Pressure-independent increases in vascular resistance in hypertension: role of sympathoadrenergic influences.

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 sympathoadrenergic system, we partially constricted or sham-constricted the abdominal aorta in rats age 6 weeks that had had adrenal demedullation and guanethidine injections to produce peripheral sympathectomy (SYMP rats, N = 13-coarcted, 14-sham-coarcted) and in sham-sympathectomized, 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 less than 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 less than 0.005). In the pump-perfused (blood, 1 ml/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 less than 0.01) and structural (p less than 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 rats, but does not account for the elevated structural component of resistance. An unknown humoral factor, or factors, may be incriminated in the latter.