Augmented input from cardiac sympathetic afferents inhibits baroreflex in rats with heart failure

Abstract

It has been established that the baroreflex is markedly decreased in chronic heart failure (CHF). Our recent study has indicated that activation of the cardiac sympathetic afferent reflex (CSAR) inhibits the baroreflex in normal rats, and in the rats with CHF the CSAR is significantly enhanced, which is related to augmented central angiotensin II (Ang II) mechanism. Therefore, the hypothesis is that the augmented CSAR in the CHF state tonically inhibits the baroreflex via central AT1 receptor. To test the hypothesis, the rats with myocardial infarction-induced CHF or sham surgery were anesthetized with alpha-chloralose and urethane, vagotomized, and recordings were made of the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). We found: (1) left ventricular epicardial application of capsaicin or electrical stimulation of the central end of the left cardiac sympathetic nerve blunted the baroreflex in both sham and CHF rats; (2) left ventricular epicardial application of lidocaine had no significant effects on the baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope, 1.7+/-0.3 to 2.9+/-0.2%/mm Hg; P<0.01); and (3) intracerebral ventricular injection of losartan had no significant effect on baroreflex in sham rats but improved the baroreflex in CHF rats (maximum slope 1.9+/-0.2 to 3.1+/-0.2%/mm Hg; P<0.01). These results suggest that tonic cardiac sympathetic afferent input plays an important role in the blunted baroreflex associated with CHF, which is mediated by central AT1 receptors.