(Hypertension. 2000;35:1253.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
From the Departments of Medical Education and Research and Internal Medicine, Veterans General Hospital-Kaohsiung, Kaohsiung, Taiwan, ROC.
Correspondence to Ching-Jiunn Tseng, MD, PhD, Department of Medical Education and Research, Veterans General Hospital-Kaohsiung, 386 Ta-Chung 1st Road, Kaohsiung, Taiwan, ROC. E-mail cjtseng{at}isca.vghks.gov.tw
AbstractRecent studies suggest that carbon monoxide (CO), which is produced in significant quantities in many brain regions, may function as a neurotransmitter. Heme oxygenase catalyzes the metabolism of heme to CO and biliverdin; however, the physiological role of CO in central cardiovascular regulation was not well understood. In the present study, we evaluated the baroreflex response of CO in the nucleus tractus solitarii (NTS) of rats. Male Sprague-Dawley rats were anesthetized with urethane, and blood pressure and heart rate were monitored intra-arterially. Unilateral microinjection (60 nL) of hematin, a heme molecule cleaved by heme oxygenase to yield CO, into the NTS produced prominent dose-related depressor and bradycardic effects. Baroreflex responses were elicited by increasing doses of phenylephrine (10 to 30 µg/kg IV) before and after intra-NTS administration of zinc deuteroporphyrin 2,4-bis-glycol (ZnDPBG) (1 nmol), an inhibitor of heme oxygenase activity, or vehicle alone. The reflex bradycardia elicited by phenylephrine was significantly inhibited by pretreatment with ZnDPBG. Furthermore, the inhibitory effect of ZnDPBG on baroreflex activation was dose dependent. These results suggest CO formed by brain heme oxygenase plays a significant role in central cardiovascular regulation and that inhibition of heme oxygenase attenuated baroreflex activation.
Key Words: bradycardia brain baroreflex
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