Effects of m-nisoldipine on anoxia-potentiated histamine and acetylcholine-induced contractions of the porcine isolated coronary artery.
Anoxia (95% N2 + 5% CO2) potentiated the contractile response to KCl 20 mmol/L, histamine (His) 5 mumol/L and acetylcholine (ACh) 0.5 mumol/L in isolated porcine coronary arterial rings. Calcium antagonists m-nisoldipine (m-Nis) and nisoldipine (Nis) 0.4-250 nmol/L produced a concentration-dependent decrease in both KCl, His and anoxia-potentiated KCl2 His or ACh-induced contractions. Chlorpheniramine 10 mumol/L but not cimetidine 10 mumol/L and atropine 10 mumol/L abolished contractions induced by His and ACh respectively. All 3 agents did not affect KCl response and the anoxia facilitation. Indomethacin 10 mumol/L markedly attenuated the further increase in tension by anoxia but failed to inhibit the response by these vasoconstrictors.
Yang
X P
XP
Department of Pharmacology, Hebei Medical College, Shijiazhuang, China.
Fu
S X
SX
Li
Y S
YS
D000109:Acetylcholine / Q000037:antagonists & inhibitors; D000818:Animals; D003331:Coronary Vessels / Q000187:drug effects; D006633:Histamine Antagonists / Q000494:pharmacology; D000860:Hypoxia / Q000503:physiopathology; D066298:In Vitro Techniques; D007213:Indomethacin / Q000494:pharmacology; D007536:Isomerism; D009119:Muscle Contraction / Q000187:drug effects*; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D015737:Nisoldipine / Q000494:pharmacology*; D013552:Swine
D006633:Histamine Antagonists; D015737:Nisoldipine; D000109:Acetylcholine; D007213:Indomethacin