Atypical antagonism of D1-receptor-mediated vasodilator responses in the perfused kidney by SCH23390

Martin, S.W.; Broadley, Kenneth J.

doi:10.1016/1043-6618(95)80034-4

Cited by 5 publications

(5 citation statements)

References 17 publications

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“…The response was abolished by the dopamine D 2 and D 3 antagonist, haloperidol ( Creese et al ., 1975 ). Vasodilatation is the usual response to dopamine in vascular beds, such as the renal and mesenteric vasculature, a response mediated by dopamine D 1 receptors ( Martin and Broadley, 1995 ). Vasoconstriction by dopamine is usually mediated by postjunctional α 1 ‐adrenoceptors ( Duval et al ., 1985 ).…”

Section: Discussionmentioning

confidence: 99%

Dietary trace amine‐dependent vasoconstriction in porcine coronary artery

Herbert

Kidd

Broadley

2008

British J Pharmacology

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Background and purpose: The dietary trace amines tyramine and b-phenylethylamine (b-PEA) can increase blood pressure. However, the mechanisms involved in the vascular effect of trace amines have not been fully established. The purpose of this study was to evaluate whether trace amine-dependent vasoconstriction was brought about by tyramine and b-PEA acting as indirect sympathomimetic agents, as previously assumed, or whether trace amine-dependent vasoconstriction could be mediated by recently discovered trace amine-associated (TAA) receptors. Experimental approach: The responses to p-tyramine and b-PEA were investigated in vitro in rings of the left anterior descending coronary arteries of pigs. Key results: p-Tyramine induced a concentration-dependent (0.1-3 mM) vasoconstriction. The maximum response and pD 2 value for p-tyramine was unaffected by endothelium removal or pre-treatment with antagonists for adrenoceptors, histamine, dopamine or 5-HT receptors. b-PEA also produced a concentration-dependent (0.3-10 mM) vasoconstriction which was unaffected by endothelium removal, b-adrenoceptor or 5-HT receptor antagonists. A substantial, but reduced, response to b-PEA was obtained in the presence of prazosin (a 1 -adrenoceptor antagonist), haloperidol (D 2 /D 3 dopamine receptor antagonist) or mepyramine (H 1 histamine receptor antagonist). The pD 2 value for b-PEA was unaffected by any of the antagonists tested. Conclusions and implications: Vasoconstriction induced by p-tyramine does not involve an indirect sympathomimetic effect, although vasoconstriction caused by b-PEA may occur, in part, by this mechanism. We therefore propose that trace aminedependent vasoconstriction is mediated by phenylethylamine-specific receptors, which are closely related to or identical to TAA receptors. These receptors could provide a target for new antihypertensive therapies.

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Section: Discussionmentioning

confidence: 99%

Dietary trace amine‐dependent vasoconstriction in porcine coronary artery

Herbert

Kidd

Broadley

2008

British J Pharmacology

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“…To assess the involvement of dopamine receptors in vasorelaxation to NADA, the dopamine receptor antagonist SCH23390 (1 mM, Martin & Broadley, 1995) was added to preparations 20 min before pre-constriction. The involvement of nitric oxide was investigated using the nitric oxide synthase inhibitor, N G -nitro-L-arginine methyl ester (L-NAME, 300 mM, Randall & Griffith, 1991).…”

Section: Experimental Protocolmentioning

confidence: 99%

Characterisation of the vasorelaxant properties of the novel endocannabinoid N‐arachidonoyl‐dopamine (NADA)

O’Sullivan

Kendall

Randall

2004

British J Pharmacology

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1 We have investigated the vascular effects of N-arachidonoyl-dopamine (NADA), a novel endocannabinoid/vanilloid. NADA caused vasorelaxant effects comparable to those of anandamide in small mesenteric vessels (G3), the superior mesenteric artery (G0) and in the aorta. 2 In G3, addition of N G -nitro-L-arginine methyl ester (300 mM) or the dopamine (D 1 ) receptor antagonist (SCH23390, 1 mM) did not affect responses to NADA. In the presence of 60 mM KCl, after de-endothelialisation, or after K þ channel inhibition with charybdotoxin (100 nM) and apamin (500 nM), relaxant responses to NADA were inhibited. 3 In G3, pretreatment with the vanilloid receptor (VR) agonist capsaicin (10 mM) or the VR antagonist capsazepine (10 mM) reduced vasorelaxation to NADA. 4 In G3, application of the CB 1 antagonist SR141716A at 1 mM but not 100 nM reduced the potency of NADA. Another CB 1 antagonist, AM251 (100 nM and 1 mM), did not affect vasorelaxation to NADA. After endothelial denudation, SR141716A (1 mM) did not reduce the responses further. A combination of capsaicin and SR141716A (1 mM) reduced vasorelaxation to NADA further than with capsaicin pretreatment alone. The novel endothelial cannabinoid (CB) receptor antagonist O-1918 opposed vasorelaxation to NADA in G3. 5 In the superior mesenteric artery (G0), vasorelaxation to NADA was not dependent on an intact endothelium and was not sensitive to O-1918, but was sensitive to capsaicin and SR141716A or AM251 (both 100 nM). 6 The results of the present study demonstrate for the first time that NADA is a potent vasorelaxant. In G3, the effects of NADA are mediated by stimulation of the VR and the novel endothelial CB receptor, while in G0, vasorelaxation is mediated through VR 1 and CB 1 receptors.

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“…It cannot be argued that the concentration of SCH23390 (1 mmol/L) employed in the present study might have been inadequate for DA 1 receptor blockade because the same concentration of SCH23390 substantially attenuated SKF38393 vasodilations. Plus, effective blockade of DA 1 receptors has been achieved by even lower concentrations of SCH23390 in previous studies (Martin and Broadley 1995b). Therefore, the finding that combined treatment of CyA and SCH23390 produced additive inhibitory effects on renal SKF38393 responses favors the involvement of 2 distinct cellular targets in the deleterious renal effects of the 2 drugs.…”

Section: Discussionmentioning

confidence: 86%

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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Atypical antagonism of D1-receptor-mediated vasodilator responses in the perfused kidney by SCH23390

Cited by 5 publications

References 17 publications

Dietary trace amine‐dependent vasoconstriction in porcine coronary artery

Dietary trace amine‐dependent vasoconstriction in porcine coronary artery

Characterisation of the vasorelaxant properties of the novel endocannabinoid N‐arachidonoyl‐dopamine (NADA)

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

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Atypical antagonism of D1-receptor-mediated vasodilator responses in the perfused kidney by SCH23390

Cited by 5 publications

References 17 publications

Dietary trace amine‐dependent vasoconstriction in porcine coronary artery

Dietary trace amine‐dependent vasoconstriction in porcine coronary artery

Characterisation of the vasorelaxant properties of the novel endocannabinoid N‐arachidonoyl‐dopamine (NADA)

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

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