Hemodynamic, neural, and humoral mechanisms of aortic coarctation hypertension in the rat.
The present study was designed: (a) to examine the contribution of the renin-angiotensin system (RAS) to elevated regional vascular resistance during the onset of aortic coarctation hypertension, and (b) to determine the role of angiotensin II ( Ang II)-neural interactions during the maintenance of high arterial pressure (AP). In the first study, rats were instrumented chronically with miniaturized pulsed Doppler flow probes on the right renal and superior mesenteric arteries 3 days prior to complete aortic ligation. After ligation, AP and renal and mesenteric vascular resistances increased significantly. In sham-ligated rats, small increases in AP and decreases in regional vascular resistances were observed. Captopril, administered 6 h postligation, reduced AP and regional vascular resistance in ligated rats to preligation levels, indicating that the RAS was responsible for these acute increases. In the second study, Ang II-neural interactions were examined by treating 12- to 14-day postligation hypertensive rats with captopril or with hexamethonium, a ganglionic blocker, followed by captopril. Depressor responses to captopril were also examined in aortic-ligated rats pretreated with hydralazine. Captopril alone and captopril after hydralazine caused similar reductions in AP (-26 +/- 2% and -27 +/- 1%, respectively). After ganglionic blockade, the depressor responses to captopril were attenuated (-13 +/- 2%). The marked differences in the efficacy of captopril to lower AP in the ganglionic-blocked group of rats suggested that the pressor actions of Ang II were mediated, in part, through indirect actions on the sympathetic nervous system.[1]References
- Hemodynamic, neural, and humoral mechanisms of aortic coarctation hypertension in the rat. Lappe, R.W., Brody, M.J. J. Cardiovasc. Pharmacol. (1986) [Pubmed]
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