Abstract
Our previous studies have shown that the cardiac sympathetic afferent reflex is enhanced in rats with chronic heart failure (CHF) induced by coronary artery ligation and contributes to the over-excitation of sympathetic activity. We sought to determine whether sympathetic activity and cardiac sympathetic afferent reflex were enhanced in adriamycin-induced CHF and whether angiotensin II (Ang II) in the paraventricular nucleus (PVN) was involved in enhancing sympathetic activity and cardiac sympathetic afferent reflex. Heart failure was induced by intraperitoneal injection of adriamycin for six times during 2 weeks (15 mg/kg). Six weeks after the first injection, the rats underwent anesthesia with urethane and α-chloralose. After vagotomy and baroreceptor denervation, cardiac sympathetic afferent reflex was evaluated by renal sympathetic nerve activity and mean arterial pressure (MAP) response to epicardial application of capsaicin (1.0 nmol). The response of MAP to ganglionic blockade with hexamethonium in conscious rats was performed to evaluate sympathetic activity. The renal sympathetic nerve activity and cardiac sympathetic afferent reflex were enhanced in adriamycin rats and the maximum depressor response of MAP induced by hexamethonium was significantly greater in adriamycin rats than that in control rats. Bilateral PVN microinjection of angiotensin II (Ang II) caused larger responses of the cardiac sympathetic afferent reflex, baseline renal sympathetic nerve activity and MAP in adriamycin rats than control rats. These results indicated that both sympathetic activity and cardiac sympathetic afferent reflex were enhanced and Ang II in the PVN was involved in the enhanced sympathetic activity and cardiac sympathetic afferent reflex in rats with adriamycin-induced heart failure.
Highlights
It is well known that sympathetic activity is overexcited in chronic heart failure (CHF) induced by coronary artery ligation[1,2]
Our previous studies have shown that Cardiac sympathetic afferent reflex (CSAR) is enhanced in rats with coronary artery ligation-induced CHF and contributes to the sympathetic overactivity[1,2]
Inhibition of the enhanced CSAR and sympathetic activity may be beneficial for coronary artery ligationinduced CHF
Summary
It is well known that sympathetic activity is overexcited in chronic heart failure (CHF) induced by coronary artery ligation[1,2]. Zhang S et al / Journal of Biomedical Research, 2012, 26(6): 425-431 duced by stimulation of cardiac sympathetic afferents with endogenous chemicals such as adenosine, bradykinin and hydrogen peroxide released from the myocardium during myocardial ischemia. This excitatory reflex results in sympathetic activation[5]. Our previous studies have shown that enhanced CSAR contributes to excessive sympathetic activity which is involved in the aggravation of CHF induced by coronary artery ligation[7,8]. The present study was designed to determine whether the CSAR and sympathetic activity were enhanced in ADR-induced heart failure rats and whether Ang II in the PVN was involved in the enhanced sympathetic activity and CSAR in ADR rats
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