Catecholamine-induced vasoconstriction is sensitive to carbonic anhydrase I activation

Brazilian Journal of Medical and Biological Research

I. Puscas²  M. Coltau²  L. Gilau¹  R. Pasca²  G. Domuta²  M. Baican¹  A. Hecht¹ 

[1] ,Simleu Silvaniei Center for Research and Medical Assistance Romanian Medical AcademySalaj,Romania

关键词: adrenergic agonists;    carbonic anhydrase;    arterial blood pressure;   

DOI  :  10.1590/S0100-879X2001000300007

来源: SciELO

【 摘 要 】

We studied the relationship between alpha- and beta-adrenergic agonists and the activity of carbonic anhydrase I and II in erythrocyte, clinical and vessel studies. Kinetic studies were performed. Adrenergic agonists increased erythrocyte carbonic anhydrase as follows: adrenaline by 75%, noradrenaline by 68%, isoprenaline by 55%, and orciprenaline by 62%. The kinetic data indicated a non-competitive mechanism of action. In clinical studies carbonic anhydrase I from erythrocytes increased by 87% after noradrenaline administration, by 71% after orciprenaline and by 82% after isoprenaline. The increase in carbonic anhydrase I paralleled the increase in blood pressure. Similar results were obtained in vessel studies on piglet vascular smooth muscle. We believe that adrenergic agonists may have a dual mechanism of action: the first one consists of a catecholamine action on its receptor with the formation of a stimulus-receptor complex. The second mechanism proposed completes the first one. By this second component of the mechanism, the same stimulus directly acts on the carbonic anhydrase I isozyme (that might be functionally coupled with adrenergic receptors), so that its activation ensures an adequate pH for stimulus-receptor coupling for signal transduction into the cell, resulting in vasoconstriction.

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