ROLE OF THE ENDOGENOUS NITRIC-OXIDE IN THE VASODILATATORY TONE AND CO2 RESPONSIVENESS OF THE ROSTRAL VENTROLATERAL MEDULLA MICROCIRCULATIONIN THE RAT

The study was designed to check the role of endogenous NO in maintaini ng the vasodilatatory tone and in mediation of local cerebral blood fl ow (CBF) responses to CO2 in rostral ventrolateral medulla (RVLM) in t he rat. The ventral surface of the medulla was exposed and CBF in the RVLM continuously recorded with a laser-Doppler flowmeter. Local vascu lar resistance (CVR) was estimated as the ratio of mean arterial press ure (MAP) to CBF. During 1 min exposure to 10% CO2 in oxygen PaCO2 ros e from 39.9 +/- 2 mm Hg to 89.7 +/- 4.6 mm Hg and pH fell from 7.4 +/- 0.04 to 7.1 +/- 0.03. After intravenous administration of 15 mg/kg L- NAME (Nitro-L-arginine-methyl ester) MAP increased by 43 +/- 2.9 mm Hg (p < 0.001), local CBF increased by 33 +/- 6% (p < 0.001) and CVR inc reased by 17 +/- 6% (p < 0.01). L-NAME significantly reduced CBF flow response to 60 s hypercapnia from 47 +/- 9% (p < 0.001) before adminis tration of L-NAME to 14 +/- 5% (p < 0.001). This effect was due to rev ersal by L-NAME of a presser response to hypercapnia to a depressor re sponse. The attenuation of CVR response to CO2 by L-NAME was too small to account alone for the significant reduction of local CBF responsiv eness to hypercapnia. We conclude that endogenous NO plays a role in m aintaining a local vasodilatory tone in RVLM, but it is less significa nt than in the cortical microcirculation. NO is not a major mediator i n the increase in local CBF in RVLM during brief hypercapnia. Endogeno us NO is critical for the neurogenic presser response to brief hyperca pnia.