Received December 2, 2007
Revised January 14, 2008
Accepted after revision February 11, 2008

¹ Nanjing Medical University

^* To whom correspondence should be addressed. E-mail: gqzhucn{at}njmu.edu.cn.

	Abstract

Our previous studies have shown that angiotensin II and reactive oxygen species in the paraventricular nucleus (PVN) modulate the cardiac sympathetic afferent reflex (CSAR). The present study was designed to more conclusively demonstrate that the PVN is an important component of the central neurocircuitry of the CSAR. In anesthetized Sprague-Dawley rats with sinoaortic denervation and cervical vagotomy, renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were continuously recorded. The CSAR was evaluated by the response of the RSNA to epicardial application of bradykinin or capsaicin. Bilateral microinjection of the reversible anaesthetic lidocaine into the PVN abolished the CSAR without significant effects on the baseline RSNA and MAP, while glutamate which excites the neurons in the PVN enhanced the CSAR and increased the baseline RSNA and MAP. Bilateral electrolytic lesions of the PVN irreversibly abolished the CSAR without significant effects on the baseline RSNA and MAP. Bilateral selective lesions of the neurons in the PVN with kainic acid induced rapid and great increases in both RSNA and MAP which returned to nearly normal levels in 60 minutes. At the 90th minute after kainic acid, epicardial application of bradykinin or capsaicin failed to induce the CSAR. These results indicate that inhibition or lesion of the PVN abolishes the CSAR, but excitation of the neurons in the PVN enhances the CSAR, suggesting that the PVN is an important component of the central neurocircuitry of the CSAR.

Key Words: Cardiovascular, Hypothalamus, Sympathetic activity