Effects of Acid-Base Balance on the Isolated Rabbit Vascular Tone

Suh, Jung Kook; Cho, Sang Yoon; Han, In Su; Kim, Kyung Hyun; Shim, Jae Chol

Abstract

The effects of acidosis and alkalosis on vascular smooth muscle contractions were studied. Ring segments(3-4 mm in length) of rabbit abdominal aorta and pulmonary artery were mounted in the tissue bath(for respiratory study) and superfusion device(for metabolic study) for isometric tension recording. Respiratory acidosis and alkalosis were obtained by increasing and lowering the PCO2(80 and 15 mmHg, respectively). Metabolic acidosis and alkalosis were obtained by lowering and increasing the HCO3 concentration(12 and 50 mEq/l, respectively). After precontraction with norepinephrine(10-7 M), Vessels were exposed to acidosis and alkalosis for 30 minutes. The study was done with and without endothelium. The mechanism of vasorelaxation and vasoconstriction were confirmed with Ca2+ activated K+ channel blocker and Ca2+ free Krebs solution. The results were as follows: 1) Respiratory and metabolic acidosis induced significant vasorelaxation in both group of abdominal aorta and pulmonary artery(p<0.05). In endothelium intact group, vasorelaxation was greater than endothelium removed group. especially in respiratory acidosis was statistically significant(p<0.05). 2) Respiratory and metabolic alkalosis induced significant vasoconstriction in both group of abdominal aorta and pulmonary artery(p<0.05). In endothelium intact group, vasoconstriction was lesser than endothelium removed group, but was not statistically significant. 3) Acidosis induced vasorelaxation was blocked by tetraethylammonium(TEA). 4) Alkalosis induced vasoconstriction was blocked by Ca2+ free Krebs solution. These results suggested that: 1) Acidosis induced vasorelaxation. 2) alkalosis induced vasoconstriction 3) Vasorelaxation during acidosis was induced by K+ efflux through the Ca2+ activated K' channel. 4) Vasoconstriction during alkalosis was induced by Ca2+ influx.