Data/hora: 11/06/2024 08:48:50

Provedor de dados: | 56
País: | Brazil
Título: | Catecholamine-induced vasoconstriction is sensitive to carbonic anhydrase I activation
Autores: | Puscas,I.; Coltau,M.; Gilau,L.; Pasca,R.; Domuta,G.; Baican,M.; Hecht,A.
Data: | 2001-03-01
Ano: | 2001
Palavras-chave: | Adrenergic agonists; Carbonic anhydrase; Arterial blood pressure.
Resumo: | 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.
Tipo: | Info:eu-repo/semantics/article
Idioma: | Inglês
Identificador: | http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2001000300007
Editor: | Associação Brasileira de Divulgação Científica
Relação: | 10.1590/S0100-879X2001000300007
Formato: | text/html
Fonte: | Brazilian Journal of Medical and Biological Research  v.34 n.3 2001
Fonte: | info:eu-repo/semantics/openAccess