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 effects of oral doses of the dopamine antagonist antiemetics metoclopramide and domperidone on baseline and dopamine stimulated renal function and systemic haemodynamics were assessed in a placebo controlled crossover study in 9 healthy volunteers. Metoclopramide did not change baseline ERPF, GFR or FF over 2 h post dosing but it significantly reduced baseline UNaV, UKV, urine flow, urinary dopamine excretion, supine and erect diastolic blood pressure and supine systolic blood pressure. Domperidone and placebo did not cause these effects. Metoclopramide caused a marked rise and domperidone a small fall in plasma aldosterone concentration (PAC) but placebo was without effect. Neither antiemetic altered plasma renin activity (PRA) but a small fall occurred with placebo. Two hours after pretreatment with placebo dopamine (2 micrograms/kg/min) increased effective renal plasma flow (ERPF), glomerular filtration rate (GFR), sodium excretion rate (UNaV), urine flow rate, urinary dopamine excretion rate, supine systolic blood pressure and supine and erect pulse rate and decreased the potassium excretion rate (UKV), filtration fraction (FF) and supine diastolic blood pressure. Metoclopramide pretreatment, did not attenuate the dopamine induced rise in ERPF, GFR, urine flow, urinary dopamine excretion or supine systolic blood pressure but it did attenuate the rise in pulse rate, the fall in diastolic pressure, and the antikaliuretic effect of dopamine leading to a net kaliuresis when compared to placebo. Domperidone was similar to placebo. Neither metoclopramide nor domperidone given orally caused clinically important antagonism of the renal haemodynamic effects of dopamine. However the effects of metoclopramide on blood pressure and electrolyte excretion may have clinical importance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metoclopramide, domperidone and dopamine in man: actions and interactions. 206 May 57

We studied the haemodynamic (systemic and renal) and humoral effects of nicardipine, a dihydropyridine calcium entry blocker in essential hypertensives and whether DA2 dopaminergic receptor blockade, induced by domperidone, might modify these effects. Eight uncomplicated mild to moderate hypertensives received placebo (saline) for 30 min followed by i.v. nicardipine (0.06 mg/min) for 30 min and repeated the same sequence introducing domperidone (10 mg i.v.) between saline and nicardipine; the effects of each treatment were followed for 30 min. The sequence was randomized with a 72-h interval between each study. Compared with placebo, nicardipine significantly reduced mean blood pressure (-14%) and renovascular resistance (-28%), increased heart rate (+15%), renal plasma flow (RPF; +21%), glomerular filtration rate (GFR; +43%) and urinary sodium excretion (+181%). The acute natriuretic effect of nicardipine was associated with an increase in the amount of filtered sodium (+43%) and with fractional sodium excretion (+110%), and a direct correlation was found between changes in RPF and in urinary sodium excretion (r = 0.68) and fractional sodium excretion (r = 0.57). Plasma renin activity (PRA) did not change, plasma aldosterone was significantly reduced (-10%) and plasma noradrenaline significantly increased (+63%). Domperidone pretreatment prevented the GFR increase induced by nicardipine and increased the noradrenaline response (+107%), but did not change the other actions of nicardipine. These data show that nicardipine, when acutely infused in essential hypertensives, while reducing blood pressure and reflexly activating the sympathetic nervous system, significantly increases urinary sodium excretion, RPF and GFR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Haemodynamic (systemic and renal) and humoral interactions between nicardipine and domperidone in hypertensives. 332 30

This study investigates the dopaminergic mechanisms involved in the control of corticosteroid secretion in normal subjects. TSH, PRL, PRA, aldosterone, and 18-hydroxycorticosterone (18-OHB) were measured before and after the administration of domperidone (10 mg, iv) to eight healthy males. Domperidone, a selective peripheral dopamine antagonist, stimulated TSH and PRL secretion. Plasma concentrations of aldosterone, 18-OHB, cortisol, and PRA were not altered by domperidone. This is in contrast to previous observations of aldosterone, 18-OHB, and PRA responses to metoclopramide, a dopamine antagonist which readily crosses the blood-brain barrier. Domperidone may fail to stimulate aldosterone, 18-OHB, and renin secretion because it does not cross the blood-brain barrier or does not function as an antagonist for adrenal dopamine receptors modulating 18-OHB and aldosterone secretion.
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PMID:Effect of domperidone, an extracerebral inhibitor of dopamine receptors, on thyrotropin, prolactin, renin, aldosterone, and 18-hydroxycorticosterone secretion in man. 703 17

Immersion of one hand into ice water (cold pressor test) in eight hypertensive subjects induces elevation of mean arterial pressure, increase in heart rate, and no significant changes of plasma renin activity and plasma aldosterone concentrations. Domperidone, a DA2 dopaminergic antagonist, attenuates heart rate increase induced by the cold pressor test, and the combination of bromocriptine, a known DA2 dopaminergic agonist, with domperidone again provoked a heart rate increase during the cold pressor test. Domperidone caused an increase of both plasma renin activity and plasma aldosterone concentrations, which were reversed by bromocriptine. These results suggest that a dopamine-receptor stimulation is taking place during the cold pressor test.
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PMID:Dopaminergic Influence on the Cardiovascular and Hormonal Responses to Cold Stress in Hypertensive Patients. 1184 49

Dopaminergic receptors have been involved in the cardiovascular and renin-angiotensin systems (RAS). We have recently reported that bromocriptine is an effective antihypertensive drug by stimulating DA(2) dopaminergic receptors. However, the nature of the dopaminergic receptors in RAS has not been established. Ten outpatients with essential hypertension were treated at the Vargas Hospital with bromocriptine (BR) (11.25 mg day(minus sign1)), a DA(2) dopaminergic agonist, for a 2-week period, after which an oral dose of 30 mg day(minus sign1) of domperidone (DO), a peripheric DA(2) dopaminergic antagonist, was added for 2 additional weeks. The active period was preceeded by a 2-week placebo period. Bromocriptine decreased blood pressure (BP) significantly by 19/9 mm Hg (systolic/diastolic BP). Bromocriptine did not cause heart rate (HR) changes. Bromocriptine decreased plasma aldosterone (ALD) without altering plasma renin activity (PRA). Domperidone partially blocked bromocriptine-induced antihypertensive submaximal treadmill effects and reversed ALD decrease. Exercise response was not significantly altered by BR + DO. We conclude the following: (1) BR is an effective antihypertensive agent; (2) BR seems to be acting at both the central and peripheric nervous systems, and (3) the nature of the dopaminergic receptor involved in renin secretion does not seem to be DA(2).
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PMID:Effect of Domperidone on the Bromocriptine-Induced Antihypertensive Action in Hypertensive Patients. 1185 Jun 82