Ai-Dong Chen

Publications (3)10.84 Total impact

• Article: Angiotensin AT1 receptors in paraventricular nucleus contribute to sympathetic activation and enhanced cardiac sympathetic afferent reflex in renovascular hypertensive rats.

  Ai-Dong Chen, Shu-Juan Zhang, Ning Yuan, Yao Xu, Wei De, Xing-Ya Gao, Guo-Qing Zhu
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  ABSTRACT: Sympathetic activity is enhanced in hypertension, which contributes to the pathogenesis of hypertension and progression of organ damage. The cardiac sympathetic afferent reflex (CSAR) is enhanced in renovascular hypertension and involved in the sympathetic activation. The present study was designed to investigate whether angiotensin II (Ang II) and Ang II type 1 (AT(1)) receptors in paraventricular nucleus (PVN) contribute to the enhanced CSAR and sympathetic outflow in experimental renovascular hypertensive rats. Hypertension was induced by the two-kidney one-clip (2K1C) method. The normotensive rats underwent sham operation (Sham). Acute experimentation was carried out at the end of the 4th week. Under urethane and α-chloralose anaesthesia, the renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded in rats with sino-aortic denervation and cervical vagotomy. The AT(1) receptor expression was determined with Western blot. The CSAR was evaluated by the response of RSNA and MAP to epicardial application of 1.0 nmol of capsaicin. The AT(1) receptor expression in the PVN was increased, and Ang II in the PVN augmented the enhanced CSAR and RSNA in 2K1C rats. The effects of Ang II were abolished by pretreatment with the AT(1) receptor antagonist, losartan, in 2K1C rats. Losartan in the PVN normalized the enhanced CSAR and decreased the RSNA and MAP in 2K1C rats. These results indicate that the increased activity of AT(1) receptors in the PVN contributes to the enhanced CSAR and excessive sympathetic activation in renovascular hypertensive rats.
  Experimental physiology 02/2011; 96(2):94-103. · 3.17 Impact Factor
• Article: Long-term administration of tempol attenuates postinfarct ventricular dysfunction and sympathetic activity in rats.

  Zhen Shi, Ai-Dong Chen, Yao Xu, Qi Chen, Xing-Ya Gao, Wei Wang, Guo-Qing Zhu
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  ABSTRACT: The purpose of this study was to determine whether the long-term administration of tempol attenuates postinfarct ventricular dysfunction and sympathetic activity in rats. Myocardial infarction (MI) was induced by left descending coronary artery ligation. Tempol was orally administered in drinking water (2 mmol/L), which was initiated 4 h after infarction and continued for 6 weeks. Tempol prevented not only the increases in left ventricular end-diastolic pressure and volume but also the decreases in ejection fraction and peak velocities of contraction in MI rats. The treatment normalized the increased renal sympathetic nerve activity (RSNA) and plasma norepinephrine level, as well as the enhanced cardiac sympathetic afferent reflex (CSAR; an excitatory cardiovascular reflex partially contributing to the sympathetic activation in chronic heart failure) and the RSNA responses to microinjection of angiotensin II into paraventricular nucleus in MI rats. Furthermore, tempol prevented the increased AT(1) receptor protein expression and superoxide anion level in both paraventricular nucleus and rostral ventrolateral medulla in MI rats. In conclusion, long-term administration of tempol attenuates ventricular dysfunction and normalizes sympathetic neural control in MI rats. The normalization of the CSAR, levels of superoxide anions and AT(1) receptor expression, and the response to angiotensin II in the paraventricular nucleus and rostral ventrolateral medulla may partially contribute to the beneficial effects of tempol on central sympathetic control.
  Pflügers Archiv - European Journal of Physiology 02/2009; 458(2):247-57. · 4.46 Impact Factor
• Article: Paraventricular nucleus is involved in the central pathway of cardiac sympathetic afferent reflex in rats.

  Ming-Kui Zhong, Yang-Can Duan, Ai-Dong Chen, Bo Xu, Xing-Ya Gao, Wei De, Guo-Qing Zhu
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  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 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.
  Experimental Physiology 07/2008; 93(6):746-53. · 3.21 Impact Factor