Dual response of cerebrocortical blood flow and arterial blood pressure to transient CO2 stimulus after inhibition of nitric oxide synthesis in rats.

Inhibition of nitric oxide synthase (NOS) by Nitro-L-arginine-methyl-ester (L-NAME 15 mg and 70 mg/kg i.v.) in 16 male Wistar rats anaesthetized with urethane, paralysed and artificially ventilated, increased significantly local peripheral vascular resistance in the parietal cortex (CVR) along with augmentation of the mean arterial blood pressure (MAP) and no change of the local cerebrocortical blood flow (CBF) recorded with a Laser-Doppler-Flowmeter. In 11 rats L-NAME reversed a pressor effect of brief hypercapnia induced by 10% CO2/air mixture (PaCO2 84.1 +/- 5 mm Hg) into a depressor response, reduced CBF response proportionally to the reduction of MAP and did not influence CVR response to CO2. In 5 rats L-NAME did not abolish the central pressor effect of a CO2-stimulus and significantly augmented CO2-induced vasodilatatory response in the cortex (43.4 +/- 24% before L-NAME and 137.8 +/- 38.8% after L-NAME) by a larger reduction of CVR (-11 +/- 8% before L-NAME and -47.1 +/- 7.6% after L-NAME). It is concluded that NO does not mediate the vasodilatatory effect of brief hypercapnia in the cortex. NO appears critical for the central pressor effect of CO2. In those rats in which the central pressor effect of a CO2-stimulus was not abolished by an NOS blocker, an increased CBF and augmented decrease in CVR was observed during brief hypercapnia. Possible mechanisms of this dual responsiveness of cortical blood flow and arterial blood pressure to CO2, induced by inhibition of NOS, are discussed.