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Experimental Physiology 93.6 pp 746-753
DOI: 10.1113/expphysiol.2007.041632
© The Physiological Society 2008
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Paraventricular nucleus is involved in the central pathway of cardiac sympathetic afferent reflex in rats

Ming-Kui Zhong1,2, Yang-Can Duan1, Ai-Dong Chen1,2, Bo Xu1, Xing-Ya Gao2, Wei De2 and Guo-Qing Zhu1,2

Departments of 1 Physiology2 Biochemical and Molecular Biology, Nanjing Medical University, Nanjing 210029, China

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 demonstrate more conclusively that the PVN is an important component of the central neurocircuitry of the CSAR. In anaesthetized 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 anaesthetic, lignocaine, into the PVN abolished the CSAR without significant effects on the baseline RSNA and MAP, while L-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 min. 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.

(Received 2 December 2007; accepted after revision 11 February 2008; first published online 15 February 2008)
Corresponding author: G.-Q. Zhu: Department of Physiology, Nanjing Medical University, Nanjing 210029, China. Email: gqzhucn{at}njmu.edu.cn







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