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1 Laboratory for Research in Neonatal Physiology, Department of Physiology, University of Tennessee Health Science Center, Memphis, TN, USA
* To whom correspondence should be addressed. E-mail: cleffler{at}physio1.utmem.edu.
Carbon monoxide (CO) and nitric oxide (NO) are important paracrine messengers in the newborn cerebrovasculature that may act as co-messengers. Here we investigated the role of NO in CO-mediated dilations in the newborn cerebrovasculature. Arteriolar branches of the middle cerebral artery (100-200 m) were isolated from 3 to 7-day-old piglets, cannulated at each end in a superfusion chamber, and intravascular pressure elevated to 30 mm Hg, which resulted in the development of myogenic tone. Endothelial removal abolished dilations of pressurized pial arterioles to bradykinin and to the COreleasing molecule Mn2(CO)10 [dimanganese decacarbonyl (DMDC)], but not dilations to isoproterenol. With endothelium intact, N-nitro-L-arginine (L-NNA), 1H-[1,2,4] oxadiazolo [4,3-a] quinoxalin-1-one (ODQ) or tetraethylammonium chloride (TEA+), inhibitors of nitric oxide synthase (NOS), guanylyl cyclase, and large conductance Ca2+- activated K channels (KCa), respectively, also blocked dilation induced by DMDC. Following inhibition of NOS, a constant concentration of sodium nitroprusside (SNP), a NO donor that only dilated the vessel 6%, returned dilation to DMDC. The stable cGMP analog, 8-bromo-cGMP, also restored dilation to DMDC in endothelium-intact, LNAtreated or endothelium-denuded arterioles, and this effect was blocked by TEA+. Similarly, in the continued presence of ODQ, 8-bromo-cGMP restored DMDC-induced dilations. These findings suggest that endothelium-derived NO stimulates guanylyl cyclase in vascular smooth muscle cells, and, thereby, permits CO to cause dilation by activating KCa channels. Such a requirement for NO could explain the endothelium dependency of CO-induced dilation in piglet pial arterioles.
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