Mechanism of impaired baroreflex control in prehypertensive Dahl salt-sensitive rats.

Abstract

Dahl salt-sensitive rats fed a low salt diet demonstrate functional impairment in baroreflex control of cardiovascular function prior to the development of hypertension. The purpose of this study was to identify the mechanism(s) responsible for impaired baroreflex control in prehypertensive Dahl salt-sensitive rats. To examine the central and efferent portions of the baroreflex arc, we electrically stimulated the aortic depressor nerve of urethane anesthetized Dahl salt-sensitive and Dahl salt-resistant rats while recording arterial pressure, heart rate, and sympathetic nerve activity. Aortic nerve stimulation produced equivalent responses in both groups, indicating that central and efferent mechanisms could not account for functional baroreflex impairment. In separate groups of Dahl rats, multifiber afferent aortic baroreceptor discharge was recorded while arterial pressure was increased with phenylephrine. Prehypertensive Dahl salt-sensitive rats demonstrated significantly less baroreceptor activation than Dahl salt-resistant rats, indicating that impaired baroreceptor discharge is the mechanism responsible for baroreflex abnormalities. Aortic arch distensibility was not different between Dahl strains, suggesting that impaired baroreceptor discharge in Dahl salt-sensitive rats is probably not due to abnormalities in vessel wall distensibility. Since arterial pressure of both Dahl strains was in the normotensive range and did not differ significantly between Dahl salt-sensitive and salt-resistant rats, baroreceptor impairment appears to be a primary defect in Dahl salt-sensitive rats, rather than being secondary to hypertension. We speculate that this impairment in baroreceptor function in Dahl salt-sensitive rats prior to any elevation in arterial pressure may contribute to the Dahl salt-sensitive rat's genetic propensity to develop hypertension.