Influence of nisoldipine on vascular resistance and vasoconstrictor responses in cats.
The influence of nisoldipine, a calcium entry antagonist, on vascular resistance and vasoconstrictor responses was investigated in the anesthetized cat. Nisoldipine, a dihydropyridine calcium entry blocking agent, decreased total peripheral resistance and dilated the intestinal vascular bed. This calcium antagonist blocked intestinal vasoconstrictor responses to BAY K 8644, a nifedipine analogue, which promotes calcium entry. The calcium entry antagonist decreased intestinal vasoconstrictor responses to sympathetic nerve stimulation, norepinephrine, and tyramine. Nisoldipine also reduced intestinal vasoconstrictor responses to potassium chloride and agonists that elicit vasoconstriction by specific receptor-mediated actions including stimulation of alpha 1- and alpha 2-adrenoceptors. The vasodilator and inhibitory effects of nisoldipine on vasoconstrictor responses were reversible, and responses returned to control value over a 60-min period. The present data suggest that an extracellular source of calcium is required for maintenance of tone and for vasoconstriction induced by neuronally released or exogenous norepinephrine as well as a diverse group of agents that act through specific receptor mechanisms or depolarize vascular smooth muscle. The present results suggest that similar sources of calcium are required for vasoconstriction elicited by alpha 1- and alpha 2-adrenoceptor agonists in the feline intestinal vascular bed.
D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001381:Azepines / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D000068438:Brimonidine Tartrate; D002302:Cardiac Output / Q000187:drug effects; D002415:Cats; D015237:Dinoprost; D004146:Dioxanes / Q000494:pharmacology; D004558:Electric Stimulation; D005260:Female; D019329:Idazoxan; D008297:Male; D008729:Methoxamine / Q000494:pharmacology; D009543:Nifedipine / Q000031:analogs & derivatives* / Q000494:pharmacology; D015737:Nisoldipine; D009638:Norepinephrine / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011450:Prostaglandin Endoperoxides, Synthetic / Q000494:pharmacology; D011460:Prostaglandins F / Q000494:pharmacology; D011810:Quinoxalines / Q000494:pharmacology; D013152:Splanchnic Circulation / Q000187:drug effects; D013449:Sulfonamides / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000502:physiology; D014439:Tyramine / Q000494:pharmacology; D014655:Vascular Resistance / Q000187:drug effects*; D014661:Vasoconstriction / Q000187:drug effects*; D000096926:Benzenesulfonamides
D019796:15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D000804:Angiotensin II; D001381:Azepines; D000068438:Brimonidine Tartrate; D015237:Dinoprost; D004146:Dioxanes; D019329:Idazoxan; D008729:Methoxamine; D009543:Nifedipine; D015737:Nisoldipine; D009638:Norepinephrine; D010656:Phenylephrine; D011450:Prostaglandin Endoperoxides, Synthetic; D011460:Prostaglandins F; D011810:Quinoxalines; D013449:Sulfonamides; D014439:Tyramine; C044648:YM 12617; D000096926:Benzenesulfonamides; C015603:azepexole