Primary resetting of left atrial sensory endings in Dahl salt-sensitive rats fed a low-salt diet.

Vagal afferent pathways contribute to vasomotor inhibition and renal sodium handling by modulating sympathetic nerve activity in rats. Low pressure or cardiopulmonary baroreflex inhibition of sympathetic nerve activity is attenuated in normotensive Dahl salt-sensitive (S) rats fed a low-salt diet. The aim of the study was to record activity in single-fiber vagal filaments from left atrial endings in Dahl S and resistant (R) rats to evaluate the mechanism for the attenuated low pressure baroreflex. Rats were fed a low-salt diet (0.1% NaCl) for 5-7 wk. Seven Dahl R and six S rats were anesthetized with urethan, and catheters were placed in the aorta and left atrium. Single-fiber recordings were obtained from the right cervical vagus. The relationship between left atrial pressure and receptor discharge was obtained during graded aortic snaring. Mean threshold for increased activation of the vagal afferents during volume expansion was 10.4 +/- 0.6 mmHg (means +/- SE) in S and 6.0 +/- 0.4 mmHg in R rats (P less than 0.002). Pressure-discharge curves were significantly shifted to the right in S rats. Maximal sensitivity of the endings expressed as delta discharge/delta LAP was not significantly different in R vs. S, but the right shift in threshold reduced the discharge of endings over a physiological range of filling pressures. We also measured left ventricular end-diastolic pressure (LVEDP) in conscious S and R rats to determine if the resetting of left atrial sensory endings could be explained by elevated left heart filling pressure.(ABSTRACT TRUNCATED AT 250 WORDS)