Huang B S, McCumbee W D, Wright G L
Department of Physiology, Marshall University School of Medicine, Huntington, WV 25704-2901.
Can J Physiol Pharmacol. 1988 Apr;66(4):332-6. doi: 10.1139/y88-057.
The in vitro contractile effect of a peptide recently isolated from the blood of spontaneously hypertensive rats was assessed on rat aortic rings. Preincubation of aortic rings with the peptide had no effect on resting tension but significantly enhanced K+ or norepinephrine-induced contractile responses. Contractile effects were abolished by removal of extracellular calcium or by additions of the calcium channel antagonists, verapamil and nifedipine. The antagonism of peptide enhancement of contraction by verapamil was noncompetitive, whereas nifedipine blockade was competitive in nature. Moreover, preincubation of aortic rings with the peptide attenuated the contractile response to Bay K 8644, a newly described synthetic calcium channel agonist. We suggest that this peptide has similar effects to Bay K 8644 and may act as an endogenous modulator of voltage-dependent calcium channels.
对从自发性高血压大鼠血液中最近分离出的一种肽在大鼠主动脉环上的体外收缩作用进行了评估。将主动脉环与该肽预孵育对静息张力没有影响,但显著增强了钾离子或去甲肾上腺素诱导的收缩反应。去除细胞外钙或添加钙通道拮抗剂维拉帕米和硝苯地平可消除收缩作用。维拉帕米对肽增强收缩作用的拮抗是非竞争性的,而硝苯地平的阻断本质上是竞争性的。此外,将主动脉环与该肽预孵育减弱了对新描述的合成钙通道激动剂Bay K 8644的收缩反应。我们认为这种肽与Bay K 8644有相似作用,可能作为电压依赖性钙通道的内源性调节剂。