Inhibition of the Plasma-Aldosterone Response to Frusemide by Bromocriptine

Edwards, C. R. W.; Miall, P; Hanker, J. P.; Thorner, Michael O.; Al-Dujaili, Emad A S; Besser, G. M.

doi:10.1016/s0140-6736(75)92132-7

Cited by 101 publications

(40 citation statements)

References 12 publications

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“…Thus, maneuvers which would be expected to alter the activity of the renin-angiotensin-aldosterone system are associated with inverse changes in urinary dopamine excretion. Recently, Edwards et al (6) demonstrated in man that the specific long-acting dopamine receptor stimulant (agonist), bromocriptine (2-brom-aergocryptine), inhibits the increase in plasma aldosterone concentration induced by furosemide without altering the concomitant increase in plasma renin ac-tivity. These observations suggest the possibility that under certain circumstances dopamine may participate directly in the regulation of aldosterone production.…”

Section: Introductionmentioning

confidence: 99%

Effects of Metoclopramide and Bromocriptine on the Renin-Angiotensin-Aldosterone System in Man

Carey¹,

Thorner²,

Ortt³

1979

J. Clin. Invest.

231

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A B S T R A C T This study was designed to investigate the possible role of dopaminergic mechanisms in the control ofthe renin-angiotensin-aldosterone system in normal man. Six normal male subjects in metabolic balance at 150 meq sodium, 60 meq potassium constant intake received the specific dopamine antagonist, metoclopramide, 10 mg i.v. or placebo followed by angiotensin II infusion 1 h later on 2 consecutive days. Metoclopramide increased plasma aldosterone concentration from 8.2+2.2 to 21.0+3.3 ng/100 ml (P <0.005) and plasma prolactin concentration from 18.0±4.0 to 91.7+4.0 nglml (P < 0.001) within 15 min of its administration. At 1 h, plasma aldosterone and prolactin concentrationis remained elevated at 16.8 ±2.1 ng/100 ml (P < 0.01) and 86.8±+15.9 ng/ml (P < 0.005), respectively. Angiotensin II at 2, 4, and 6 pmol/kg per miim further increased plasma aldosterone concentration to 27.2+3.4, 31.9+5.7, and 36.0+6.7 ng/100 ml (P < 0.02), respectively. Placebo did not alter plasma aldosterone or prolactin concentrations, but angiotensin II increased plasma aldosterone concentration to 13.7±2.4, 19.0+ 1.9, and 23.3+3.2 ngIl00 ml (P < 0.005). The increment of plasma aldosterone concentration in response to angiotensin II was similar after metoclopramide or placebo.The six subjects also received the dopamine agonist, bromocriptine, 2.5 mg or placebo at 6 p.m., midnight, and 6 a.m. followed by angiotensin II infusion on 2 consecutive d. Bromocriptine suppressed prolactin to <3 ng/ml. After placebo, plasma aldosterone concentration increased from 5.2± 1.4 to 12.3+1.7, 17.2 +2.2, and 21.8+3.5 ng/100 ml (P < 0.01) and after bromocriptine from 7.2±1.0 to 14.7+. and 23.4±1.6 ng/100 ml (P < 0.001) with each respective angiotensin II dose. No difference in the response to angiotensin II after bromocriptine or placebo was observed. Plasma renin activity, free 11-hydroxycorticoid concentration, and serum potassium concentration were unchanged by metoclopramide or bromocriptine.The results suggest that aldosterone production is under maximum tonic dopaminergic inhibition which can be overridden with stimulation by angiotensin II in normal man. INTRODUCTION Dopamine, a precursor of the sympathetic neurotransmitter norepinephrine, may itself be a major transmitter of the peripheral autonomic nervous system (1). The adrenergic component of this system is important in controlling renin release (2, 3), but little is known concerning the role of dopamine in the regulation of the renin-angiotensin-aldosterone system. Cuche et al. (4) have shown in man that the increase in plasma renin activity with upright posture is associated with a decrease in urinary dopamine and an increase in norepinephrine and epinephrine excretion. Alexander and colleagues (5) have reported that sodium-depleted subjects respond to dietary or intravenous sodium loading with an increase in urinary dopamine and a decrease in urinary norepinephrine. Thus, maneuvers which would be expected to alter the activity of the renin-angiotensin-aldosterone system are ass...

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Section: Introductionmentioning

confidence: 99%

Effects of Metoclopramide and Bromocriptine on the Renin-Angiotensin-Aldosterone System in Man

Carey¹,

Thorner²,

Ortt³

1979

J. Clin. Invest.

231

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“…It has previously been reported that some essential hypertensive patients, particularly those with low PRA, have increased PA responses to All when studied under conditions of moderate to high sodium intake."" 28 On the other hand, decreased PA responses to All have been reported in essential hypertensives when sodium intake was markedly restricted. 27 Williams et al 2 " have suggested that this apparent discrepancy is probably related to the fact that the sodium-dependent swing in adrenal All responsiveness in essential hypertensives is smaller than normal.…”

mentioning

confidence: 99%

Dopaminergic modulation of pressor and hormonal responses in essential hypertension.

Sowers¹,

Golub²,

Berger³

et al. 1982

Hypertension

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“…In support of this notion it has been demonstrated that administration of DA or the DA agonist bromocriptine produced a significant suppression of the aldosterone response to angiotensin 11, diuretics, and posture (13, [29][30][31]. Moreover, MTC has been found to cause a rise in aldosterone secretion without changes in the known regulators of aldosterone production such as PRA, ACTH.…”

Section: Resultsmentioning

confidence: 92%

The Effect of Metoclopramide Administration on Electrolyte Status and Activity of Renin-Angiotensin-Aldosterone System in Premature Infants

et al. 1985

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ABSTRACT. The present study has been carried out to define whether endogenous dopamine contributes to the regulation of renal sodium handling and the function of the renin-angiotensin-aldosterone system in low birth weight premature infants. Twelve premature infants with mean birth weight of 1420 g and mean gestational age of 29.2 wk were given metoclopramide (MTC) in a dose of 0.1 mg/ kg/day to treat delayed gastric emptying, regurgitation, and abdominal distension at the age of 17-23 days. Infants were kept on either a low (2-3 mEq/kg/day) or high (4-7 mEq/kg/day) sodium diet to modulate activity of RAAS. Prior to and after a 3-day period of M T C administration, blood samples were taken, and in six male infants 24-h urine collections were made to determine plasma and urine electrolytes, plasma renin activity, plasma aldosterone concentration, and urinary aldosterone excretion. We demonstrated that plasma sodium and potassium concentrations and plasma renin activity were not altered by MTC. O n the other hand, in response to MTC, there was a significant increase in urinary sodium excretion (1.8 + 0.3 versus 2.3 + 0.3 mEq/kg/day) and a decrease in potassium excretion (1.2 + 0.2 versus 0.8 + 0.1 mEq/kg/day); plasma aldosterone concentration and urinary aldosterone excretion decreased significantly from initial values of 2101 + 274 pg/ ml and 2.91 + 0.52 pg/day to 1500 + 207 pglml ( p < 0.01) and 2.21 2 0.43 pg/day ( p < 0.01), respectively, after M'TC. These alterations were independent of the pretreatment hormone levels. We conclude that in low birth weight premature infants endogenous dopamine has no influence on plasma renin activity and enhances rather than inhibits aldosterone production and renal tubular sodium reabsorption. (Pediatr Res 19: 912-915, 1985) Abbreviations DA, dopamine RAAS, renin-angiotensin-aldosterone system PRA, plasma renin activity pAldo, plasma aldosterone concentration UAE, urinary aldosterone excretion MTC, metoclopramideIn recent years several lines of evidence have suggested a role of DA in thc regulation of renal sodium excretion and the involvement of dopaminergic mechanisms in the control of the RAAS system. Urinary DA excretion has been demonstrated to correlate positively with sodium intake and urinary sodium excretion ( 1-4), and a dose-dependent increase in urinary sodium excretion has been reported after DA administration (5-7) suggesting a natriuretic role for DA. Moreover, DA has been shown to increase renin release (8-lo), to inhibit angiotensin-induced aldosterone production (1 1-13), and to enhance the renal response to aldosterone (14).Very few data are available on the interactions among dopaminergic mechanisms, sodium homeostasis, and the RAAS during the neonatal period. It has been observed, however, that DA given to sick premature infants in a dose of 0.5-4.0 pg/min/kg increased sodium and water diuresis (15) and enhanced PRA, but did not cause significant alteration in pAldo (16). In an attempt to define the relationship between endogenous DA, renal sodium exc...

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Inhibition of the Plasma-Aldosterone Response to Frusemide by Bromocriptine

Cited by 101 publications

References 12 publications

Effects of Metoclopramide and Bromocriptine on the Renin-Angiotensin-Aldosterone System in Man

Effects of Metoclopramide and Bromocriptine on the Renin-Angiotensin-Aldosterone System in Man

Dopaminergic modulation of pressor and hormonal responses in essential hypertension.

The Effect of Metoclopramide Administration on Electrolyte Status and Activity of Renin-Angiotensin-Aldosterone System in Premature Infants

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