Dopaminergic regulation of aldosterone secretion: How credible?

Ganguly, Arnab

doi:10.1042/cs0660631

Cited by 27 publications

(20 citation statements)

References 38 publications

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“…The general concept of dopaminergic inhibition of aldosterone sccl-etion has been questioned (35) because of recent studies in rats, rabbits, and dogs which failed to demonstrate an increased aldosterone secretion after MTC (36,37). These observations lend support to the view that the inhibitory effect of DA on aldosterone production is species specific.…”

Section: Resultssupporting

confidence: 69%

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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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Section: Resultssupporting

confidence: 69%

“…Nevertheless its consistency in humans and nonhuman primates has been adequately substantiated. However, there is evidence that MTC produces its effect on aldosterone production by nondopaminergic mechanisms as we11 (35).…”

Section: Resultsmentioning

confidence: 99%

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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“…A large mass of findings seems to indicate that the dopaminergic system is involved in the modulation of the secretory activity of the adrenal zona glomerulosa (for review see [4,10]). A series of investigations has shown that many factors, which participate in the regulation of the secretory activity of this adrenal zone (i.e., angiotensin II, K +, ACTH, somatostatin, a-MSH, and enkephalins) also exerts a striking adrenoglomerulotrophic effect (for review see [37]).…”

Section: Introductionmentioning

confidence: 99%

Investigations on the possible involvement of the dopaminergic system in the modulation of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa: A coupled morphometric and biochemical study

et al. 1987

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The effects of metoclopramide (MTC) and bromocriptine (BRC) (two drugs which act as antagonist and agonist of DOPA-receptors, respectively) on the zona glomerulosa of dexamethasone/ACTH-treated rats were investigated by coupled biochemical and morphometric techniques. Short-term (1-h) MTC administration significantly increased the plasma concentration of aldosterone, while long-term (7-day) MTC administration, as well as short- and long-term treatment with BRC did not cause any apparent change. Long-term MTC administration was found to significantly potentiate both the rise in the plasma level of aldosterone and the hypertrophy of the zona glomerulosa and its parenchymal cells induced by a prolonged treatment with angiotensin II (AII), but not those evoked by a chronic sodium deprivation alone or combined with AII infusion. Long-term BRC administration notably counteracted the effects of sodium restriction (coupled or not with AII infusion), but not those induced by the administration of AII alone. Long-term MTC administration partially reversed both the lowering of the plasma concentration of aldosterone and the atrophy of the zona glomerulosa and its parenchymal cells caused by a prolonged sodium-loading (combined or not with captopril infusion), but not those produced by the administration of captopril alone. On the other hand, long-term BRC treatment induced a further significant reduction in the blood level of aldosterone and the volume of zona glomerulosa and its cells only in captopril-treated animals. These findings are consistent with the view that the dopaminergic system exerts a maximal tonic inhibitory effect not only on the secretory activity, but also on the growth and steroidogenic capacity of the rat zona glomerulosa. Furthermore, they suggest that the activity of the dopaminergic system is in turn controlled by the sodium balance, being almost completely suppressed by a prolonged sodium deprivation.

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“…The presence of chromaffin cells originating from the medulla in the cortical layers is strong evidence supporting the concept of the neurohormonal control of zona glomerulosa cell secretion (5). Dopamine D2-like receptors have been found (9,19) to play a pivotal role in inhibiting aldosterone secretion. We (31) and other investigators (23) have demonstrated that two subtypes of dopamine receptors, D2 and D4 receptors (D2R and D4R), are expressed in the adrenal cortex, mainly in the zona glomerulosa, and exert opposite effects on aldosterone secretion.…”

mentioning

confidence: 81%

D4 dopamine receptor enhances angiotensin II-stimulated aldosterone secretion through PKC-ε and calcium signaling

Chang

Wu²,

Huang³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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-Aldosterone secretion is subjected to dopaminergic regulation. Our previous study showed that both human D2 and D4 dopamine receptors (D2R and D4R) modulate aldosterone secretion, but in opposing directions. The inhibitory effect of D2R is mediated by attenuating protein kinase C-(PKC-) and calcium-dependent signaling. The mechanism of D4R effect on angiotensin II (AII)-stimulated aldosterone secretion is explored in this study. Experiments were done with primary human adrenal cortical cells and human adrenocarcinoma (NCI-H295R) cells. Activation of different PKC isoforms was detected by specific phospho-PKC antibodies and PKC translocation. The role of calciumdependent signaling was examined by measuring the cytoplasmic inositol 1,4,5-triphosphate (IP3) and calcium ([Ca 2ϩ ]i). The D4R agonist PD-168,077 enhanced AII-stimulated aldosterone synthesis and secretion as early as 30 min following exposure independently of the modulation of aldosterone synthase (CYP11B2) transcription. CYP11B2 mRNA level elevated by AII was augmented by D4R in the later period. These effects were reversed by the D4R antagonist L-745,870. AII activated PKC-␣/␤II, -ε, and -but not PKC-␦, -, or -/ of H295R cells. The D4R agonist selectively enhanced AIIstimulated PKC-ε phosphorylation and its translocation to the cell membrane. Furthermore, the D4R agonist enhanced the AII-stimulated elevation of intracellular IP 3 and [Ca 2ϩ ]i. Inhibition of PKC-ε translocation by the PKC-ε-specific inhibitory peptide attenuated AII-stimulated aldosterone secretion, CYP11B2 mRNA expression, and elevation of intracellular IP 3 and [Ca 2ϩ ]i. We conclude that D4R augmented aldosterone synthesis/secretion induced by AII. The mechanisms responsible for this augmentation are mediated through enhancing PKC-ε phosphorylation and [Ca 2ϩ ]i elevation.aldosterone-producing adenoma; protein kinase C-ε; hypertension THERE IS INCREASING EVIDENCE (8, 12) that aldosterone plays a direct role in the pathogenesis of chronic heart failure and vascular inflammation. The vascular and perivascular inflammatory responses to angiotensin II (AII) infusion and salt loading, both reported to increase cardiovascular aldosterone synthesis (28,29), are completely prevented by adrenalectomy (25). This suggests that the regulation of adrenal aldosterone production is more important than that of local cardiac and/or vascular synthesis of aldosterone. Although the regulation of aldosterone production by AII is well established, the modulating factors affecting itself or its downstream signaling are controversial and far from being completely delineated. The presence of chromaffin cells originating from the medulla in the cortical layers is strong evidence supporting the concept of the neurohormonal control of zona glomerulosa cell secretion (5). Dopamine D2-like receptors have been found (9, 19) to play a pivotal role in inhibiting aldosterone secretion. We (31) and other investigators (23) have demonstrated that two subtypes of dopamine receptors, D2 and D4 receptors (D2R and D4R)...

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Dopaminergic regulation of aldosterone secretion: How credible?

Cited by 27 publications

References 38 publications

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

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

Investigations on the possible involvement of the dopaminergic system in the modulation of the growth and steroidogenic capacity of the rat adrenal zona glomerulosa: A coupled morphometric and biochemical study

D4 dopamine receptor enhances angiotensin II-stimulated aldosterone secretion through PKC-ε and calcium signaling

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