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 renin, erythropoietin and chorionic gonadotropin levels were evaluated in 57 patients with renal adenocarcinoma. Renin elevation, found in 37 per cent, was unrelated to blood pressure levels but was associated with high grade, high stage lesions of mixed histologic cell type and predicted a poor prognosis. Erythropoietin was raised in 63 per cent of patients and was more sensitive than renin in indicating the presence of renal adenocarcinoma. However, it was less specific and did not correlate directly with tumor grade, stage, histologic type, prognosis or hematocrit and hemoglobin levels. None of the patients had elevated chorionic gonadotropin levels. Therefore, we believe that renin and erythropoietin determinations may be of value as biochemical tumor markers in renal adenocarcinoma.
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PMID:Hormones in renal cancer. 85 Mar 15

Plasma renin, erythropoietin and chorionic gonadotropin levels were evaluated in 57 patients with renal adenocarcinoma. Renin elevation, found in 37 per cent, was unrelated to blood pressure levels but was associated with high grade, high stage lesions of mixed histologic cell type and predicted a poor prognosis. Erythropoietin was raised in 63 per cent of patients and was more sensitive than renin in indicating the presence of renal adenocarcinoma. However, it was less specific and did not correlate directly with tumor grade, stage, histologic type, prognosis or hematocrit and hemoglobin levels. None of the patients had elevated chorionic gonadotropin levels. Therefore, we believe that renin and erythropoietin determinations may be of value as biochemical tumor markers in renal adenocarcinoma.
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PMID:Hormones in renal cancer. 103 May 44

Renin gene expression in the mouse kidney and submandibular gland (SMG) are differentially regulated by cAMP. In this study, we examined the potential molecular mechanism responsible for this tissue-specific regulation. 32P end-labeled synthetic oligonucleotide containing mouse renin cAMP-responsive element (CRE) was incubated with kidney nuclear extracts from either control or cAMP-treated mice and analyzed by gel mobility shift assay. Our results demonstrated that cAMP induced a nuclear protein which complexed with the CRE oligonucleotide in a specific manner. This nuclear protein-DNA binding was competed effectively by the oligonucleotide containing human chorionic gonadotropin alpha-subunit CRE but not by the mouse renin DNA fragment from which the CRE was deleted by site-directed mutagenesis. In contrast, no DNA-protein complex formation could be detected when this [32P]CRE oligonucleotide was incubated with the SMG nuclear extract from control or cAMP-treated mice. However, CRE-binding protein complex formation was demonstrated in the SMG nuclear extract when the incubation was performed in the presence of 0.8% sodium deoxycholate and 1.2% Nonidet P-40, detergents that dissociate protein-protein complexes. Furthermore, in the absence of deoxycholate, we observed that SMG nuclear extract attenuated the binding of the kidney CRE-binding protein to mouse renin CRE in a dose-dependent manner and this inhibitory effect of SMG nuclear extract disappeared in the presence of sodium deoxycholate. This inhibitory nuclear protein in SMG is specific for CRE-binding protein since it does not affect nuclear protein binding to synthetic DNA oligonucleotides of human collagenase AP-1 and human metallothionein AP-2. Our data further suggest that inhibitory nuclear protein is present in lower quantities in other extrarenal tissues, i.e. testes, liver, brain, heart, but is not detectable in the kidney. Taken together, these results suggest that the SMG and certain extrarenal tissues contain nuclear trans-acting factor(s) that interact with CRE-binding protein, thereby interfering with its binding to mouse renin CRE. The presence of this inhibitory protein in the mouse SMG nucleus may contribute to the tissue-specific regulation of the renin gene expression by cAMP.
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PMID:Molecular mechanism of tissue-specific regulation of mouse renin gene expression by cAMP. Identification of an inhibitory protein that binds nuclear transcriptional factor. 165 39

The renin gene is expressed, primarily as prorenin, in the ovary, uterus and placenta. High concentrations of prorenin are present in human ovarian follicular and amniotic fluids and ovarian secretion causes increases in plasma prorenin at mid-menstrual cycle and during pregnancy. Plasma prorenin is low but detectable in nephrectomized human subjects. Comparative studies in female cats revealed several differences. Cat plasma prorenin became undetectable after bilateral nephrectomy. Neither plasma prorenin nor renin increased during pregnancy. Renin and prorenin were undetectable in ovarian follicular, amniotic and allantoic fluids. Human chorionic gonadotropin-induced ovulation caused only small increases in plasma prorenin. In contrast, renin and prorenin were clearly present in extracts of reproductive tissues. Ovarian total renin was lowest during anestrus (169 +/- 27 ng/g per h) and estrus (258 +/- 58 ng/g per h) and increased with ovulation (385 +/- 31 ng/g per h). Higher ovarian levels were found during pseudopregnancy (1370-2030 ng/g per h) and early pregnancy (1312-2700 ng/g per h) and in the placental chorion disc of early pregnancy (1755-1184 ng/g per h). In the uterus, the level was 98-183 ng/g per h during gestation. These results demonstrate that, in marked contrast to humans, only the cat kidney secretes prorenin into body fluids. Nonetheless, total renin increases in cat ovaries during follicle maturation, ovulation, pregnancy and pseudopregnancy, in the uterus during gestation and in the placental chorion disc. These results are consistent with an autocrine or paracrine role for the tissue renin system in cat reproductive tissues.
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PMID:Tissue renin and prorenin increase in female cats during the reproductive cycle without commensurate changes in plasma, amniotic or ovarian follicular fluid. 165 92

Tumors of the female genital tract may be associated with a variety of unusual clinical manifestations. Uncommon endocrine and paraendocrine syndromes include production of human chorionic gonadotropin by tumors other than those of germ cell origin, hyperthyroidism associated with struma ovarii and gestational trophoblastic disease, the carcinoid syndrome, the Zollinger-Ellison syndrome, hypercalcemia, Cushing's syndrome, hypoglycemia, hypertension related to renin or aldosterone production, hyperprolactinemia, inappropriate secretion of antidiuretic hormone, and virilization associated with Nelson's syndrome and placental site trophoblastic tumor. Paraneoplastic syndromes associated with gynecological tumors include disorders of the nervous system, connective tissue, and skin, as well as hematologic abnormalities and the nephrotic syndrome. Heritable and other congenital syndromes associated with these tumors are the Peutz-Jeghers syndrome, the nevoid basal-cell carcinoma syndrome, Ollier's disease and Maffucci's syndrome, hereditary leiomyomatosis, ataxia-telangiectasia, von Hippel-Lindau's disease, thyroid abnormalities associated with Sertoli-Leydig cell tumors, and Carney's complex. Other syndromes associated with tumors of the female genital tract include Meigs' syndrome, hyperamylasemia, uveal melanocytic lesions, and pyrexia.
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PMID:Clinical syndromes associated with tumors of the female genital tract. 175 57

We examined whether renin (prorenin plus renin) is secreted from the human placenta into the maternal or fetal circulation and compared the secretion rate to that of human chorionic gonadotropin (hCG), progesterone, and estradiol. While estradiol and progesterone passed into both circulations, renin (mostly prorenin) and hCG were secreted predominantly into the maternal circulation. To examine if prorenin passed from the maternal to the fetal circulation and vice versa, we perfused both circuits separately with exogenous recombinant human prorenin. No prorenin passed from maternal to fetal circulations, but a small amount (less than 10%) slowly passed from fetal to maternal, beginning 15 min after the addition of prorenin. Exogenous prorenin was not converted to renin in either circulation. Perfusate total renin had close to 10% active renin, whereas that of tissue extracts was closer to 50%. In conclusion, the results are consistent with some tissue activation of prorenin, either in vitro or in vivo, but no activation in the maternal or fetal circulations. The human placenta may secrete prorenin into the maternal but not into the fetal circulation. The possibility that the placenta may secrete a small amount of active renin into the maternal circulation was not ruled out.
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PMID:Prorenin secretion from human placenta perfused in vitro. 205 64

Angiogenesis is a feature of ovarian follicle and corpus luteum development. Ovarian homogenates and follicular fluid (FF) contain factors that stimulate new vessel formation. Because the renin-angiotensin system has been shown to facilitate angiogenesis, renin activity was measured in FF and plasma from 20 normal, ovulatory women who were undergoing in vitro fertilization and were therefore stimulated with human menopausal gonadotropin/human chorionic gonadotropin. Serum estradiol (E2) and FF E2 and progesterone (P) were also determined and correlated with FF and plasma renin activity. FF renin activity was significantly higher than plasma renin activity (55.8 +/- 7.9 versus 3.8 +/- 0.7 ng of angiotensin I/ml/hour, P less than 0.001). Positive correlations were found between FF E2 and renin activity (r = 0.53, P less than 0.05). There was also a correlation between plasma renin activity and serum E2 (r = 0.69, P less than 0.05). No correlation was present between FF P and renin activity. The high renin-like activity present in FF after stimulation with gonadotropins could be involved in the mechanism of angiogenesis and may play an important role in events related to reproductive processes.
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PMID:Renin-like activity in ovarian follicular fluid. 241 Mar 2

To clarify a possible participation of the renin-angiotensin-system (RAS) in physiological processes of pregnancy, findings are listed about occurrence and variations of RAS components in uterus, placenta, amniotic fluid, fetal membranes, fetus and serum. There exist complete and independent RAS in the respective organs and tissues. During pregnancy concentrations and/or activities of the components change, but in different ways and non-uniforming. The information now available does not yet allow a definite view on the role of RAS during pregnancy and on the correlations to estrogens, progesterone, chorionic gonadotropin, prostaglandins etc. Supposedly RAS may be involved to a high degree in the local regulation of blood flow and the maintenance of fetal vascular homeostasis. Furthermore, there are relations between fetoplacental components of RAS and pregnancy-induced hypertension. Further investigations are necessary. They are expected to offer therapeutic possibilities for influencing pathological processes in which RAS plays a role.
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PMID:[Possible involvement of the renin-angiotensin system in reproduction. III. Occurrence and role in pregnancy]. 255 Nov 7

A 26-year-old man with hypothalamic hypodipsia-hypernatremia syndrome is reported, who presented with adipsia, hypernatremia, and impaired osmolality-mediated arginine vassopressin (AVP) secretion. A chorionic gonadotropin-secreting tumor was detected in the anterior hypothalamus and treated with external irradiation. After the treatment, hypernatremia persisted and was not corrected by fluid loading, osmolality-mediated AVP secretion remained impaired. Despite the absence of signs of hydropenia, hypovolemia was suggested by low blood pressure and elevated plasma indices of the renin-angiotensin system, and supported by blood volume determination. The plasma aldosterone concentrations were inappropriately low for the renin-angiotensin status. The plasma atrial natriuretic polypeptide (ANP) level was normal in spite of hypovolemia and increased more than double after fluid loading. Hypernatremia, primarily caused by hypodipsia and impaired osmolality-mediated AVP secretion, secondarily sustained ANP secretion and suppressed aldosterone release, which conceivably contributed to the development and perpetuation of hypovolemia in this patient.
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PMID:Pathogenesis of extracellular fluid abnormalities of hypothalamic hypodipsia-hypernatremia syndrome. 297 77

Renin-like activity and angiotensin II/III immunoreactivity in follicular fluids from 34 women stimulated with human menopausal gonadotropin and human chorionic gonadotropin (56.8 +/- 6.5 ng angiotensin I per milliliter per hour and 187 +/- 21 pg/ml [mean +/- SEM], respectively) were much higher (p less than 0.001) than in follicular fluids from 12 unstimulated preovulatory women (1.41 +/- 0.37 ng angiotensin I per milliliter per hour and 58.5 +/- 13.7 pg/ml) and in simultaneously drawn plasma (4.47 +/- 0.73 ng angiotensin I per milliliter per hour and 31.8 +/- 11.6 pg/ml, respectively; p less than 0.001). Plasma renin-like activity and angiotensin II/III immunoreactivity in stimulated cycles did not differ from unstimulated cycles. Follicular fluid angiotensin II/III immunoreactivity correlated significantly with follicular fluid renin-like activity in stimulated (r = 0.72; p less than 0.01) and in unstimulated samples (r = 0.86; p less than 0.01). Significant correlation was found also between follicular fluid renin-like activity and estradiol. A sharp preovulatory rise of renin-like activity and angiotensin II/III immunoreactivity was noted in unstimulated follicular fluid samples collected on cycle days 13 and 14 compared to days 9 through 12 (p less than 0.01). The findings that follicular fluid renin-like activity and angiotensin II/III immunoreactivity are correlated, and that gonadotropins have a stimulatory effect on follicular fluid concentrations support our concept of a physiologic intrinsic ovarian renin-angiotensin system.
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PMID:The ovarian renin-angiotensin system: renin-like activity and angiotensin II/III immunoreactivity in gonadotropin-stimulated and unstimulated human follicular fluid. 310 87


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