Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to elucidate the role of the dopaminergic system in the control of aldosterone secretion in acromegaly with arterial hypertension 10 patients and 10 healthy volunteers were studied. Plasma aldosterone and prolactin were determined by radioimmunological methods after dopaminergic receptor blockade with metoclopramide and sulpiride. Plasma aldosterone was also determined after adrenal stimulation with synthetic corticotrophin (Synacthen). In patients with acromegaly and hypertension, the aldosterone secretion in response to metoclopramide was completely inhibited whereas induced with corticotrophin was lower than in controls. Also prolactin secretion in response to metoclopramide or sulpiride was markedly lower as compared with that in controls. Sulpiride did not stimulate aldosterone secretion either in patients or in healthy controls. The results indicate that the dopaminergic control of aldosterone secretion in acromegaly with arterial hypertension is altered.
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PMID:Arterial hypertension in acromegaly: altered dopaminergic control of aldosterone secretion. 283 67

The effects of d-Sulpiride (25 mg i.v.) and 1-Sulpiride (25 mg i.v.) administration in the control of arterial blood pressure (ABP) and PRL-GH secretion have been analyzed in five normal male volunteers. It was observed a quite different action on ABP, 1-Sulpiride causing a long lasting hypotension and d-Sulpiride a short-lived hypertension. The correlation between ABP, heart rate and PRL-GH levels suggests a probable central cation for 1-Sulpiride and a possible peripheral action for d-Sulpiride effects on ABP.
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PMID:[Effects of sulpiride isomers in the control of blood pressure in man]. 745 1

In eight young healthy subjects on a 240 mM Na diet mean arterial pressure (MAP), renal hemodynamics and renal handling of Na and exogenous Li were measured at baseline and during acute nitric oxide (NO) inhibition with 90-minute infusion of 3.0 microg/kg x min(-1) of N(G)-L-arginine methyl ester (L-NAME). The same experiment was repeated with infusion of 50 microg/kg x min(-1) of DA2 receptor blocker L-Sulpiride (L-SULP) alone and, finally, with simultaneous infusion of both L-NAME and L-SULP. L-SULP alone did not elicit any effect. L-NAME alone produced no changes in MAP from 0 to 45 minutes (P1) and a 6.6% increase at 45 to 90 minutes (P2) of infusion. Effective renal plasma flow (ERPF, PAH clearance) and glomerular filtration rate (GFR, inulin clearance) declined by 10.2% and 7.6%, respectively, in P1 and by 15.3% and 11.5% in P2. Filtration Fraction (FF) rose by 4.2% in P2. Calculated renal vascular resistance (RVR) increased by 13.0% to 25.6%. Fractional excretion of Na (FENa) and Li (FELi) fell by 20.0% and by 16.0%, respectively, in P1 and by 40.0% and 25.1% in P2. All these variations, except for MAP and GFR, were significantly greater during coinfusion of L-NAME and L-SULP. ERPF declined by 17.8% to 33.7%, FENa by 26.7% to 53.3%, FELi by 13.8% to 34.8%, while RVR rose by 22.5% to 59.1% and FF by 10.1% to 29.3%. The present data confirm that NO blockade with low-dose systemic infusion of L-NAME produces renal vasoconstriction, reduced GFR with slight increase in FF, and enhanced tubular Li, and Na reabsorption. Since increase in RVR and FF and decrease in FENa and FELi are markedly potentiated by the simultaneous infusion of DA2 blocker L-SULP, which exerts no effects by itself, we suggest that DA interactions between DA system at the level of DA2 receptors and basal NO production play a physiological role in the regulation of renal function in humans.
Hypertension 1998 Jan
PMID:Dopamine-2 receptor blockade potentiates the renal effects of nitric oxide inhibition in humans. 945 16