[Angiotensin II participates in stress-induced high blood pressure via stimulating hypothalamic vasopressin synthesis and release].

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Experiments were carried out in male Sprague-Dawley rats. The animals were randomly divided into three groups: control, stressed and stress + captopril. Stress stimulations were composed of repeated electric foot-shock combined with noise, twice one day (2 h each session) for 15 consecutive days. Animals in the stress+captopril group were administered with captopril (50 mg/kg.d) intraperitoneally. The results showed that at the end of the 15-day experiment the systolic pressure of the tail artery in stressed rats was significantly higher than that of the control rats, i.e., 19.75+/ C1.0 kPa (n=8, P<0.05) versus 16.32+/ C0.55 kPa (n=7); the vasopressin (AVP) mRNA level in the hypothalamus of the stressed rats also increased significantly compared with that of the control rats, i.e., 12990.33+/ C1533.58 (n=6, P<0.001) versus 7332.66+/ C522.65 (n=6). However, in the stress + captopril rats, both the tail artery systolic pressure and hypothalamic AVP mRNA level were significantly higher than those of the control rats, but lower than those of the stressed rats. In the control rats, no significant change in mean blood pressure (MBP) was observed after intracerebroventricular (icv) injection of 0.3 microgram of d(CH(2))(5)Tyr(Me)AVP, a selective AVP V(1) receptor antagonist; however, a decrease in MBP was observed in both stressed and stress+captopril rats (P<0.05), but the decrease in stress+captopril rats was more obvious than that of the stressed rats after icv a same dose of d(CH(2))(5)Tyr(Me)AVP. These results indicate that the endogenous renin-angiotensin system participates in the mechanism of the stress-induced high blood pressure in rats, and that the effect of Ang II is mediated mainly by stimulating hypothalamic AVP synthesis and release, which in turn result in an increase in blood pressure by acting on the central V (1) receptors.

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