Effects of dopamine blockade on renal sodium excretion

Pelayo, Juan C.; Fildes, Robert D.; Eisner, Gilbert M.; José, Pedro A.

doi:10.1152/ajprenal.1983.245.2.f247

Cited by 66 publications

(61 citation statements)

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“…These results are not surprising since conflicting results have been reported concerning dopamine values in essential AHT: similar (10, 11) as well as increased (12,13) or decreased levels (14,15) have been observed. Our data are in agreement with the fact that the involvement of ERD in resting eunatremic conditions seems to be unlikely (16,18) asking the question of the reality of a dopaminergic basal tone (17).…”

Section: Discussionsupporting

confidence: 91%

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Sanchez

Damase‐Michel²,

Tran

et al. 1995

Hypertens Res

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The effect of chronic salt loading (10 g of NaCI for a period of 7 days) on urinary dopamine release has been investigated in 3 groups of beagle dogs: normotensive dogs (group 1: n = 7), and 2 groups of dogs made hypertensive by chronic sinoaortic denervation [group 2: (n = 6) during the first 4 months after sinoaortic denervation i.e. a model of arterial hypertension with high levels of plasma catecholamines and group 3: (n = 6) one year after denervation i. e. a model of arterial hypertension with normal sympathetic tone]. In normal dogs (group 1), salt loading induced an increase in urinary dopamine excretion during the two first days after salt loading. The rise in urinary dopamine was blunted in group 2. It was not observed in group 3. Salt loading failed to change arterial pressure and heart rate in the three groups of animals. These data show an alteration of the renal dopaminergic system in hypertensive sinoaortic denervated dogs suggesting that a dopaminergic impairment can appear during the development of arterial neurogenic hypertension.(Hypertens Res 1995; 18 Suppl. I: 5187-5190)Key Words: dopamine, hypertension, sinoaortic denervation, kidneyAlthough its physiological relevance is still unclear, it is now admitted that endogenous renal dopamine (ERD) plays a role in the regulation of sodium excretion (1) through activation of specific receptors (2). Moreover, as alteration of sodium handling is one of the factors involved in pathophysiology of arterial hypertension (AHT), a great interest focuses on the potential role of ERD in this pathology. Indeed, several studies showed impairment of renal dopamine mobilization during salt loading in hypertensive models (3). Most of the time, these studies concerned models of genetic AHT. The aim of our work was to investigate whether ERD could be altered during the development of acquired AHT elicited by sinoaortic denervation in dogs. Material and MethodsNineteen beagle dogs weighting from 13 to 16 kg were studies: seven normal normotensive dogs (group 1) were compared to 12 animals made hypertensive by sinoaortic denervation (SAD) as previously described (4). Briefly, carotid and aortic nerves were cut under chloralose anesthesia (80 mg/kg iv.) during 2 successive procedures, 1 at time 0, and the second 7 weeks later. During surgery, care was taken to keep both vagal and sympathic fibers in the vagus intact. The effectiveness of baroreceptor denervation was checked by the failure of norepinephrine (2 mg/kg) to induce bradycardia and nitroglycerine (1, 3, 10 and 30 mg/kg) to induce tachycardia. During the 4 first months, AHT elicited by SAD is associated with a high level in plasma catecholamines. One year after SAD, plasma catecholamine levels return to basal values (4). Furthermore, functional (5) and histological (6) renal alterations are similar to those observed in human AHT.

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Section: Discussionsupporting

confidence: 91%

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Sanchez

Damase‐Michel²,

Tran

et al. 1995

Hypertens Res

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“…15 We have previously reported that dopamine blockade in hydropenia does not affect sodium excretion. 17 However, dopamine blockade did attenuate the natriuresis associated with saline loading. 17 This effect of dopamine blockade on sodium excretion is due primarily to occupation of DA!…”

Section: Discussionmentioning

confidence: 96%

“…17 However, dopamine blockade did attenuate the natriuresis associated with saline loading. 17 This effect of dopamine blockade on sodium excretion is due primarily to occupation of DA! receptors, since DA, antagonists 5 -1318 more consistently de- Values are mean±SEM.…”

Section: Discussionmentioning

confidence: 96%

Attenuated renal response to dopaminergic drugs in spontaneously hypertensive rats.

et al. 1990

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Activation of renal dopamine-1 receptors decreases sodium transport. However, the spontaneously hypertensive rat retains sodium despite increased renal dopamine concentration. We tested the hypothesis that the abnormal sodium handling in spontaneously hypertensive rats (Okamoto-Aoki strain) is related to a decreased dopaminergic response by studying the effects of the intrarenal infusion of the dopamine-1 agonist SKF-38393 and the dopamine-1 antagonist SCH-23390 in hypertensive and in normotensive Wistar-Kyoto rats. Rats (9-16 weeks old) were studied with renal nerves intact under pentobarbital anesthesia (n=5-6 in each group). Specificity of dopamine-1 effects of SKF-38393 was verified because its natriuretic effect was blocked in a dose-related manner by the dopamine-1 antagonist SCH-23390 (n=5). Intrarenal arterial infusion of the dopamine-1 agonist SKF-38393 did not affect glomerular filtration rate but resulted in a dose-related natriuresis and diuresis in normotensive but not in hypertensive rats. Intrarenal arterial infusion of the dopamine-1 antagonist SCH-23390 alone induced an antinatriuresis, without affecting glomerular filtration rate, in normotensive but not in hypertensive rats. Addition of the dopamine-2 antagonist YM-09151 to the dopamine-1 antagonist infusion did not enhance the effect of the dopamine-1 antagonist The lack of response to the dopamine-1 agonist or antagonist in hypertensive rats was not due to differences in renal dopamine-1 receptor density ( U ± 0 J pmol/mg protein for spontaneously hypertensive rats, n=4; l±0.2 for Wistar-Kyoto rats, n=4) or affinity, distribution determined by autoradiography was also similar. The abnormal renal sodium handling in 9-16-week-old spontaneously hypertensive rats is in part due to decreased response distal to the dopamine-1 receptor. (Hypertension 1990;15:560-569) T he sympathetic nervous system contributes to the development of hypertension in rats with genetic hypertension, including the spontaneously hypertensive rat (SHR) of the Okamoto-Aoki strain, in part by promoting sodium retention.

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“…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.…”

mentioning

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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Effects of dopamine blockade on renal sodium excretion

Cited by 66 publications

References 0 publications

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Attenuated renal response to dopaminergic drugs in spontaneously hypertensive rats.

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

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Effects of dopamine blockade on renal sodium excretion

Cited by 66 publications

References 0 publications

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Involvement of Renal Dopaminergic System in Experimental Neurogenic Arterial Hypertension

Attenuated renal response to dopaminergic drugs in spontaneously hypertensive rats.

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

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