Primary impairment of cardiopulmonary baroreflexes in Dahl salt-sensitive rats.
Neural mechanisms contribute to salt-induced hypertension in Dahl salt-sensitive (DS) rats. We examined whether cardiopulmonary (CP) baroreflexes are impaired in prehypertensive DS rats. Dahl salt-resistant (DR) and DS rats fed low salt diet were urethane-anaesthetized and sino-aortic denervated. Reductions in sympathetic activity (SNA, splanchnic nerve recording) were measured while CP baroreceptors were stimulated by volume expansion by dextran infusion (stimulus quantitated by changes in left ventricular end-diastolic pressure, LVEDP). Baseline arterial pressure, LVEDP and SNA were similar in the two groups. With dextran administered in equal amounts, LVEDP rose 25% more but SNA fell 20% less in DS than DR rats. Maximal CP baroreflex gain calculated as delta SNA/ delta LVEDP (in %/mmHg) was -3.6 +/- 0.4 in DS and -6.3 +/- 0.6 in DR rats (P less than 0.005). Heart weight and left atrial distensibility were similar in DR and DS rats. Thus DS rats with normal cardiac mechanical properties and blood pressure have impaired CP baroreflexes. This may contribute to salt-hypertension in these animals.
D000818:Animals; D004039:Diet, Sodium-Restricted; D006321:Heart / Q000503:physiopathology*; D006325:Heart Atria / Q000503:physiopathology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology; D008168:Lung / Q000503:physiopathology*; D011311:Pressoreceptors / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains / Q000502:physiology*; D012018:Reflex / Q000502:physiology*; D012965:Sodium Chloride / Q000633:toxicity*; D013153:Splanchnic Nerves / Q000503:physiopathology
D012965:Sodium Chloride