Selective Inhibition of the Renal Dopamine Subtype D
            <sub>1A</sub>
            Receptor Induces Antinatriuresis in Conscious Rats

Wang, Zhiqin; Felder, Robin A.; Carey, Robert M.

doi:10.1161/01.hyp.33.1.504

Cited by 49 publications

(36 citation statements)

References 40 publications

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“…5 Also, when D 1 R expression in rat kidney is reduced by local tissue administration of specific antisense oligodeoxynucleotides, a significant antinatriuresis occurs during both normal and high Na ϩ intake. 18 On the other hand, activation of AT 1 Rs, the major renal Ang II receptors in the kidney, inhibits adenylyl cyclase and increases Na ϩ transport in the RPT via NHE-3 and Na/KATPase, resulting in antinatriuresis. 19 Ang II, via AT 1 Rs, constricts both afferent and efferent arterioles and contracts the glomerular mesangium, resulting in decreased intrarenal blood flow and glomerular filtration rate.…”

Section: Discussionmentioning

confidence: 99%

Intrarenal Dopamine D ₁ -Like Receptor Stimulation Induces Natriuresis via an Angiotensin Type-2 Receptor Mechanism

et al. 2007

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Abstract-We explored the effects of direct renal interstitial stimulation of dopamine D 1 -like receptors with fenoldopam, a selective D 1 -like receptor agonist, on renal sodium excretion and angiotensin type-2 (AT 2 ) receptor expression and cellular distribution in rats on a high-sodium intake. In contrast to vehicle-infused rats, sodium excretion increased in fenoldopam-infused rats during each of three 1-hour experimental periods (Ͻ0.001 Key Words: angiotensin Ⅲ dopamine Ⅲ receptors Ⅲ sodium excretion Ⅲ natriuresis Ⅲ receptor trafficking Ⅲ kidney T he kidney is endowed with 2 local hormonal systems that play a major role in the regulation of sodium (Na ϩ ) transport across the renal proximal tubule (RPT): the reninangiotensin system and the dopaminergic system. In vitro studies show that angiotensin II (Ang II), the major effector peptide of the renin-angiotensin system, acts at angiotensin type-1 (AT 1 ) receptors on RPT cell membranes to increase Na ϩ transport across the cell from the lumen into the interstitial space and peritubular capillaries by stimulating Na ϩ -hydrogen (H ϩ ) exchanger-3 (NHE-3) and Na ϩ ,K ϩ -ATPase activities, respectively. 1 On the other hand, dopamine (DA), synthesized in and secreted from RPT cells, activates D 1 -like receptors (D 1 and D 5 receptor subtypes) on RPT cells to inhibit Na ϩ reabsorption by inhibiting NHE-3 and Na ϩ ,K ϩ -ATPase activities. 2,3 Although these 2 hormonal systems act in opposite directions on RPT Na ϩ transport in vitro, little is known regarding the physiological interactions of intrarenal Ang II and DA in the control of Na ϩ excretion in vivo. Approximately 50% of basal Na ϩ excretion is mediated by the paracrine action of renal DA on RPT D 1 -like receptors. 4,5 However, the mechanisms of receptor interaction that govern DA-induced natriuresis are incompletely understood. DA downregulates AT 1 receptors (AT 1 Rs) in the RPT. 6 However, Ang II binds to angiotensin type-2 (AT 2 ) receptors (AT 2 Rs), as well as AT 1 Rs, and the effects of DA on AT 2 Rs are unknown.AT 2 Rs are expressed in the RPT but have a low degree of renal expression compared with that of AT 1 Rs. 7 The present study explores the direct renal interstitial (RI) stimulation of D 1 receptors with fenoldopam, a selective D 1 -like receptor agonist, and its effects on renal Na ϩ excretion and AT 2 R expression in the rat. We demonstrate that natriuresis induced by stimulation of renal D 1 -like receptors requires AT 2 R expression and recruitment to the RPT plasma membrane. In the presence of AT 2 R inhibition, D 1 -like receptor stimulation is not able to induce renal Na ϩ excretion.

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Section: Discussionmentioning

confidence: 99%

Intrarenal Dopamine D ₁ -Like Receptor Stimulation Induces Natriuresis via an Angiotensin Type-2 Receptor Mechanism

et al. 2007

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“…The external portions of the tubes were placed in a stainless steel spring. While the mice were still under general anesthesia, an indwelling renal interstitial infusion catheter, constructed as described previously, 12 was implanted into the left renal cortex through a small hole made with a 26-gauge needle. Mice were housed under controlled conditions.…”

Section: Animal Preparationmentioning

confidence: 99%

Angiotensin AT ₂ Receptors Directly Stimulate Renal Nitric Oxide in Bradykinin B ₂ -Receptor–Null Mice

2003

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Abstract-Both bradykinin B 2 and angiotensin II type 2 (AT 2 ) receptors are known to stimulate renal production of nitric oxide (NO). To evaluate the individual contributions of AT 2 and B 2 receptors to renal NO production, we monitored renal interstitial, stable NO metabolites and cGMP by a microdialysis technique in conscious, bradykinin B 2 -null and wild-type mice (nϭ8 in each group) during low sodium intake alone or with the angiotensin AT 1 or AT 2 receptor blockers, valsartan (0.5 g/min) or PD123319 (0.15 g/min), or both. During normal salt intake, renal interstitial fluid NO and cGMP levels in B 2 -null mice were not different from those of wild-type mice. Low sodium intake increased NO and cGMP in wild-type mice but not in B 2 -null mice. Valsartan increased NO and cGMP in both wild-type and B 2 -null mice but to a significantly greater degree in the wild-type than in B 2 -null mice. PD123319 decreased NO and cGMP in both wild-type and B 2 -null mice. Combined valsartan and PD123319 decreased NO and cGMP in both wild-type and B 2 -null mice, but there was no significant difference during combined treatment from their levels after administration of PD123319 alone. Our results indicate that during ingestion of a low-salt diet, production of NO is mediated mainly via the AT 2 -B 2 receptor cascade. Blockade of the AT 1 receptor enhances the production of NO via the AT 2 receptor in both wild-type and B 2 -null mice. We conclude that NO can be produced by 2 alternative pathways: directly through the Key Words: nitric oxide Ⅲ receptors, angiotensin II Ⅲ animals, transgenic Ⅲ receptors, bradykinin Ⅲ angiotensin II Ⅲ cyclic GMP P revious studies demonstrated that angiotensin II type 1 (AT 1 ) receptor blockade increases renal nitric oxide (NO) and that this increase is abolished by angiotensin II type 2 (AT 2 ) receptor blockade, proving that the AT 2 receptor is responsible for the increase in NO. 1,2 Similarly, activation of the AT 2 receptor results in an increase in renal cGMP. 3 Because cGMP functions as a second messenger for NO, its increase in response to AT 2 receptor stimulation is thought to be mediated by NO 3 . Furthermore, AT 2 receptor stimulation increases renal bradykinin (BK), 4,5 which in turn increases NO production. 6 Thus, previous studies demonstrated that the AT 2 receptor mediates a vasodilator 5 cascade that includes BK, NO, and cGMP. These observations raise the question as to whether BK is an obligatory intermediate in the putative BK-NO-cGMP signaling cascade mediated by the AT 2 receptor.BK, the major effector hormone of the kallikrein-kinin system, acts mainly through the BK B 2 -subtype (B 2 ) receptor to mediate the majority of its cardiovascular and renal actions. 7 Studies in mice that lack the B 2 receptor (B 2 -/-) have reported normal development, blood pressure, and renal function. 8 -10 It is not known how B 2 -/-mice produce NO to maintain their normal blood pressures.In the present study, we investigated whether the AT 2 receptor can directly stimulate renal NO prod...

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“…The inhibition of Na ϩ -K ϩ -ATPase activity by the D 1 -like dopamine receptors appears to have been conserved in phylogenetically distinct organisms. In mammalian renal tubule cells under conditions of moderate sodium excess, the D 1 -like dopamine receptors are responsible for decreasing renal sodium transport by at least 50% (10,18,24,50,51). Mammalian renal tubule cells can adapt in an environment of low (50 mosmol/kgH 2 O) to high osmolality (1,200 mosmol/kgH 2 O) (30), similar to conditions to which euryhaline crustaceans are exposed during their migration from low-to high-salinity water.…”

Section: Perspectives and Significancementioning

confidence: 99%

D₁-like dopamine receptors downregulate Na⁺-K⁺-ATPase activity and increase cAMP production in the posterior gills of the blue crabCallinectes sapidus

Arnaldo

Villar

Konkalmatt

et al. 2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Dopamine-mediated regulation of Na+-K+-ATPase activity in the posterior gills of some crustaceans has been reported to be involved in osmoregulation. The dopamine receptors of invertebrates are classified into three groups based on their structure and pharmacology: D1- and D2-like receptors and a distinct invertebrate receptor subtype (INDR). We tested the hypothesis that a D1-like receptor is expressed in the blue crab Callinectes sapidus and regulates Na+-K+-ATPase activity. RT-PCR, using degenerate primers, showed the presence of D1βR mRNA in the posterior gill. The blue crab posterior gills showed positive immunostaining for a dopamine D5 receptor (D5R or D1βR) antibody in the basolateral membrane and cytoplasm. Confocal microscopy showed colocalization of Na+-K+-ATPase and D1βR in the basolateral membrane. To determine the effect of D1-like receptor stimulation on Na+-K+-ATPase activity, intact crabs acclimated to low salinity for 6 days were given an intracardiac infusion of the D1-like receptor agonist fenoldopam, with or without the D1-like receptor antagonist SCH23390. Fenoldopam increased cAMP production twofold and decreased Na+-K+-ATPase activity by 50% in the posterior gills. This effect was blocked by coinfusion with SCH23390, which had no effect on Na+-K+-ATPase activity by itself. Fenoldopam minimally decreased D1βR protein expression (10%) but did not affect Na+-K+-ATPase α-subunit protein expression. This study shows the presence of functional D1βR in the posterior gills of euryhaline crabs chronically exposed to low salinity and highlights the evolutionarily conserved function of the dopamine receptors on sodium homeostasis.

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Selective Inhibition of the Renal Dopamine Subtype D _1A Receptor Induces Antinatriuresis in Conscious Rats

Cited by 49 publications

References 40 publications

Intrarenal Dopamine D ₁ -Like Receptor Stimulation Induces Natriuresis via an Angiotensin Type-2 Receptor Mechanism

Intrarenal Dopamine D ₁ -Like Receptor Stimulation Induces Natriuresis via an Angiotensin Type-2 Receptor Mechanism

Angiotensin AT ₂ Receptors Directly Stimulate Renal Nitric Oxide in Bradykinin B ₂ -Receptor–Null Mice

D₁-like dopamine receptors downregulate Na⁺-K⁺-ATPase activity and increase cAMP production in the posterior gills of the blue crabCallinectes sapidus

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Selective Inhibition of the Renal Dopamine Subtype D 1A Receptor Induces Antinatriuresis in Conscious Rats

Cited by 49 publications

References 40 publications

Intrarenal Dopamine D 1 -Like Receptor Stimulation Induces Natriuresis via an Angiotensin Type-2 Receptor Mechanism

Intrarenal Dopamine D 1 -Like Receptor Stimulation Induces Natriuresis via an Angiotensin Type-2 Receptor Mechanism

Angiotensin AT 2 Receptors Directly Stimulate Renal Nitric Oxide in Bradykinin B 2 -Receptor–Null Mice

D1-like dopamine receptors downregulate Na+-K+-ATPase activity and increase cAMP production in the posterior gills of the blue crabCallinectes sapidus

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Product

Resources

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Selective Inhibition of the Renal Dopamine Subtype D _1A Receptor Induces Antinatriuresis in Conscious Rats

Intrarenal Dopamine D ₁ -Like Receptor Stimulation Induces Natriuresis via an Angiotensin Type-2 Receptor Mechanism

Intrarenal Dopamine D ₁ -Like Receptor Stimulation Induces Natriuresis via an Angiotensin Type-2 Receptor Mechanism

Angiotensin AT ₂ Receptors Directly Stimulate Renal Nitric Oxide in Bradykinin B ₂ -Receptor–Null Mice

D₁-like dopamine receptors downregulate Na⁺-K⁺-ATPase activity and increase cAMP production in the posterior gills of the blue crabCallinectes sapidus