Selective peripheral dopamine-1 receptor stimulation. Differential responses to sodium loading and depletion in humans.

Ragsdale, N V; Lynd, M; Chevalier, Robert L.; Felder, Robin A.; Peach, Michael J.; Carey, Robert M.

doi:10.1161/01.hyp.15.6.914

Cited by 28 publications

(49 citation statements)

References 22 publications

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“…Urine Sodium Excretion (U Na V) U Na V (baseline [vehicle, control] and enalapril) was greater on the HS than the LS diet and increased with fenoldopam 39 on the HS (absolute and %, Table 4A, Figure 3A) but not the LS diet, as reported previously, 22 despite less stringent salt restriction employed in the current study (50 mmol sodium/24 h) versus the previous study (10 mmol sodium/24 h). 22 Enalapril alone did not affect U Na V on LS or HS diets (Table 4A, Figure 4A).…”

Section: Urine Flowsupporting

confidence: 81%

“…Heart rates and systolic BP 22,34 on LS and HS diets were similar and unchanged with fenoldopam, 22,34 enalapril, or the combination of fenoldopam and enalapril. Diastolic and mean BPs were similar at baseline on both salt diets establishing the saltresistant phenotype.…”

Section: Cardiovascular and Renal Hemodynamic Parameters In Response mentioning

confidence: 89%

“…22 Enalapril alone did not affect U Na V on LS or HS diets (Table 4A, Figure 4A). 40 The addition of fenoldopam to enalapril increased U Na Von LS but not HS diets (absolute and %, Table 4A, Figure 5A).…”

Section: Urine Flowmentioning

confidence: 92%

“…30 By contrast, D 1 -like and AT 2 receptors cooperate to inhibit renal proximal sodium transport, 31 causing natriuresis. 32 In the current study, we tested the hypothesis that the previously reported attenuated natriuretic effect of D 1 -like receptor agonists in normotensive humans 22 during salt restriction is caused, in part, by increased RAAS activity. In this double-blind, placebo-controlled, balanced crossover study, we examined the effect of inhibition of the angiotensin converting enzyme with enalapril on the natriuretic effect of D 1 -like receptor stimulation with fenoldopam in salt-resistant normotensive subjects on low-salt (LS) and high-salt (HS) diets.…”

mentioning

confidence: 97%

“…[22][23][24] During salt restriction, the ability of renal endogenous dopamine to inhibit sodium transport is abolished. 22 This phenomenon is attributable to decreased renal dopamine production, altered dopamine receptor subtype expression, and postreceptor mechanisms in the renal tubule, and to overriding effects of salt-conserving mechanisms such as the sympathetic nervous system, the RAAS, and other saltretaining hormones.…”

mentioning

confidence: 99%

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The Renin-Angiotensin and Renal Dopaminergic Systems Interact in Normotensive Humans

Natarajan¹,

Eisner

Armando³

et al. 2016

Journal of the American Society of Nephrology

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The renin-angiotensin-aldosterone (RAAS) and renal dopaminergic systems interact to maintain sodium balance. High NaCl intake increases renal synthesis of dopamine and dopaminergic receptor activity, decreasing epithelial sodium transport, whereas sodium deficit activates the RAAS, increasing epithelial sodium transport. We tested the hypothesis that attenuation of the natriuretic effect of dopamine D 1 -like receptors during salt restriction results in part from increased RAAS activity in seven salt-resistant normotensive adults using a double-blind placebo-controlled balanced crossover design. All subjects attained sodium balance on low (50 mmol Na + /day) and high (300 mmol Na + /day) NaCl diets, administered 4 weeks apart. Sodium, potassium, lithium, para-aminohippurate, and creatinine clearances were measured before, during, and after a 3-hour infusion of fenoldopam, a D 1 -like receptor agonist, with and without pretreatment with enalapril, an angiotensin converting enzyme inhibitor. On the high NaCl diet, fenoldopam-induced natriuresis was associated with the inhibition of renal proximal and distal tubule sodium transport. On the low NaCl diet, fenoldopam decreased renal distal tubule sodium transport but did not cause natriuresis. The addition of enalapril to fenoldopam restored the natriuretic effect of fenoldopam and its inhibitory effect on proximal tubule sodium transport. Thus, on a high NaCl diet fenoldopam causes natriuresis by inhibiting renal proximal and distal tubule transport, but on a low NaCl diet the increased RAAS activity prevents the D 1 -like receptor from inhibiting renal proximal tubule sodium transport, neutralizing the natriuretic effect of fenoldopam. These results demonstrate an interaction between the renin-angiotensin and renal dopaminergic systems in humans and highlight the influence of dietary NaCl on these interactions. During salt depletion, sodium balance is maintained by increased activity of several systems, including the renin-angiotensin-aldosterone (RAAS) and sympathetic nervous systems.

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Section: Urine Flowsupporting

confidence: 81%

Section: Cardiovascular and Renal Hemodynamic Parameters In Response mentioning

confidence: 89%

Section: Urine Flowmentioning

confidence: 92%

mentioning

confidence: 97%

mentioning

confidence: 99%

See 3 more Smart Citations

The Renin-Angiotensin and Renal Dopaminergic Systems Interact in Normotensive Humans

Natarajan¹,

Eisner

Armando³

et al. 2016

Journal of the American Society of Nephrology

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Dopamine and Renal Function and Blood Pressure Regulation

Armando

Villar

José

2011

Comprehensive Physiology

108

215

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Dopamine is an important regulator of systemic blood pressure via multiple mechanisms. It affects fluid and electrolyte balance by its actions on renal hemodynamics and epithelial ion and water transport and by regulation of hormones and humoral agents. The kidney synthesizes dopamine from circulating or filtered L-DOPA independently from innervation. The major determinants of the renal tubular synthesis/release of dopamine are probably sodium intake and intracellular sodium. Dopamine exerts its actions via two families of cell surface receptors, D1-like receptors comprising D1R and D5R, and D2-like receptors comprising D2R, D3R, and D4R, and by interactions with other G protein-coupled receptors. D1-like receptors are linked to vasodilation, while the effect of D2-like receptors on the vasculature is variable and probably dependent upon the state of nerve activity. Dopamine secreted into the tubular lumen acts mainly via D1-like receptors in an autocrine/paracrine manner to regulate ion transport in the proximal and distal nephron. These effects are mediated mainly by tubular mechanisms and augmented by hemodynamic mechanisms. The natriuretic effect of D1-like receptors is caused by inhibition of ion transport in the apical and basolateral membranes. D2-like receptors participate in the inhibition of ion transport during conditions of euvolemia and moderate volume expansion. Dopamine also controls ion transport and blood pressure by regulating the production of reactive oxygen species and the inflammatory response. Essential hypertension is associated with abnormalities in dopamine production, receptor number, and/or posttranslational modification.

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