da Silva R K, Menani J V, Saad W A, Renzi A, Silveira J E, Luiz A C, Camargo L A
Department of Physiology, School of Dentistry, Paulista State University, Araraquara, Brazil.
Brain Res. 1996 Apr 22;717(1-2):38-43. doi: 10.1016/0006-8993(95)01553-1.
The present experiments were conducted to investigate the role of the alpha 1-, alpha 2- and beta-adrenergic receptors of the median preoptic area (MnPO) on the water intake and urinary electrolyte excretion, elicited by central injections of angiotensin II (ANG II). Prazosin (an alpha 1-adrenergic receptor antagonist) and yohimbine (an alpha 2-adrenergic receptor antagonist) antagonized the water ingestion, Na+, K+, and urine excretion induced by ANG II. Administration of propranolol, a beta-adrenergic receptor antagonist increased the Na+, K+, and urine excretion induced by ANG II. Previous treatment with prazosin and yohimbine reduced the pressor responses to ANG II. These results suggest that the adrenergic neurotransmission in the MnPO may actively participate in ANG II-induced dipsogenesis, natriuresis, kaliuresis, diuresis and pressor responses in a process that involves alpha 1-, alpha 2-, and beta-adrenoceptors.
本实验旨在研究正中视前区（MnPO）的α1、α2和β肾上腺素能受体在中枢注射血管紧张素II（ANG II）引起的水摄入和尿电解质排泄中的作用。哌唑嗪（一种α1肾上腺素能受体拮抗剂）和育亨宾（一种α2肾上腺素能受体拮抗剂）可拮抗ANG II诱导的水摄入、钠、钾和尿排泄。β肾上腺素能受体拮抗剂普萘洛尔的给药增加了ANG II诱导的钠、钾和尿排泄。先前用哌唑嗪和育亨宾治疗可降低对ANG II的升压反应。这些结果表明，MnPO中的肾上腺素能神经传递可能在涉及α1、α2和β肾上腺素能受体的过程中积极参与ANG II诱导的饮水、利钠、利尿、排钾和升压反应。
