Nakanishi T, Gu H, Momma K
Department of Pediatric Cardiology, Tokyo Women's Medical College, Japan.
J Mol Cell Cardiol. 1996 Aug;28(8):1715-26. doi: 10.1006/jmcc.1996.0161.
The purpose of the present study was to determine the effect of various types of acidosis on vessel diameter, intracellular pH (pHi), and calcium concentration ([Ca2+]i) in a cannulated preparation of the mesenteric arteriole of the rabbit. The effect of acidosis on vessel contraction was also studied in the wire-mounted preparation. In the cannulated preparation, pre-contracted by noradrenaline, hypercapnia caused vasoconstriction and increases in [Ca2+]i. In the wire-mounted preparation pre-contracted by either noradrenaline or high KCl, hypercapnia caused a transient vasoconstriction. In contrast, in the cannulated preparation pre-contracted by high KCl, hypercapnia caused a transient vasorelaxation and decreases in [Ca2+]i. Intracellular acidosis, induced by a NH4Cl prepulse, caused vasoconstriction and increases in [Ca2+]i even in the cannulated preparation pre-contracted by high KCl. The decrease in pHi during hypercapnia was similar to that observed after NH4Cl withdrawal. These data suggest that: (1) the effect of acidosis on vascular tone and [Ca2+]i is different depending upon the type of preparation and the mode of pre-activation, and (2) [Ca2+]i may, at least partly, regulate vascular contraction and relaxation during acidosis.
本研究的目的是确定不同类型的酸中毒对兔肠系膜小动脉插管标本中血管直径、细胞内pH值(pHi)和钙浓度([Ca2+]i)的影响。还在钢丝固定标本中研究了酸中毒对血管收缩的影响。在插管标本中,用去甲肾上腺素预收缩后,高碳酸血症引起血管收缩和[Ca2+]i升高。在分别用去甲肾上腺素或高钾预收缩的钢丝固定标本中,高碳酸血症引起短暂的血管收缩。相反,在高钾预收缩的插管标本中,高碳酸血症引起短暂的血管舒张和[Ca2+]i降低。由氯化铵预脉冲诱导的细胞内酸中毒即使在高钾预收缩的插管标本中也会引起血管收缩和[Ca2+]i升高。高碳酸血症期间pHi的降低与氯化铵撤除后观察到的相似。这些数据表明:(1)酸中毒对血管张力和[Ca2+]i的影响因标本类型和预激活方式而异;(2)[Ca2+]i可能至少部分调节酸中毒期间的血管收缩和舒张。