Pharmacological Characterization of Neuronal Dopamine Receptors in the Rat Hindquarters, Renal and Superior Mesenteric Vascular Beds

Dupont, Alain; Vanderniepen, P.; Lefebvre, Romain; Bogaert, Marcus

doi:10.1111/j.1474-8673.1986.tb00658.x

Cited by 14 publications

(7 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the kidney, prejunctional D 2 -like receptors have been shown to inhibit norepinephrine release (373,519,520). Dopamine can vasodilate the renal vasculature via prejunctional D 2 -like receptors (144, 209, 515, 519, 555, 604). This effect is mainly evident when renal nerve activity is increased, a situation that is seen during anesthesia and sodium-depleted states.…”

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

108

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: Structure and Function Of The Renal Dopaminergic Systemmentioning

confidence: 99%

Dopamine and Renal Function and Blood Pressure Regulation

Armando

Villar

José

2011

Comprehensive Physiology

108

215

View full text Add to dashboard Cite

show abstract

“…Therefore, dopexamine-binding sites in this region are most likely DA? receptors located on sympathetic nerve endings reported to be involved in the inhibition of neurogenic va soconstriction [19][20][21], The /-sulpiride-sen sitive dopexamine-binding sites in the in tima may be identical with intimal nonprejunctional DA2 sites which we have recently described [10]. The functional significance of these sites is not yet properly character ized.…”

Section: Discussionmentioning

confidence: 88%

Anatomical Localization of the Binding and Functional Characterization of Responses to Dopexamine Hydrochloride in the Rat Mesenteric Vasculature

et al. 1991

View full text Add to dashboard Cite

Dopamine receptors of the DA₁ subtype have been identified in mesenteric blood vessels, stimulation of which leads to vasodilation. In this study, we have determined the anatomical localization of dopexamine-hydrochloride-binding sites and carried out functional characterization of responses to this DA₁-receptor and β₂-adrenoceptor agonist in rat mesenteric vasculature. Autoradiographic studies showed the presence of [³H]-dopexamine-binding sites in all the different layers of the mesenteric artery. The DA₁ receptor antagonist, SCH 23390 (IC50 = 4.9 μmol/l), and the β-adrenoceptor antagonist, propranolol (IC50 = 6.0 μmol/l), inhibited the binding of dopexamine. The inhibitory effect of these compounds on dopexamine binding was selective for different regions of the mesenteric artery. Also, dopexamine produced concentration-related increases in cAMP formation in membrane particles from superior mesenteric artery and its main branches. The presence of both SCH 23390 and propranolol was required to completely abolish dopexamine-induced increases in cAMP formation. In functional studies, dopexamine (1 and 3 μg/kg/min) produced dose-related increases in mesenteric blood flow (23 and 38%, respectively) which were accompanied by concomitant decreases in the calculated mesenteric vascular resistance. As seen with increases in cAMP, the vascular responses to dopexamine could be completely abolished only by prior treatment with both SCH 23390 and propranolol. These results suggest that in mesenteric vasculature of rat dopexamine binds primarily to DA₁ receptors and β₂-adrenoceptors. The activation of these receptors by dopexamine leads to vasodilation which is mediated by an increase in the intracellular levels of cAMP.

show abstract

“…This inhibitory effect of apomorphine is synaptic vasodilator dopamine receptors in the antagonized by the selective DA2-receptor antagonist superior mesenteric arterial bed of the rat. We have domperidone, but not by the selective DA,-receptor demonstrated that, in vivo, the dopamine receptor antagonist SCH 23390, indicating that these presynapagonist apomorphine inhibits neurogenic vasocon-tic dopamine receptors can be classified as DA2-recepstriction in the superior mesenteric vascular bed of the tors (Dupont et al, 1986b). rat by interaction with presynaptic inhibitory…”

Section: Introductionmentioning

confidence: 84%

“…In the first group of rats no antagonist was administered, but in the second and third groups either SCH 23390 or domperidone was injected locally immediately after the first stimulation. The dose of domperidone (10 gg kg-') used antagonizes the inhibitory effect of apomorphine on neurogenic vasoconstriction in this preparation (Dupont et al, 1986b). In preliminary experiments it was shown that lower doses of domperidone failed to antagonize the effect of quinpirole.…”

Section: Animals and General Proceduresmentioning

confidence: 99%

Influence of the dopamine receptor agonists fenoldopam and quinpirole in the rat superior mesenteric vascular bed

Dupont

Lefebvre

Vanderniepen

1987

British J Pharmacology

View full text Add to dashboard Cite

1 The effect of local administration of the dopamine2 (DA2)-receptor agonist quinpirole and of the DA,-receptor agonist fenoldopam was studied in the in situ, constant flow autoperfused, superior mesenteric vascular bed of the rat.2 Local infusion of quinpirole (30 pg kg-'min-' for 5min) had no effect on baseline perfusion pressure; it reduced the pressor responses to electrical stimulation (4 Hz, 1 ms, supramaximal voltage) of the periarterial sympathetic nerves to 45.6 ± 2.1% of its original value but did not modify similar pressor responses produced by locally administered noradrenaline.3 The inhibitory effect of quinpirole was antagonized by the selective DA2-receptor antagonist domperidone (10 pg kg-') but not by the selective DA,-receptor antagonist SCH 23390 (50 pg kg-'). 4 Local infusion of fenoldopam (30 pg kg-' min-' for 5 min) reduced baseline perfusion pressure to 89.9 ± 1.9%, increased the pressor response to electrical stimulation (4Hz, 1 ms, supramaximal voltage) of the periarterial nerves to 134.7 ± 14.0%, but reduced the pressor response to locally administered noradrenaline to 37.2 ± 8.2%. Similar pressor responses induced by the selective a,-adrenoceptor agonist phenylephrine were also reduced by fenoldopam (to 38.4 ± 6.4%), but responses to locally administered angiotensin II were not modified.5 Pretreatment with SCH 23390 (50 pg kg-') antagonized the effect of fenoldopam on baseline perfusion pressure, but had no influence on the effect of fenoldopam on responses to electrical stimulation or to noradrenaline.6 Pretreatment with the selective az-adrenoceptor antagonist rauwolscine (100 pg kg-') had no effect on the reduction in baseline perfusion pressure induced by fenoldopam nor on its inhibitory effect on the response to noradrenaline, but it antagonized the stimulatory effect of fenoldopam on the response to electrical stimulation.7 The results show that quinpirole inhibits neurogenic vasoconstriction in the rat superior mesenteric vascular bed through stimulation of presynaptic DA2-receptors while fenoldopam stimulates postsynaptic vasodilatory DA,-receptors. In addition, our results suggest that the inhibitory effect of fenoldopam on the vasoconstrictor response to noradrenaline may be due to an antagonistic action at postsynaptic a,-adrenoceptors, while its potentiating effect on neurogenic vasoconstriction is due to blockade of presynaptic oi2-adrenoceptors.

show abstract

Pharmacological Characterization of Neuronal Dopamine Receptors in the Rat Hindquarters, Renal and Superior Mesenteric Vascular Beds

Cited by 14 publications

References 13 publications

Dopamine and Renal Function and Blood Pressure Regulation

Dopamine and Renal Function and Blood Pressure Regulation

Anatomical Localization of the Binding and Functional Characterization of Responses to Dopexamine Hydrochloride in the Rat Mesenteric Vasculature

Influence of the dopamine receptor agonists fenoldopam and quinpirole in the rat superior mesenteric vascular bed

Contact Info

Product

Resources

About