Aalkjaer C, Mortensen F V, Jensen P E, Nielsen H
Department of Pharmacology and Danish Biomembrane Research Centre, University of Aarhus, Universitetsparken, DK-8000 Aarhus C, Denmark.
Pflugers Arch. 1998 Oct;436(5):705-11. doi: 10.1007/s004240050692.
In vitro both acetate and hyperosmolarity cause vasodilation, which could be physiologically important during food ingestion and during peritoneal dialysis. The purpose of this study was to investigate the role of the intracellular calcium concentration ([Ca2+]i, measured with fura-2), membrane potential (measured with glass microelectrodes) and intracellular pH [pHi, measured with bis-carboxyethylcarboxyfluorescein (BCECF)] in the vasodilation. Hyperosmolar sodium acetate (30 mM) concentration dependently relaxed noradrenaline-precontracted arteries. This response was associated with hyperpolarization and a fall in [Ca2+]i. In arteries precontracted with 50 mM K+ the relaxation was associated with a decrease of [Ca2+]i but no change in membrane potential. Isoosmolar sodium acetate neither relaxed or affect [Ca2+]i of K+-precontracted arteries, but induced a small relaxation with no reduction in [Ca2+]i in noradrenaline-precontracted arteries. Hyperosmolar acetate caused a transient reduction of pHi that was unrelated to relaxation. It is concluded that the mechanisms responsible for the relaxation to hyperosmolar acetate involve a decrease of [Ca2+]i, which is only partly explained by hyperpolarization and probably a decrease in the sensitivity of the contractile proteins to [Ca2+]i. pHi seems not to play a role in these effects.
在体外，醋酸盐和高渗都可引起血管舒张，这在食物摄入和腹膜透析过程中可能具有重要的生理意义。本研究的目的是探讨细胞内钙浓度（[Ca2+]i，用fura-2测量）、膜电位（用玻璃微电极测量）和细胞内pH值（[pHi]，用双羧乙基羧基荧光素（BCECF）测量）在血管舒张中的作用。高渗醋酸钠（30 mM）浓度依赖性地舒张去甲肾上腺素预收缩的动脉。这种反应与超极化和[Ca2+]i下降有关。在50 mM K+预收缩的动脉中，舒张与[Ca2+]i降低有关，但膜电位无变化。等渗醋酸钠既不舒张也不影响K+预收缩动脉的[Ca2+]i，但在去甲肾上腺素预收缩的动脉中引起小幅度舒张且[Ca2+]i无降低。高渗醋酸盐导致pHi短暂降低，这与舒张无关。得出的结论是，高渗醋酸盐舒张的机制涉及[Ca2+]i降低，这仅部分由超极化解释，可能还有收缩蛋白对[Ca2+]i敏感性的降低。pHi似乎在这些效应中不起作用。
