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Abraham G, Simon G: Autopotentiation of pressor responses by subpressor angiotensin II in rats. Am J Hypertens. 1994 Mar;7(3):269-75.
The mechanisms whereby the continuous administration of initially subpressor doses of angiotensin II (ANG II) leads to pressor hyperresponsiveness and gradual development of hypertension were investigated. Male Sprague-Dawley rats (350 to 400 g) were given ANG II intraperitoneally, 200 ng/kg/min, for 24 h, 7 to 10 days, or 6 weeks. Vehicle-infused rats were controls. Pressor responses to incremental doses of ANG II, norepinephrine (NE), and serotonin were measured in chloralose-anesthetized rats, before and after neurohumoral blockade, and the main findings were confirmed in awake, free-moving rats with implanted catheters. Pressure responses to ANG II and NE were also measured in the isolated, pump-perfused mesenteric circulation of rats after 7 to 10 days of ANG II or sham infusion. Compared with control rats, there were no hemodynamic changes in ANG II-treated rats at 24 h. After 7 to 10 days of ANG II treatment, tail systolic blood pressure rose by 13 mm Hg (P < .01) and pressor responses to ANG II (P < .01) but not to NE or serotonin were increased. Pressor hyperresponsiveness was due in part to potentiation of vascular responses because pressure responses to ANG II (P < .002) but not to NE were also increased in the mesenteric circulation of ANG II-treated rats. By 6 weeks, mild hypertension was well established in ANG II-treated rats and pressor responses were increased to both ANG II (P < .05) and NE (P < .01).(ABSTRACT TRUNCATED AT 250 WORDS) |
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