The Abnormal Renal Vasodilator Response to D1-Like Receptor Stimulation in Conscious SHR Can Be Normalized by AT1 Blockade

Vries, P A M de; Zeeuw, Dick de; Jong, Paul E. de; Navis, Gerjan

doi:10.1097/00005344-200411000-00009

Cited by 5 publications

(5 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Infusion of D 1 -like receptor agonists, YM-435 or fenoldopam, into the renal artery blocks angiotensin II-induced afferent and efferent arteriolar constriction (98, 610). Blockade of AT 1 R normalizes the impaired renal vasodilator effect of D 1 -like receptor stimulation in the SHR (134). The increased vasodilatory effect of a D 3 R/D 4 R agonist (quinpirole) (203, 548) after renal denervation may also depend on a decreased activity of the renin-angiotensin system (379).…”

Section: Dopamine Receptor Interactionsmentioning

confidence: 99%

“…The inhibitory effect of dopamine on ion transport is exerted via its own receptors (10, 83, 123, 173, 204, 210, 220, 352, 396, 401, 402, 457–459, 597, 628, 690) and via the regulation of the release or secretion of other hormones/humoral substances. Such hormones may directly inhibit ion transport, interact with dopamine to increase [e.g., ANP (118,318,392, 393,481), nitric oxide (631), prolactin (280), and eicosanoids (272, 328)] their inhibition of ion and water transport, and/or prevent their stimulatory effect on sodium transport [e.g., angiotensin II (100,101,116,134,274,321,363,558,628), insulin (44,45,682), and vasopressin (16,559)]. Dopamine receptors also inhibit renal nerve activity (520), although the natriuretic effect of D 1 -like receptor stimulation persists even after renal denervation (307).…”

Section: Structure and Function Of The Renal Dopaminergic Systemmentioning

confidence: 99%

See 1 more Smart Citation

Dopamine and Renal Function and Blood Pressure Regulation

Armando

Villar

José

2011

Comprehensive Physiology

104

215

View full text Add to dashboard Cite

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.

show abstract

Section: Dopamine Receptor Interactionsmentioning

confidence: 99%

Section: Structure and Function Of The Renal Dopaminergic Systemmentioning

confidence: 99%

Dopamine and Renal Function and Blood Pressure Regulation

Armando

Villar

José

2011

Comprehensive Physiology

104

215

View full text Add to dashboard Cite

show abstract

“…Systemic infusion of dopamine, at low doses, causes renal vasodilation via D1 [ 32 ] and D2-like receptors [ 33 ]. Stimulation of D1 receptors increases RBF without affecting GFR in the adult Wistar Kyoto rat but this vasodilation is blunted in the SHR counterpart [ 34 ]. However, pretreatment with an AT1R blocker, restores the RBF response and also increases GFR in SHR in response to D1 receptor stimulation [ 34 ].…”

Section: Discussionmentioning

confidence: 99%

“…Stimulation of D1 receptors increases RBF without affecting GFR in the adult Wistar Kyoto rat but this vasodilation is blunted in the SHR counterpart [ 34 ]. However, pretreatment with an AT1R blocker, restores the RBF response and also increases GFR in SHR in response to D1 receptor stimulation [ 34 ]. In SHR and rats subjected to subtotal nephrectomy renal D1R dysfunction associated with receptor G-protein uncoupling occurs [ 35 , 36 ].…”

Section: Discussionmentioning

confidence: 99%

Beneficial effects of brief early life angiotensin-converting enzyme inhibition wane with time in sheep with solitary functioning kidney

et al. 2023

View full text Add to dashboard Cite

A child with a congenital solitary functioning kidney (SFK) may develop kidney disease from early in life due to hyperfiltration injury. Previously, we showed in a sheep model of SFK that brief angiotensin converting enzyme inhibition (ACEi) early in life is reno-protective and increases renal functional reserve (RFR) at 8 months of age. Here we investigated the long-term effects of brief early ACEi in SFK sheep out to 20 months of age. At 100 days gestation (term=150 days) SFK was induced by fetal unilateral nephrectomy, or sham surgery was performed (controls). SFK lambs received enalapril (SFK+ACEi; 0.5mg/kg, once daily, orally) or vehicle (SFK) from 4 to 8 weeks of age. At 8, 14 and 20 months of age urinary albumin excretion was measured. At 20 months of age, we examined basal kidney function and RFR via infusion of combined amino acid and dopamine (AA+D). SFK+ACEi resulted in lower albuminuria (40%) at 8 months, but not at 14 or 20 months of age compared with vehicle-SFK. At 20 months, basal GFR (13%) was lower in SFK+ACEi compared with SFK, but renal blood flow (RBF), renal vascular resistance (RVR) and filtration fraction were similar to SFK. During AA+D, the increase in GFR was similar in SFK+ACEi and SFK animals, but the increase in RBF was greater (46%) in SFK+ACEi than SFK animals. Brief ACEi in SFK delayed kidney disease in the short-term but these effects were not sustained long-term.

show abstract

“…In humans with essential hypertension and rodents with genetic hypertension (SHRs and Dahl salt-sensitive rats), D 1 -like receptor agonist-mediated natriuretic and diuretic responses are impaired [46,47]. The ability of D 1 -like receptors to stimulate adenylyl cyclase activity in renal arteries is also impaired in SHRs [48] and we have also reported an impaired ability of D 1 receptors to dilate the mesenteric arteries of SHRs [49]. Other studies have shown that the D 1 receptor is hyperphosphorylated and uncoupled from G protein subunits, leading to the D 1 receptor dysfunction in SHRs, which precedes the onset of hypertension and co-segregates with the hypertensive phenotype [10,50].…”

Section: Discussionmentioning

confidence: 99%

Impaired dopamine D1 receptor-mediated vasorelaxation of mesenteric arteries in obese Zucker rats

Han

Wang

et al. 2014

Cardiovasc Diabetol

View full text Add to dashboard Cite

BackgroundObesity plays an important role in the pathogenesis of hypertension. Renal dopamine D1-like receptor-mediated diuresis and natriuresis are impaired in the obese Zucker rat, an obesity-related hypertensive rat model. The role of arterial D1 receptors in the hypertension of obese Zucker rats is not clear.MethodsPlasma glucose and insulin concentrations and blood pressure were measured. The vasodilatory response of isolated mesenteric arteries was evaluated using a small vessel myograph. The expression and phosphorylation of D1 receptors were quantified by co-immunoprecipitation and immunoblotting To determine the effect of hyperinsulinemia and hyperglycemia on the function of the arterial D1 receptor, we studied obese Zucker rats (six to eight-weeks old) fed (6 weeks) vehicle or rosiglitazone, an insulin sensitizer (10 mg/kg per day) and lean Zucker rats (eight to ten-weeks old), fed high-fat diet to induce hyperinsulinemia or injected intraperitoneally with streptomycin (STZ) to induce hyperglycemia.ResultsIn obese Zucker rats, the vasorelaxant effect of D1-like receptors was impaired that could be ascribed to decreased arterial D1 receptor expression and increased D1 receptor phosphorylation. In these obese rats, rosiglitazone normalized the arterial D1 receptor expression and phosphorylation and improved the D1-like receptor-mediated vasorelaxation. We also found that D1 receptor-dependent vasorelaxation was decreased in lean Zucker rats with hyperinsulinemia or hyperglycemia but the D1 receptor dysfunction was greater in the former than in the latter group. The ability of insulin and glucose to decrease D1 receptor expression and increase its phosphorylation were confirmed in studies of rat aortic smooth muscle cells.ConclusionsBoth hyperinsulinemia and hyperglycemia caused D1 receptor dysfunction by decreasing arterial D1 receptor expression and increasing D1 receptor phosphorylation. Impaired D1 receptor-mediated vasorelaxation is involved in the pathogenesis of obesity-related hypertension.

show abstract

The Abnormal Renal Vasodilator Response to D1-Like Receptor Stimulation in Conscious SHR Can Be Normalized by AT1 Blockade

Abstract: These results suggest that the RAAS accounts for the blunted renal vasodilator response to a D1-like receptor agonist in SHR. A dysbalance between the dopaminergic system and the RAAS may be involved in the abnormal renal hemodynamic regulation in SHR.

Cited by 5 publications

References 28 publications

Dopamine and Renal Function and Blood Pressure Regulation

Dopamine and Renal Function and Blood Pressure Regulation

Beneficial effects of brief early life angiotensin-converting enzyme inhibition wane with time in sheep with solitary functioning kidney

Impaired dopamine D1 receptor-mediated vasorelaxation of mesenteric arteries in obese Zucker rats

Contact Info

Product

Resources

About