Abnormalities in neural circulatory control contribute to salt-induced hypertension in Dahl sensitive (DS) rats. This study tested the hypothesis that there is impairment in cardiopulmonary baroreflex function in prehypertensive DS rats. The study was performed in DS and Dahl resistant (DR) rats fed low-salt diet. Arterial baroreceptors were denervated. Sympathetic activity was recorded from the splanchnic nerve during stimulation of cardiopulmonary baroreceptors with volume expansion (iv dextran). Resting mean arterial pressure averaged 93 +/- 6 (SE) in DS vs. 98 +/- 5 mmHg in DR rats. Resting left ventricular end-diastolic pressure (LVEDP) was 13.5 +/- 1.0 in/DS vs. 11.4 +/- 0.9 mmHg in DR rats. Volume expansion with the same amount of dextran caused greater increases in LVEDP in DS (+13 +/- 1 mmHg) than DR (+10 +/- 1 mmHg) but less inhibition of sympathetic activity (-40 +/- 4 vs. -50 +/- 2%) in DS compared with DR rats, respectively. Cardiopulmonary baroreflex gain calculated as percent inhibition of sympathetic activity divided by increases in LVEDP was -3.2 +/- 0.2 in DS vs. -4.9 +/- 0.6%/mmHg in DR rats. Reflex responses to dextran were abolished by vagotomy. Volume expansion also induced increases in mean arterial pressure. These were/greater in DS than DR rats (+43 +/- 4 vs. +28 +/- 5 mmHg, respectively) before vagotomy but were similar in the two groups after vagotomy. The distensibility (delta volume/delta pressure) of the left atrium was similar in DS and DR rats. We conclude that prehypertensive DS rats have impairment of the cardiopulmonary baroreflex.(ABSTRACT TRUNCATED AT 250 WORDS)
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