Vascular dopamine receptors: Demonstration and characterization by studies

Brodde, Otto‐Erich

doi:10.1016/0024-3205(82)90406-4

Cited by 81 publications

(24 citation statements)

References 51 publications

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“…This effect was similar to previous reports on rabbit mesenteric and splenic arteries (Brodde et al 1981;Hilditch & Drew 1981) and the ferret pulmonary artery (Gorman 1988). SKF 38393 also appeared to act as a DAI partial agonist as previously reported (Brodde 1982;Hoshino et at. 1986).…”

Section: Discussionsupporting

confidence: 91%

“…Dopamine (DA) has a vasodilatory effect in several vascular beds of human and various species of animals, and the existence of the specific DA receptors in these vasculatures has been reported (McNay et al 1965;Toda & Goldberg 1979;Brodde 1982). Furthermore, the subtype of DA receptors in the dog renal and rabbit mesenteric and splenic arteries was reported to be DAI receptors (Brodde et al 1981;Goldberg et al 1984;Ohlstein et al 1984).…”

Section: Introductionmentioning

confidence: 99%

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Endothelium‐dependent And‐independent Relaxation by Dopamine in the Rabbit Pulmonary Artery

Yamauchi

Kobayashi

Shimoura

et al. 1992

Clin Exp Pharma Physio

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1. The relaxing response of dopamine (DA) was studied in the rabbit pulmonary artery. DA caused concentration-related relaxation in helically cut strips of the artery contracted with prostaglandin F2 alpha in the presence of prazosin. 2. The DA-induced relaxation in endothelium-denuded strips was reduced to about 40% compared with that in endothelium-intact strips. 3. Methylene blue and haemoglobin, inhibitors of endothelium-dependent relaxation, reduced the DA-induced relaxations in endothelium-intact strips to the level of endothelium-denuded strips. These results indicate that the DA-induced relaxation is partially mediated or modified by the release of endothelium-derived relaxing factor (EDRF). 4. Apomorphine, as a DA agonist, caused concentration-dependent relaxation in endothelium-intact strips. Bromocriptine, a DA2 agonist, produced only a little relaxation at higher concentration. 5. In endothelium-intact strips, haloperidol, a DA antagonist, and the DA1 antagonists, fluphenazine and SCH 23390 inhibited DA-induced relaxations. On the other hand spiperone and domperidone, DA2 antagonists, were inactive. 6. In endothelium-denuded strips, fluphenazine and SCH 23390 inhibited DA-induced relaxations, but domperidone was inactive. 7. These results indicate that the DA-induced relaxation is mediated by DA receptors, and that DA1 receptors are involved in both endothelium-dependent and -independent relaxation in the rabbit pulmonary artery.

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Section: Discussionsupporting

confidence: 91%

Section: Introductionmentioning

confidence: 99%

Endothelium‐dependent And‐independent Relaxation by Dopamine in the Rabbit Pulmonary Artery

Yamauchi

Kobayashi

Shimoura

et al. 1992

Clin Exp Pharma Physio

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“…Collectively, the findings of the present study argue against any role for DA 1 receptors in CyA-SKF38393 interaction and, by the same token, implicate adrenergic receptors of the a 1 subtype in the interaction. Furthermore, the present findings are in accordance with earlier reports (Brodde 1982;Ohlstein et al 1984) that non-a 1 -adrenoceptor vasoconstrictors, such as PGF 2a or potassium chloride, are more appropriate for studying DA 1 -receptor-mediated vasodilations.…”

Section: Discussionsupporting

confidence: 95%

The α₁-adrenergic receptor not the DA₁-dopaminergic receptor mediates cyclosporine–SKF38393 renovascular interaction

El‐Mas

El-Din

El‐Gowilly

et al. 2005

Can. J. Physiol. Pharmacol.

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In this study, we investigated the effect of acute exposure to cyclosporine A (CyA) on renal vasodilations evoked by the DA(1) dopaminergic agonist SKF38393 and whether dopamine DA(1) receptors are directly involved in the interaction. Changes evoked by CyA in SKF38393 vasodilations were evaluated in phenylephrine-preconstricted isolated perfused rat kidneys in the absence and presence of SCH23390, a DA(1) receptor antagonist. SKF38393 (3 x 10(-8) to 3 x 10(-6) mol) produced dose-dependent reductions in the renal perfusion pressure that were significantly attenuated in tissues pretreated with SCH23390 or CyA. Unlike SKF38393, the vasodilatory action of sodium nitroprusside, a nitrovasodilator, was not altered by CyA. The attenuating effect of CyA on SKF38393 vasodilations was preserved in preparations pretreated with SCH23390, suggesting that sites other than DA(1) receptors may be involved in CyA-SKF38393 interaction. The study was then extended to investigate the possible involvement of renal alpha1-adrenoceptors in the interaction. Blockade of alpha(1)-adrenoceptors by prazosin (30 nmol/L) significantly reduced the vasodilatory effect of SKF38393 and virtually abolished the CyA-induced attenuation of SKF38393 responses. Further, CyA failed to alter SKF38393 vasodilations when the renal tone was raised with prostaglandin F2alpha (PGF2alpha), a vasoconstrictor whose effect is independent of alpha(1)-adenoceptors. Together, these findings support earlier reports that both DA(1) and alpha(1)-receptors mediate the renal vasodilatory action of SKF38393 and suggest that CyA interacts selectively with the alpha(1)-receptor component to compromise SKF38393 responses.

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“…Histochemical and physiological investigations have indicated a central cholinergic innervation of small blood vessels in the brain (Rennels et al, 1977;Estrada et al, 1983;Eckenstein and Baughman, 1984). In addition, a noradrenergic innervation ofintraparenchymal blood vessels originating in the locus coeruleus has long been suspected (Hart-man et al, 1972;Rennels and Nelson, 1975;Swanson et al, 1977) and dopaminergic innervation of blood vessels has been reported in experimental animals (see Brodde, 1982).…”

Section: Introductionmentioning

confidence: 95%

Adrenergic, serotoninergic, histaminergic, and imipramine binding sites in post-mortal human cerebral microvessel preparations

O’Neill

Fowler

Marcusson

et al. 1988

J. Neural Transmission

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Cerebral microvessels were prepared from fresh and frozen human brain samples obtained from autopsy cases. Structural integrity and purity of the microvessels were confirmed by light and electron microscopy, and by measurement of the enzymatic marker gamma-glutamyltranspeptidase. Similar morphological and enzymatic characteristics were found for the microvessels prepared from fresh and frozen brain samples. Radioligand binding experiments indicated the presence both in the "fresh" and "frozen" microvessel preparations of specific alpha 1-, alpha 2-, and beta-adrenergic, histamine H1, serotonin S1 and imipramine binding sites, although the density of beta-adrenergic and histamine H1 specific binding sites were lower in the frozen samples than in the fresh samples. Low levels of specific binding to muscarinic, GABAergic and serotonin S2 sites (with respect to the specific binding densities in the crude homogenates) were found in the microvessel preparations.

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Vascular dopamine receptors: Demonstration and characterization by studies

Cited by 81 publications

References 51 publications

Endothelium‐dependent And‐independent Relaxation by Dopamine in the Rabbit Pulmonary Artery

Endothelium‐dependent And‐independent Relaxation by Dopamine in the Rabbit Pulmonary Artery

The α₁-adrenergic receptor not the DA₁-dopaminergic receptor mediates cyclosporine–SKF38393 renovascular interaction

Adrenergic, serotoninergic, histaminergic, and imipramine binding sites in post-mortal human cerebral microvessel preparations

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Vascular dopamine receptors: Demonstration and characterization by studies

Cited by 81 publications

References 51 publications

Endothelium‐dependent And‐independent Relaxation by Dopamine in the Rabbit Pulmonary Artery

Endothelium‐dependent And‐independent Relaxation by Dopamine in the Rabbit Pulmonary Artery

The α1-adrenergic receptor not the DA1-dopaminergic receptor mediates cyclosporine–SKF38393 renovascular interaction

Adrenergic, serotoninergic, histaminergic, and imipramine binding sites in post-mortal human cerebral microvessel preparations

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The α₁-adrenergic receptor not the DA₁-dopaminergic receptor mediates cyclosporine–SKF38393 renovascular interaction