Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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 effect of TRH induced secretion of TSH and prolactin (hPrl) on plasma renin activity (PRA), water and electrolyte excretion, was studied in 7 normal males before and after an intravenous injection of 2 ml normal saline or 200 microgram TRH. Plasma hPrl and TSH rose significantly (p less than 0.01) in all 7 subjects after TRH but not after saline injection. No significant differences in the hourly excretion of sodium, potassium and free water clearance were noted before and after either saline or TRH injection. Mean PRA values of the 7 subjects were similar after either the 2 ml saline of TRH injection. Our results indicate that despite a correlation between basal hPrl and sodium excretion as well as free water clearance, acute TRH induced elevation of hPrl is not associated with changes of urinary sodium and potassium excretion, free water clearance and PRA in normal males. These findings provide some evidence against a direct osmoregulatory role of hPrl in man.
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PMID:The effects of TRH on prolactin, plasma renin activity, water and electrolyte excretion in normal males. 41 66

The present prospective study was conducted in order to investigate the effect of an acute decrease in serum T3 levels on ANP, aldosterone, angiotensin II, renin and ADH. All patients showed a pathologic TRH stimulation test prior to organ harvesting. Our patients developed secondary T3 hypothyroidism of different severity dependent on intensive care unit (ICU) stay. T3 values in group 1 (ICU stay > or = 77 h) were smaller than 70 ng/dl, those of group 2 (ICU stay < or = 53 h) were greater than 70 ng/dl. In both groups a severe elevation of plasma renin activity was measured, with almost high-normal values for ANP in group 1 and slightly elevated values in group 2 [not significant (n.s.)]. Results demonstrate that, contrary to patients who are not critically ill, brain-dead patients develop a dissociation of the renin-angiotensin-aldosterone mechanism. No statistical significant difference was found between the groups in serum levels of ADH and aldosterone. This endocrine dissociation, however, seems to have no clinical significance with regard to organ function after transplantation in kidney recipients.
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PMID:Atrial natriuretic peptide (ANP), aldosterone, angiotensin II and renin in the 'low T3 syndrome' in organ donors. 830 64

To evaluate the effect of bromocriptine withdrawal after dopaminergic long-term treatment (15.0 +/- 6.8 mg/day, mean +/- SD) in 12 acromegalic patients on body composition, bioelectrical impedance was measured before and at the end of two weeks of drug withdrawal. During withdrawal basal hGH and IGF-I increased from 2.5 +/- 1.9 micrograms/l and 2.1 +/- 0.8 kU/l to 9.1 +/- 11.7 micrograms/l and 4.9 +/- 2.2 kU/l, respectively, and the hGH secretion deteriorated significantly both after oral glucose load and in the TRH test, indicating recurrence of active acromegaly. Reactance and resistance decreased by 5 +/- 4 and 23 +/- 19 omega, respectively (p less than 0.01), whereas body weight remained constant (+0.4 +/- 2.1 kg). Bioelectrical impedance analysis indicated evident shifts in body composition, i.e. a significant reduction of body fat (-2.0 +/- 1.7 kg) and a simultaneous increase in both lean body mass (+2.4 +/- 2.2 kg) and total body water (+1.8 +/- 1.6 l). The changes in body composition were related to a combined effect of unsuppressed hypersomatotropism and the lack of bromocriptine actions other than inhibition of hGH secretion (for example stimulation of the renin-angiotensin-aldosterone system by both the recurred hypersomatotropism and the absence of dopaminergic bromocriptine effects). We conclude that bioelectrical impedance analysis is a good additional tool to assess the pathophysiological effects of bromocriptine withdrawal in long-term treated acromegalic patients.
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PMID:Effect of bromocriptine withdrawal in acromegaly on body composition as assessed by bioelectrical impedance analysis. 195 Mar 40

We recently reported that renin, angiotensinogen, and angiotensin-converting enzyme were present in normal human pituitary lactotroph cells and PRL-secreting adenomas. Angiotensin-II and -III have also been shown to modulate PRL release in vitro. The present study was designed to determine whether angiotensin modulates PRL secretion in vivo. In 36 hypertensive patients with widely varying renin levels, active renin and basal PRL levels did not correlate. In 10 normal volunteers, both a sustained infusion of angiotensin-II and a graded infusion of angiotensin-III induced a 2- to 3-fold increase in aldosterone levels, but had no effect on PRL secretion. Administration of the angiotensin-converting enzyme inhibitor captopril had no effect on PRL circadian rhythm in 10 normal subjects or on PRL concentrations in 11 patients with PRL-secreting adenomas. Cross-over administration of placebo and captopril did not affect the peak PRL level measured after TRH treatment in 10 hypertensive men (placebo, 43.1 +/- 5.4; captopril, 40.0 +/- 6.2 micrograms/L; P = NS) or the rise in PRL induced by doperidone in 6 normal women (placebo, 129.5 +/- 16.2; captopril, 150.0 +/- 35.7 micrograms/L; P = NS). Further, administration of enalapril for 30 days to 6 hypertensive patients did not alter basal PRL concentrations or the peak concentrations induced by TRH. These data indicate that in humans the circulating renin-angiotensin system does not interact with diurnal PRL release or with the response to TRH or domperidone.
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PMID:Effect of the circulating renin-angiotensin system on prolactin release in humans. 210 27

Recent observations implicate angiotensin-II (AII) as a possible PRL-releasing factor. These observations prompted us to investigate the role of the renin-angiotensin system in PRL release in man. Nine normal volunteers ingesting a 20-40 mmol/day sodium, 70 mmol/day potassium diet and eight normal volunteers ingesting a 120 mmol/day sodium, 70 mmol/day potassium diet were infused with metoclopramide (2.5 mg over 1 min) and later with TRH (500 micrograms), two agents known to cause PRL release. The infusions were repeated after 36 h of oral administration of converting enzyme inhibitor [CEI; captopril (50 mg, orally, four times daily) or enalapril (5 mg, orally, twice daily)]. On a separate occasion, AII was infused at 10 ng/kg.h for 1 h into normal volunteers on normal salt diet. CEI administration lowered mean arterial pressure by 6-7 mm Hg and stimulated the release of active renin. The PRL responses on low and normal salt diet as well as before and after CEI were not statistically different. There was also no difference in the PRL responses of patients placed on captopril vs. those on enalapril. AII increased blood pressure by 11-25 mm Hg, but did not increase PRL significantly above basal concentrations during the control dextrose infusion. Five hyperprolactinemic volunteers were also given CEI for up to 4 weeks. They demonstrated no significant change in serum PRL levels. We conclude that AII in the pituitary does not significantly alter either basal PRL levels or metoclopramide- and TRH-induced PRL responses in normal subjects on low and high salt diets. In addition, CEI is not a useful therapy in patients with pathological hyperprolactinemia. These findings, however, do not exclude a role for AII in physiological regulation, since CEI does not cross the blood-brain barrier and would not be expected to alter hypothalamic AII.
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PMID:The effect of angiotensin-converting enzyme inhibition on prolactin responses in normal and hyperprolactinemic subjects. 250 32

The effect of insulin administration on water intake, was studied in children submitted to standard protocols for stimulation of secretion of hypophyseal hormones by i.v. treatment with several different drugs: insulin, insulin plus TRH and LH-RH; and propranolol, clonidine or LH-RH. Drinking was measured from 0 to 90 min after drug administration; from blood samples taken at 60 min for hypophyseal hormones analysis, microhaematocrit values were measured, as well as plasma renin activity (PRA) and glycaemia. Water intake was significantly higher in both groups of patients receiving insulin than in the control group (no insulin). Haematocrit values did not change after 60 min. There was a significant correlation of glycaemia of individuals from all three groups and water intake at 60 min. PRA was significantly higher in insulin treated individuals.
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PMID:Effect of insulin administration on water drinking in children. 250 49

A 68-yr-old man had developed intractable vomiting soon after recovering from a flu-like illness. The use of Compazine as an antiemetic produced classic dystonic manifestations which resolved rapidly after discontinuation and treatment with Artane. However, he later developed a variety of neurobehavioral disturbances which led to his admission to the hospital. Extensive diagnostic procedures failed to identify any gastrointestinal or neurological causes. His condition unceasingly worsened until hypocortisolemia was serendipitously discovered, and all of his symptoms disappeared rapidly and completely with glucocorticoid replacement. Over the course of hospitalization, other than a single episode of orthostatic hypotension, the patient did not manifest any signs of adrenal insufficiency or endocrinopathy. Although detectable, his plasma ACTH level was markedly low in the presence of hypocortisolemia. His adrenal function was subnormal in the cortisol response to ACTH stimulation. His renin-angiotensin-aldosterone system and catecholamine levels were normal. He had normal pituitary responses to GnRH, TRH, and insulin, with rises in plasma levels of LH, FSH, TSH, PRL, and GH, but no stimulation of ACTH. Repeated CRH tests revealed no stimulation of ACTH and cortisol. No circulating anti-ACTH, antiadrenal, or antipituitary antibody was detected. We conclude that this elderly patient had a rare syndrome of selective corticotroph dysfunction which resulted in secondary adrenal failure and exacerbated his mental and neuromuscular abnormalities. To our knowledge, these symptoms, which clearly relate to hypocortisolism, have not been previously reported.
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PMID:Delirium and neuromuscular symptoms in an elderly man with isolated corticotroph-deficiency syndrome completely reversed with glucocorticoid replacement. 255 16

The role of the tonic inhibitory effect of dopamine on aldosterone secretion has been investigated in 10 patients with chronic renal failure (CRF) on hemodialysis, in 8 normotensive renal transplant recipients (Tx) with normal renal function and in 8 normotensive volunteers (NV). The following tests were performed: the response of plasma aldosterone (PA) to metoclopramide administration; the response of plasma prolactin (PRL) to TRH administration, and the changes induced by Lisuride (a dopaminergic agonist, on the values of PA and PRL). The basal values of PA and PRL were higher in CRF than in NV and Tx. The inverse was true for plasma renin activity (PRA) values. The response of PA and PRL to metoclopramide showed blunted increases in CRF when compared to NV, in the absence of changes of PRA, cortisol and potassium. After TRH administration, PRL increase in CRF was also inferior. Lisuride induced a decrease of both PA and PRL both in CRF and NV. In Tx, basal values of PA and PRL were similar to NV. Nevertheless, the response to metoclopramide and TRH were partially blunted when compared to that of NV. These results point to the existence of a deranged dopaminergic regulation of aldosterone secretion in end-stage renal failure patients. The alterations are partially corrected by a well-functioning kidney graft.
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PMID:Dopamine control of aldosterone secretion in end-stage renal failure. 309 88

To investigate the influence of critical illness on plasma renin activity and aldosterone levels and to examine potential inhibitory effects of dopamine therapy on aldosterone responsiveness, we measured plasma renin activity, and potassium and creatinine in serum, as well as the responses of aldosterone, cortisol and prolactin levels to TRH 200 micrograms i.v. + Synacthen 0.25 mg i.v. in 63 unselected, critically ill patients (32 females, 31 males, aged 18-84 years). Of the patients 19 received dopamine treatment (3-13 micrograms/kg/min i.v.); 21 of the patients died in the further course of their disease. Plasma renin activity was increased in 66.7% of the patients and aldosterone levels were elevated in 90.5% of the patients. There were correlations (P less than 0.05) of lethality with plasma renin activity and cortisol levels and correlations (P less than 0.01) of aldosterone concentrations with plasma renin activity and cortisol levels. Whereas dopamine treatment had no inhibitory effect on aldosterone levels before and after stimulation, prolactin stimulation was decreased in dopamine-treated patients. Thus, dopamine does not generally lose its potency of hormone inhibition in critically ill patients, but has no influence on the secondary aldosteronism developing regularly in the early phase of critical illness, which is apparently mainly due to the stimulatory effect of ACTH (or ACTH-related pituitary peptides) and is considered an epiphenomen of the stress mechanisms acting upon the patients in this condition.
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PMID:[Plasma renin activity and aldosterone behavior in critically ill patients]. 310 59

The effect of TRH (200 micrograms) on blood pressure, pulse rate, TSH and GH release was investigated in 10 acromegalics, four patients with non-GH secreting pituitary tumours, and seven normal controls. TRH produced a rapid-onset, short-lived pressor response in the acromegalic group (delta mean blood pressure 33 mmHg) compared to the two control groups (P less than 0.001). There was no response to the same volume of saline. The pressor response in the acromegalic group was not different in those who did or did not release GH. The pressor response to TRH was linearly related over the range 50-200 micrograms. Measurement of plasma noradrenaline and plasma renin activity during TRH testing in six acromegalics indicated that the pressor effect was neither mediated by adrenergic mechanisms, nor the renin-angiotensin system. Echocardiographic monitoring in five of these six patients showed that there was a significant increase in directly measured end systolic, end diastolic dimensions and heart rate (all P less than 0.02), and calculated stroke volume (P less than 0.001) and cardiac output (P less than 0.01) without changes in systemic vascular resistance. These data suggest that increase in preload, probably via venoconstriction, is the most likely factor producing the pressor response to TRH in acromegalics.
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PMID:Cardiovascular and hormonal responses to thyrotrophin releasing hormone in acromegalics. 311 46


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