Abstract
Carbon monoxide is formed in the process of degradating heme from biliverdin by heme oxygenase (HO) in the various tissues, including central nervous system (CNS). Previous studies suggested that inhibition of HO activity increased arterial pressure (AP) mediated by the autonomic nervous system. The present study was designed to investigate the sympathetic nerve response to inhibition of HO activity by a direct renal nerve recording in conscious rats. Zinc deuteroporphyrin 2, 4-bis glycol (ZnDPBG), an inhibitor of HO activity, was administered ip in chronically instrumented Wistar rats: 8 intact, 8 atropine-treated, and 7 sinoaortic denervated (SAD). ZnDPBG induced significant increases in mean AP (MAP) from 95.9 ± 1.6 to 116.9 ± 4.7 mmHg and renal sympathetic nerve activity (RSNA) from 100.0 to 186.7 ± 19.2%, but no significant change in heart rate (HR) in intact rats. In atropine-treated rats, ZnDPBG also induced significant increases in MAP from 96.7 ± 1.5 to 110.6 ± 2.0 mmHg and RSNA from 100.0 to 184.7 ± 22.5%, but induced no change in HR. In SAD rats, ZnDPBG induced significant increases in MAP from 91.4 ± 5.7 to 118.8 ± 8.5 mmHg, HR from 356.8 ± 10.4 to 409.1 ± 14.4 beats/min, and RSNA from 100.0 to 211.6 ± 18.9%. The present study suggested that inhibition of HO activity caused sympatho-excitation via a direct action on CNS, resulted in an increase in AP. Further study is required to investigate the underlying mechanism of HR response to HO inhibition. [J Physiol Sci. 2006;56 Suppl:S135]
