Armstead W M, Lippton H L, Hyman A L, Kadowitz P J
Am J Physiol. 1987 Apr;252(4 Pt 2):H816-25. doi: 10.1152/ajpheart.1987.252.4.H816.
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.
在麻醉猫身上研究了钙通道拮抗剂尼索地平对血管阻力和血管收缩反应的影响。尼索地平是一种二氢吡啶类钙通道阻滞剂,可降低总外周阻力并扩张肠道血管床。这种钙拮抗剂可阻断肠道对BAY K 8644(一种硝苯地平类似物,可促进钙内流)的血管收缩反应。钙通道拮抗剂可降低肠道对交感神经刺激、去甲肾上腺素和酪胺的血管收缩反应。尼索地平还可降低肠道对氯化钾以及通过特定受体介导作用(包括刺激α1和α2肾上腺素能受体)引起血管收缩的激动剂的血管收缩反应。尼索地平对血管收缩反应的血管舒张和抑制作用是可逆的,反应在60分钟内恢复到对照值。目前的数据表明,细胞外钙源对于维持张力以及由神经元释放的或外源性去甲肾上腺素以及通过特定受体机制起作用或使血管平滑肌去极化的多种药物诱导的血管收缩是必需的。目前的结果表明,猫肠道血管床中由α1和α2肾上腺素能受体激动剂引起的血管收缩也需要类似的钙源。