Neurohumoral mechanisms in acute aortic coarctation in conscious and anesthetized dogs.

To study the interactions of the renin-angiotensin system, sodium balance, and the sympathetic nervous system in the development of coarctation hypertension, an aortic gradient was created with a pneumatic cuff in 11 chronically instrumented conscious dogs. Significant hypertension associated with a significant rise in plasma renin activity and sodium retention occurred within 48 h. Competitive angiotensin II blockade caused a greater decrease in arterial pressure after coarctation than before coarctation. In contrast, plasma norepinephrine decreased significantly from control levels after coarctation, and alpha-adrenergic blockade with phentolamine caused less of a decrease in arterial pressure than before coarctation. This decrease in sympathetic activity was also accompanied by a decreased blood pressure response to pressor doses of angiotensin II and methoxamine after coarctation. To assess carotid baroreceptor influence on acute coarctation hypertension, aortic blood pressure responses to pressor agents were determined in 12 chlorolose-urethan-anesthetized dogs while carotid sinus pressure was independently varied. Maintaining carotid pressure at control levels after aortic constriction restored blood pressure responses to pressor agents to before-coarctation levels. These results suggest that 1) activation of the renin-angiotensin system and sodium retention contribute to the development of coarctation hypertension, and 2) there is a carotid sinus baroreceptor-mediated decrease in alpha-adrenergic activity with acute coarctation hypertension.