SUMMARY Experimental aortic coarctation in rats is accompanied by non-pressure-related increases in hindlimb total vascular resistance and its neurogenic and structural components. To investigate the role of the sympattaoadrenergic system, we partially constricted or sham-constricted toe abdominal aorta in rats age 6 weeks that had had adrenal demedullation and guanethidine injections to produce peripheral sympatfaectomy (SYMP rats, N •= 13-coarcted, 14-sham-coarcted) and in sham-sympatbectomized, sham-demedullated control rats (SHAM rats, n = 14-coarcted, 11-sham-coarcted). In both SHAM and SYMP rats with coarctation, tail and femoral arterial pressures did not increase but carotid pressures rose by 18-25% (p < 0.01), accompanied by significant increases in heart weight/body weight. However, arterial pressures in SYMP were 30% lower than those in SHAM rats (p < 0.005). In the pump-perfused (blood, lml/min), innervated, isolated hindlimbs of SYMP, compared to SHAM rats, the effect of acute section of local nerves on resistance was reduced and denervation hypersensitivity was documented. In contrast to SHAM, coarctation in SYMP rats was not accompanied by increases in total hindlimb resistance and its neurogenic component; there were, however, significant rises in the humoral-myogenic (p < 0.01) and structural (p < 0.05) components. Thus, the sympatho-adrenergic system influences arterial blood pressure and accounts for the elevated neurogenic component of peripheral vascular resistance in coarctation hypertension In rats, but does not account for the elevated structural component of resistance. An unknown humoral factor, or factors, may be incriminated in the latter. hindquarters vascular bed in rats with aortic coarctation hypertension, we observed several structural and functional abnormalities that could not be the result of local elevation of intravascular pressure.1 ' These abnormalities included an increased hindlimb vascular resistance, with a large contribution by an elevated neurogenic component and also a significant contribution by an elevated structural component. The purpose of the present experiments was to further explore the role of sympathoadrenergic influences in the underlying mechanisms of these abnormalities in resistance. Hindlimb resistance was studied in coarcted rats that had had the peripheral sympathoadrenergic system ablated by guanethidine injections as newborns 4 and later had surgical adrenal demedullation.
MethodsThe protocols we used to ablate the peripheral sympathoadrenergic system and to coarct the aorta were identical to those previously reported.1 " Briefly, newborn male, Sprague-Dawley rats (Zivic-Miller Labs, Inc.) received guanethidine sulfate (Ismelin Sulfate, kindly supplied by CIBA-GEIGY), 50 mg/kg/day i.p., 5 days per week for 3 weeks. At age 28 days these rats underwent bilateral surgical adrenal demedullation; they were designated "sympathectomized" rats. Control rats, designated "sham-sympathectomized" rats, received saline injections and sham adrenal demedullatio...