Activation of angiotensin Ⅱ type 1 receptors in the median preoptic nucleus induces a diuretic and natriuretic response in rats

• Published in: Journal of Nanjing Medical University Vol. 23; no. 6; pp. 410 - 414
• Main Authors: Gao, Yuan, Luo, Lei, Liu, Hong
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.11.2009
• Subjects: angiotensin AT1 receptor; endogenous digitalis-like factor; median preoptic nucleus; Na +,K +-ATPase; natriuresis; rat; 核受体; 血管紧张素; natriuresis; angiotensin AT1 receptor; median preoptic nucleus; rat; Na +,K +-ATPase; endogenous digitalis-like factor
• ISSN: 1007-4376; 1876-4819
• DOI: 10.1016/S1007-4376(09)60091-5

Objective： To investigate the effect of activation of angiotensin Ⅱ（AngⅡ） type 1 （AT1） receptors in the median preoptic nucleus （MnPO） of rats on renal sodium excretion. Methods： After anesthesia, the rats were injected into the MnPO via an implanted cannula. Urine samples were collected via a bladder cannula, and the urine sodium concentration was assayed with flame spectrophotometry. The serum level of endogenous digitalis-like factor （EDLF） and Na^＋,K^＋-ATPase activity in the renal cortex tissue were assayed respectively with a radioimmunoassay and with an ammonium molybdophosphate-based kit. Results： Both the urinary volume and the sodium excretion peaked 60 min after AngⅡ was administered into the MnPO. The responses were accompanied by an increase in serum EDLF and a decrease in Na^＋,K^＋-ATPase activity in the renal cortex. The responses of diuresis and natriuresis, as well as an increase in serum EDLF and a decrease in Na^＋,K^＋-ATPase activity in the renal cortex induced by MnPO adminstration with AngⅡ were inhibited by pior treatment with the AngⅡ receptor blocking agent losartan into the MnPO. Conclusion： These results suggest that activation of AT1 receptors in the MnPO of rat induces diuretic and natriuretic responses. The responses are associated with an increase release of EDLF and with the inhibition of Na^＋,K^＋-ATPase activity in renal cortex tissue.