Exacerbation of central baroreflex impairment in Dahl rats by high-salt diets.
To determine whether baroreflex impairment progresses in hypertensive Dahl rats, we recorded reflex responses to drug-induced changes in blood pressure in hypertension-sensitive (DS) and hypertension-resistant (DR) rats maintained on low- or high-salt diets for 7 wk. Chronotropic responses, manifested as either bradycardia for phenylephrine or tachycardia for sodium nitroprusside, were always smaller in awake DS rats on high-salt diet than in any others. When the same rats were later anesthetized, related changes in afferent aortic and efferent splanchnic nerve activity were similarly reduced. Regardless of dietary salt intake, reflex bradycardia elicited by electrical stimulation of aortic nerve afferents was also weaker in DS than in DR rats, but attendant decreases in mean aortic pressure and splanchnic nerve activity did not differ significantly. These results are compatible with an impairment of afferent and central components of the reflex arc. Even though exact sites of dysfunction were not identified, our findings suggest that in hypertensive DS rats high-salt diets may aggravate baroreflex impairment, at least in part, by acting centrally.
D000344:Afferent Pathways / Q000503:physiopathology; D000818:Animals; D001011:Aorta / Q000294:innervation; D001919:Bradycardia / Q000209:etiology; D001921:Brain / Q000503:physiopathology*; D004032:Diet; D004198:Disease Susceptibility; D004558:Electric Stimulation; D006973:Hypertension / Q000235:genetics / Q000503:physiopathology*; D008297:Male; D011311:Pressoreceptors / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains; D012018:Reflex / Q000502:physiology*; D012965:Sodium Chloride / Q000008:administration & dosage*; D013997:Time Factors; D014630:Vagus Nerve / Q000503:physiopathology
D012965:Sodium Chloride