INTERACTION BETWEEN CALCIUM AND HYDROGEN-IONS IN CANINE CORONARY-ARTERIES
INTERACTION BETWEEN CALCIUM AND HYDROGEN-IONS IN CANINE CORONARY-ARTERIES
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DOI：
10.1016/s0022-2828(87)80388-7
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发表时间：
1987-08-01
影响因子：
5
通讯作者：
CINGOLANI, HE
中科院分区：
文献类型：
--
作者：
RINALDI, GJ;CATTANEO, EA;CINGOLANI, HE
本实验采用离体实验研究了高钾预收缩犬冠状动脉时“呼吸性”和“代谢性”酸碱变化的影响。碱中毒（pH 7.70 ±. 0.02）使冠状动脉张力增加33 . ±. 3%（P < 0.05）和酸中毒（pH7.10 ±. 0.01）下降了30 .+-。3%（P < 0.05）。张力稳定在约15分钟，其变化是相似的程度，无论是在细胞外pH值的变化产生的PCO 2或碳酸氢盐浓度的变化。收缩的变化没有废除既不α或β肾上腺素能阻滞，也不内皮剥脱。当平滑肌收缩性和这些离子浓度之间的关系达到平台时，pH的影响不能通过改变细胞外钾或钙来抵消。当肌条和[Ca 2 +]0的张力被绘制成曲线图时，DTmax在酸中毒时显著增加，在酸中毒时显著降低。未检测到Ca 50 [（Ca 2 +]0获得50%的最大力所需）的显著变化，pH值变化不会改变Ca 2+内流，但硝苯地平诱导的类似程度的松弛导致Ca 2+内流可检测到的减少。Ca 2+流出增加酸中毒和抑郁症。我们的数据不支持氢离子变化诱导钙内流改变的竞争方式作为收缩或舒张导管冠状动脉的机制。相反，他们认为酸碱变化通过调节Ca ~（2+）流出来改变血管平滑肌的收缩活动。
In vitro experiments were carried out to study the effects of "respiratory" and "metabolic" acid-base alterations on canine coronary arteries precontracted by high potassium. Alkalosis (pH 7.70 .+-. 0.02) increased the coronary tone by 33 .+-. 3% (P < 0.05) and acidosis (pH 7.10 .+-. 0.01) decresed in by 30 .+-. 3% (P < 0.05). The tension stabilized in approximately 15 mins and its variation was of similar extent whether changes in extracellular pH were produced by changes in PCO2 or in bicarbonate concentration. The contractile changes were not abolished neither by alpha or beta adrenergic blockade nor by endothelium denudation. The effect of pH could not be offset by altering extracellular potassium or calicum when the plateau of the relationship between contractility of the smooth muscle and concentration of these ions were reached. When tonus developed by the strips and [Ca2+]0 were plotted reciprocally, DTmax significantly increased in alkalosis and decreased in acidosis. No significant changes in Ca50 [(Ca2+]0 necessary to obtain 50% of maximal force) were detected pH changes did not modify Ca2+ influx but a relaxation of similar extent induced by nifedipine produced a detectable decrease in Ca2+ influx. Ca2+ efflux was augmented in acidosis and depressed in alkalosis. Our data do not support the hypothesis of hydrogen ion changes inducing calcium influx alterations in a competitive fashion as the mechanism involved to contract or relax conduit coronary arteries. On the countrary, they suggest that acid-base variations alter the contractile activity of vascular smooth muscle by modulating Ca2+ efflux.