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)

This double-blind, placebo-controlled human study was performed to determine the endocrine responses to intravenously administered indomethacin at two dose rates (0.36 or 0.72 mg/kg bolus followed by 0.071 or 0.143 mg/kg/hr for 150 min.). A 5% hypertonic saline infusion was used for further assess the hormonal systems regulating body fluid and electrolyte balance. Plasma renin activity (PRA) and concentrations of aldosterone and vasopressin (AVP) were unaffected by indomethacin. Hypertonic saline caused a 5% increase in plasma sodium and a 4.2% increase in serum osmolality, with a concomitant two-fold rise in plasma AVP levels and significant declines in PRA and aldosterone. Indomethacin had no effects on these responses, and did not affect plasma catecholamine concentrations, but the hypertonic saline infusion doubled the noradrenaline levels in plasma. Atrial natriuretic peptide (ANP)-like immunoreactivity in plasma was not affected by indomethacin nor by hypertonic saline. The higher dose rate of indomethacin resulted in significant stimulation of growth hormone release, but plasma prolactin levels were not influenced. Thus acute intravenous administration of indomethacin proved to be devoid of significant effects on the multihormonal system regulating fluid and electrolyte balance.
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PMID:Hormonal, haemodynamic, and subjective effects of intravenously infused indomethacin: no change in the physiological response to hypertonic saline challenge. 253 May 7

Serotonergic stimulation can increase the secretion of several hormones through the involvement of different serotonin (5-HT) receptor subtypes. RU 24969, a 5-HT agonist with highest affinity at 5-HT1A and 5-HT1B receptors, increased plasma renin activity (PRA) and plasma renin concentration (PRC) as well as plasma corticosterone and prolactin concentrations in a dose-dependent manner. Inasmuch as 5-HT2 receptors mediate the serotonergic stimulation of renin secretion, we examined the ability of two selective 5-HT2 antagonists, ritanserin and LY53857, to inhibit the neuroendocrine effects of RU 24969. To determine whether the 5-HT receptors which are involved in the stimulation of these hormones are pre- or postsynaptic, RU 24969 was also injected to rats whose brain serotonergic neurons were chemically destroyed by i.c.v. injection of 5,7-dihydroxytryptamine. Both ritanserin and LY53857 blocked the effect of RU 24969 on PRA and PRC, but did not inhibit the RU 24969-induced elevation in plasma corticosterone concentrations. Ritanserin did not inhibit the effect of RU 24969 on prolactin levels, but LY53857 produced a partial inhibition of the RU 24969-induced elevation of prolactin concentrations. In rats with chemical lesions of serotonergic neurons the dose-response curves of RU 24969 for PRA and PRC as well as corticotropin, corticosterone and prolactin shifted to the left, suggesting functional up-regulation of postsynaptic 5-HT receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuroendocrine evidence for denervation supersensitivity of serotonin receptors: effects of the 5-HT agonist RU 24969 on corticotropin, corticosterone, prolactin and renin secretion. 255 18

Data presented in this study suggest existence of hyperendorphinism in uraemic patients. This hyperendorphinism may be regarded both as a primary beneficial compensatory mechanism counteracting disturbances of the internal environment, while causing secondary harmful side effects, which contribute to the uraemic state. Erythropoietin treatment of uraemic, haemodialyzed patients is followed by marked endocrine alterations (suppression of plasma levels of STH, ACTH, prolactin, glucagon, aldosterone, cortisol and plasma renin activity, elevation of plasma insulin and atrial natriuretic levels, lack of influence on plasma PTH, CT and AVP). It remains to be clarified whether the erythropoietin induced endocrine alterations are due to correction of the existing anaemia or reflect a specific effect of this hormone.
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PMID:Endocrine abnormalities in patients with endstage renal failure. 256 Mar 46

The modifying effect on exercise performance and neuroendocrine response of the nonselective beta blocker timolol (10 mg b.i.d. for 5 days) and the beta 1-selective beta blocker metoprolol (100 mg b.i.d. for 5 days) was studied. The hormones studied were growth hormone, prolactin, cortisol, renin, epinephrine, dopamine, and norepinephrine. The response was studied during short-term maximal dynamic exercise, using two different exercise protocols; continuous (n = 11) and intermittent (n = 9) bicycle ergometry, in normal healthy young men. Accumulated work on placebo was nearly identical in the two studies, but was significantly reduced by 10.4% and 6.6% with timolol and by 4.7% and 6.7% with metoprolol, during continuous and intermittent exercise, respectively. During continuous exercise, accumulated work was 5.8% lower (p less than 0.05) with timolol than with metoprolol. The hormonal plasma concentrations of all hormones except renin were higher during continuous exercise than during intermittent exercise. Beta blockade had no effect on baseline hormonal levels, but the response was markedly changed during exercise. Maximum epinephrine, cortisol, and prolactin responses increased after beta blockade; dopamine remained nearly unchanged; while the renin responses were attenuated. Norepinephrine concentrations were slightly increased during continuous exercise by beta blockade and rose in direct proportion to the increase in workload. During intermittent exercise, maximum norepinephrine levels were significantly reduced by beta blockade compared with placebo. Thus the effect of beta 1-selective and nonselective beta receptor blockade on circulating hormones does not seem to explain the reduced exercise capacity following beta blockade.
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PMID:Effect of beta-adrenergic blockade on hormonal responses during continuous and intermittent exercise. 257 80

In rats, angiotensin II appears to be synthesized in the anterior pituitary gland and stored in gonadotropes in the same granules as the beta-subunit of luteinizing hormone (LH). The gonadotropes also contain renin-like and angiotensin-converting enzyme-like immunoreactivity, but angiotensinogen-like immunoreactivity is found in a separate population of cells and does not colocalize with any of the known anterior pituitary hormones. This suggests that angiotensinogen shuttles to the gonadotropes in a paracrine fashion. There are angiotensin II receptors on lactotropes and corticotropes, but no definite function has been established for pituitary angiotensin II in the regulation of prolactin and adrenocorticotropic hormone.
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PMID:Renin-angiotensin system in the anterior pituitary of the rat. 265 Jul 14

Renin, prorenin and cathepsin B were localized in human lactotrophs using immunoelectron microscopic techniques. Renin and prorenin were found in numerous cytoplasmic granules. Cathepsin B, a lysosomal enzyme known to be able to activate prorenin into renin, was also present in cytoplasmic granules of lactotrophs. The co-localization of renin and prolactin in the same secretory granules was demonstrated by double immunolabelling. Renin and cathepsin B were co-localized in some granules by the same technique. These results suggest a local activation of renin in the secretory granules of lactotrophs and support the hypothesis of a possible autocrine action of the renin-angiotensin system on prolactin release.
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PMID:Renin and cathepsin B in human pituitary lactotroph cells. An ultrastructural study. 265 57

The present studies were undertaken to determine the involvement of neurons in the hypothalamic paraventricular nucleus (PVN) in stress-induced renin secretion. The stressor was a 10-min conditioned emotional response (CER) paradigm. Bilateral electrolytic lesions in the PVN prevented the stress-induced increase in plasma renin activity (PRA), and plasma renin concentration (PRC). Stress-induced corticosterone secretion was also blocked, supporting the histological verification and suggesting that the lesion included corticosterone-releasing factor neurons in the PVN. Stress-induced renin secretion appears to be restricted to the PVN, as electrolytic lesions in the nucleus reuniens, dorsal and caudal to the PVN, did not prevent the stress-induced increase in either PRA or PRC. The next step was to determine whether cell bodies in the PVN or fibers of passage through the PVN mediate the stress-induced increase of these hormones. For this purpose, bilateral stereotaxic injections of the cell-selective neurotoxin ibotenic acid (10 micrograms/microliter; 0.3 microliters per side) were performed 14 days prior to the stress procedure. Histological evaluation of the tissue revealed cell death and lysis in the PVN. Ibotenic acid injection into the PVN prevented the effect of stress on PRA, PRC and corticosterone levels. None of the lesions prevented the stress-induced rise in plasma prolactin concentration. These results suggest that neurons in the PVN play an important role in mediating stress-induced increases in renin and corticosterone but not prolactin secretion.
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PMID:Neuronal cell bodies in the hypothalamic paraventricular nucleus mediate stress-induced renin and corticosterone secretion. 266 72

The effect of captopril on the response of plasma aldosterone (PA) and plasma renin activity (PRA) to 10 mg metoclopramide i.v. was studied in 9 normal subjects. In the same conditions the prolactine response was studied in 6 healthy males. Metoclopramide induced a significant increase of PA during control study, as well as after treatment with captopril. The maximal increase of PA was of similar magnitude and occurred 15 mn after injection of metoclopramide on both occasions. PRA did not change appreciably after metoclopramide neither during control study nor during captopril. The prolactin response to metoclopramide was blunted by treatment with captopril. In conclusion, captopril did not alter the aldosterone response to metoclopramide, which suggests that dopaminergic control of aldosterone secretion is independent of modifications in the renin-angiotensin system.
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PMID:[Effect of captopril on the plasma aldosterone response to metoclopramide in normal subjects]. 268 76

This review examines the role of serotonin (5-HT) in depression. Dysfunction of serotonergic neurons has been implicated as one of the causes of endogenous depression. Since serotonergic neurons innervate the hypothalamus and these neurons send collaterals to several other brain areas, it is possible that hypothalamic sites which control hormone secretion receive the same serotonergic afferents that innervate other limbic areas in the brain. Several investigators have devised neuroendocrine challenge tests measuring the effect of 5-HT agonists on plasma cortisol and prolactin in depressed patients. These tests help to identify dysfunctional 5-HT neurons, and are a "window into the brain." The secretion of cortisol and prolactin is increased predominantly by 5-HT1 receptors. However, changes in 5-HT2 receptors have also been implicated in depression. Results from our laboratory and by others suggest that brain serotonergic neurons stimulate renin and vasopressin secretion by activation of 5-HT2 receptors. Therefore, the renin and vasopressin response to 5-HT agonists should be included in neuroendocrine tests of serotonergic function in affective disorders. Since antidepressants produce a decrease in the density of 5-HT2 receptors, renin and vasopressin could be used to evaluate the antidepressant potential of new drugs.
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PMID:Neuroendocrine aspects of the serotonergic hypothesis of depression. 269 29

In this review an attempt has been made to summarize our current knowledge on the involvement of various endocrine systems in the adaptation of the neonate to extrauterine life. Clinical and experimental evidence has been provided to indicate the role of catecholamines, glucocorticoids, prostaglandins, vasopressin, endorphins and the renin-angiotensin-aldosterone system in the cardiovascular and respiratory adaptation. Furthermore, the contribution of prolactin, vasopressin and the renin-angiotensin system to the redistribution of the body fluid compartments after birth and to the regulation of neonatal salt and water metabolism has been demonstrated. It has been concluded that the endocrine reactions induced by birth process and perinatal pathological events are important regulators of successful transition.
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PMID:Endocrine factors in the neonatal adaptation. 270 Nov 49


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