Hisa H, Hayashi Y, Satoh S
J Pharmacol Exp Ther. 1985 Nov;235(2):481-6.
Effects of intrarenal infusions of prazosin (0.7 microgram/kg/min), yohimbine (1 microgram/kg/min), propranolol (4 micrograms/kg/min) and sulpiride (20 micrograms/kg/min) on renal prostaglandin (PG) E2 and renin release in response to renal nerve stimulation (RNS) were examined in anesthetized dogs. RNS (2.5-5 Hz, for 10 min) decreased renal blood flow and increased both PGE2 and renin secretion rates. The blood flow response was inhibited by prazosin but not by other antagonists. Prazosin and propranolol, but not yohimbine or sulpiride, attenuated the renin response. However, none of these antagonists affected the PGE2 response. The results suggest that the RNS-induced renin release is mediated by alpha adrenoceptors, which seem to be alpha-1 type, and beta adrenoceptors, but the RNS-induced PGE2 release is not mediated by these adrenoceptors. Renal dopaminergic component may play no significant role in the RNS-induced PGE2 or renin release.
在麻醉犬中,研究了肾内输注哌唑嗪(0.7微克/千克/分钟)、育亨宾(1微克/千克/分钟)、普萘洛尔(4微克/千克/分钟)和舒必利(20微克/千克/分钟)对肾神经刺激(RNS)引起的肾前列腺素(PG)E2和肾素释放的影响。RNS(2.5 - 5赫兹,持续10分钟)降低肾血流量,并增加PGE2和肾素分泌率。哌唑嗪可抑制血流量反应,而其他拮抗剂则无此作用。哌唑嗪和普萘洛尔可减弱肾素反应,而育亨宾或舒必利则无此作用。然而,这些拮抗剂均不影响PGE2反应。结果表明,RNS诱导的肾素释放由α肾上腺素能受体介导,似乎是α-1型,以及β肾上腺素能受体介导,但RNS诱导的PGE2释放并非由这些肾上腺素能受体介导。肾多巴胺能成分在RNS诱导的PGE2或肾素释放中可能不起重要作用。