fraction (r = 0.492, P less than 0.003) indicated that individuals with greatest impairment of GFR had the lowest filtration fraction and increased overall renal vascular resistance, indicating dependence of GFR on afferent, rather than efferent vasoconstriction, under conditions of low renal perfusion. Mean vasoactive hormones and blood volume were increased, but without clear cut correlation with GFR. The greatest impairment of GFR was observed in elderly CHF patients, as renal blood flow and function demonstrated an age-dependent decline, in addition to the adverse effects of CHF. In a multiple regression model, renal blood flow and filtration fraction accounted for 69% and 25%, respectively, of the variability of GFR, with a co-linear influence of age. Thus, we have identified age-related, abnormal renal hemodynamic patterns in CHF, and the fragile nature of GFR in the elderly CHF population.

Adult↗
PubMed1988

A longitudinal study of urinary creatinine and creatinine clearance in normal subjects. Race, sex, and age differences.

The purpose of this study was to examine the variability of 24-hour urinary and serum creatinine levels and creatinine clearance in normal subjects and to develop nomograms for assessing the adequacy of 24-hour urine collections. The data were from a longitudinal research program examining biochemical, hormonal, and hemodynamic parameters in normal subjects. Bloods and 24-hour urine specimens were collected at yearly intervals from 144 people over 9 years, and from an additional 110 over 4 years. The subjects were originally distributed equally by sex, race (black, white), blood pressure (three groups within the normal range), and age (three groups). Men had 33% higher urine creatinines per weight than females (P less than 0.001). Because they only had 8% higher creatinine clearance per weight they also exhibited 21% higher serum creatinine. Blacks had 5% higher urine creatinine per weight than whites, perhaps reflecting greater muscle mass, but their serum creatinines were not different from those of whites, reflecting a 5% higher creatinine clearance by weight than whites (P less than 0.01). Interestingly, older black men (age greater than 60 years) had 12% lower urine creatinine/weight than younger black men (P less than 0.001). They also had 13% lower creatinine clearance by weight, resulting in no net difference in serum creatinine. The intraindividual variability in urine creatinine excretion averaged 15% and did not differ between blacks and whites and men and women. The within individual variability in serum creatinine and creatinine clearance averaged 14 and 20%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

On the renal basis for essential hypertension: nephron heterogeneity with discordant renin secretion and sodium excretion causing a hypertensive vasoconstriction-volume relationship.

We propose herein that there are two functionally abnormal nephron populations in essential hypertension: (1) a group of ischemic nephrons with impaired sodium excretion which chronically hypersecrete renin. Numerically, these ischemic nephrons comprise a minor subgroup since most patients with essential hypertension exhibit no overt evidence of renal insufficiency. (2) In reaction to this, a more numerous group of normal nephrons appears in adaptive hypernatriuresis. They have an increased distal sodium supply and consequently, a chronically suppressed renin secretion. One difference between patients with renovascular hypertension and those with essential hypertension is the intermingling of these two populations of nephrons. In our hypothesis, the adapting hyperfiltering normal nephrons accomplish the hypernatriuresis in response to saline infusion, that is characteristic of all essential hypertension. However, the unsuppressed secretion of renin, that arises from the ischemic nephron population attenuates this compensatory natriuresis in the following ways: (1) by inappropriately acting on the hyperfiltering nephrons to enhance proximal tubular sodium reabsorption; (2) by activating TGF-mediated afferent constriction in these nephrons, and (3) simultaneously, the reactive secretion of renin from ischemic nephrons is diluted by non-participation of the adapting hypernatriuretic nephrons so that plasma renin settles at a level which is insufficient to fully compensate GFR in the ischemic nephrons. These adaptive responses provide a basis for the observation that the inhibition of renin activity with converting enzyme inhibitors in essential hypertension increases renal blood flow and sodium excretion. They also explain why converting enzyme inhibitors can effectively reduce blood pressure, even when renin levels are not absolutely elevated, since any circulating renin imposed upon the adapting hypernatriuretic nephrons inappropriately impairs their sodium excretion. In addition, the theory explains why basal renin secretion is either not suppressed or inadequately suppressed in patients with essential hypertension. As a result, whole kidney homeostatic function is compromised because individual nephrons are responding to their individual stimuli to fulfil their individual need, rather than acting in concert with other nephrons. The net effect of this uncoordinated response is to shift total renal function so that systemic arterial hypertension is sustained by abnormal sodium retention for the inappropriately high plasma renin level, or vice versa.(ABSTRACT TRUNCATED AT 400 WORDS)

Homeostasis↗
PubMed1988

The ovarian prorenin-angiotensin system. Lessons from IVF.

Recent evidence suggests that prorenin and other active components of the renin-angiotensin system may be linked to ovarian physiology. Prorenin, the inactive form of the enzymatically active renin, is present in the fluid of mature human ovarian follicles in concentrations more than 10 times higher than that found in the plasma of women undergoing ovarian stimulation. Only 1% of the renin in follicular fluid is in active form. Concentrations of prorenin in fluid of immature follicles are lower than levels detected in concomitantly aspirated mature follicles. Study of prorenin levels disclosed a positive correlation to testosterone and E2 in fluids of mature follicles. Plasma prorenin increases about twofold at midcycle at the time of the LH surge; the peak of prorenin is sustained for about 40 hours. In patients undergoing ovarian stimulation for IVF, hCG administration results in much higher plasma prorenin levels and the height of prorenin response is directly related to the number of mature follicles. It peaked 4 to 6 days after hCG injection and then fell, close to baseline, by about 12 days after hCG administration. Examination of the time course of hormonal changes in response to hCG revealed a temporal relationship between prorenin and both plasma E2 and progesterone. In women who conceived, prorenin began to rise again on days 8 to 12 after embryo transfer when endogenous hCG was detected in the blood. No such changes in prorenin occurred in women with ovarian failure who conceived after transfer of a donor egg. These findings indicate that prorenin is produced by the mature follicle and the corpus luteum in response to LH/hCG. Since angiotensin II affects intracellular calcium and phospholipase activity, there are many potential roles for prorenin via angiotensin II action. Putative actions of the ovarian renin system may include control of oocyte maturation, ovulation, ovarian blood flow, and ovarian steroid biosynthesis. Future work to elucidate the function of this new renin system may have relevance to many basic and clinical aspects of human reproduction.

Enzyme Precursors↗
PubMed1988

Prorenin secretion from human testis: no evidence for secretion of active renin or angiotensinogen.

To determine if the testis secretes active renin and prorenin, we collected internal spermatic venous blood from 29 young men undergoing varicocelectomy and measured plasma prorenin and active renin together with angiotensinogen and testosterone. Prorenin was higher in internal spermatic venous plasma than in peripheral plasma (+5.3 +/- 1.2 (+/- SE) ng/mL.h [+1.21 ng/(L.s)]; P less than 0.001) as was testosterone [+344 +/- 32 ng/mL [(+1193 nmol/L; P less than 0.001], but there was no significant difference in either active renin (-0.74 +/- 0.45 ng/mL.h [-0.17 ng/(L.s)] or angiotensinogen [+12 +/- 24 ng/mL (+0.01 mumol/L)]. These results demonstrate that the testis secretes prorenin, but not active renin or angiotensinogen, into the general circulation. They support the hypothesis that extrarenal renin systems cannot process prorenin to renin.

Adult↗
PubMed1987

Plasma prorenin response to human chorionic gonadotropin in ovarian-hyperstimulated women: correlation with the number of ovarian follicles and steroid hormone concentrations.

Plasma prorenin and active renin were measured before and after human chorionic gonadotropin (hCG) administration in two groups of patients undergoing ovarian stimulation for 4-6 days with follicle-stimulating hormone alone or in combination with luteinizing hormone, for in vitro fertilization. Baseline total plasma renin (prorenin plus active renin; n = 12) averaged 25 +/- 8 ng/ml per hr (mean +/- SD). Total renin did not change during ovarian stimulation but it increased to 46 +/- 16 ng/ml per hr (P less than 0.05) 1 or 2 days later, just before hCG administration. Thirty-six hours after hCG administration, just before laparoscopy and egg retrieval, total renin was 123 +/- 97 ng/ml per hr; a peak of 182 +/- 143 ng/ml per hr occurred 2-6 days later--i.e., during the luteal phase of the menstrual cycle. In eight of the patients who did not conceive, total renin returned to baseline 14 days after hCG administration. In four who conceived, a nadir was reached (57 +/- 13 ng/ml per hr) 8-12 days after hCG administration and then total renin increased again as the plasma beta hCG measurement began to rise. By day 16 it averaged 225 +/- 157 ng/ml per hr. In a second group of five patients active renin and prorenin were measured separately. Active renin comprised less than 20% of the total renin at all times. It was unchanged until day 4 after hCG administration and then increased significantly only when plasma progesterone was high. Thus, the initial response to hCG was entirely due to an increase in prorenin. A highly significant correlation was observed between the number of follicles and the total renin increases on the day of aspiration (r = 0.93, P less than 0.001) and at the peak (r = 0.89, P less than 0.001). After hCG administration, a temporal relationship was observed between the rise in total renin and plasma estradiol and progesterone levels. These results demonstrate that plasma prorenin increases markedly after administration of hCG and that the rise is directly related to the number of ovarian follicles and to plasma estrogen and progesterone levels. The findings suggest that prorenin is produced by the mature ovarian follicle and by the corpus luteum in response to gonadotropin stimulation.

Chorionic Gonadotropin↗
PubMed1987

Ovarian prorenin-renin-angiotensin system.

Renin is classically considered to be an enzyme that is synthesized by the kidneys and secreted into the circulation where it affects angiotensin production. We review here recent evidence that suggests the existence of an extra-renal renin system, the ovarian prorenin-renin-angiotensin system, which may be linked to reproductive function. Prorenin, the inactive form of the enzyme renin, is present in the fluid of mature human ovarian follicles in extremely high concentrations; however, only 1 per cent of the renin in follicular fluid is in the active form. Plasma prorenin increases about 2-fold at midmenstrual cycle at the time of the LH surge, and the peak of prorenin is sustained for about 2 days. No change in plasma active renin levels occurs at this time. Administration of hCG to women whose ovaries have been stimulated with gonadotropins results in much higher plasma prorenin levels and the height of prorenin response is directly related to the number of mature follicles. Plasma prorenin also increases 10-fold during the early stages of pregnancy. It begins to rise on days 8 to 12 after embryo transfer, in parallel with the rise in endogenous hCG. The ovaries are the apparent source of the increase in plasma prorenin in early pregnancy since no such increase in prorenin occurred in a woman with ovarian failure who conceived after receiving a donor egg. These results suggest that prorenin is synthesized and secreted by the mature ovarian follicle and by the corpus luteum in response to LH/hCG. They also suggest that an ovarian renin system exists that is regulated by changes in prorenin.(ABSTRACT TRUNCATED AT 250 WORDS)

Chorionic Gonadotropin↗
PubMed1987

Altered renin and aldosterone excretion in patients treated for metastatic germ cell tumours.

Twenty-four patients with metastatic germ cell tumours were studied for abnormalities in the renin-aldosterone axis and for persistent abnormalities of renal function 9+ to 54+ months following completion of cisplatin based chemotherapy. Increased plasma renin activity and aldosterone were identified in fourteen of nineteen (79%) patients. The mean serum magnesium was subnormal. Statistically lower serum phosphorus levels, and higher urea and creatinine levels were also observed. No patients was hypertensive or on diuretics at the time of study. Since vascular toxicity has been reported after cisplatin based chemotherapy and hypomagnesaemia and increased plasma renin activity have been linked to cardiovascular events, these data imply that germ cell tumour patients treated with cisplatin based chemotherapy should be carefully observed for delayed cardiovascular toxicity.

Aldosterone↗