AJP - Regulatory, Integrative and Comparative Physiology, Vol 266, Issue 2 518-R525, Copyright © 1994 by American Physiological Society

ARTICLES

Nitro-L-arginine attenuates hypercapnic cerebrovasodilation without affecting cerebral metabolism

C. Iadecola and X. Xu
Department of Neurology, University of Minnesota, Minneapolis 55455.

We have previously demonstrated that topical cortical application of nitro-L-arginine (L-NA), a potent inhibitor of nitric oxide (NO) synthesis, attenuates resting cerebral blood flow (CBF) and the cerebrovasodilation elicited by hypercapnia. In this study, we sought to determine whether these cerebrovascular effects of L-NA are secondary to a depression in cerebral metabolism. Rats were anesthetized (chloralose, 80 mg/kg) and artificially ventilated. Arterial pressure and blood gases were monitored. The frontal cortex was exposed and superfused with normal Ringer (pH 7.3-7.4; 37 degrees C) or with Ringer containing L- or D-NA. CBF or cerebral glucose utilization (CGU) was measured autoradiographically using the [14C]iodoantipyrine or 2-[14C]deoxy-D-glucose method, respectively. Application of normal Ringer did not affect CBF at the site of superfusion (n = 5; P > 0.05, paired t test). Application of L-NA (1 mM; n = 5), but not D-NA (1 mM; n = 6), attenuated resting CBF by 33 +/- 5% (P < 0.05; analysis of variance). During hypercapnia (partial pressure of CO2 = 55-60 mmHg), L-NA attenuated the CBF increase by 78 +/- 6% (n = 5/group; P < 0.05 from Ringer), whereas D-NA had no effect (P > 0.05). Resting CBF and the CBF response to hypercapnia were largely unaffected in brain regions outside the field of superfusion. In contrast to hypercapnia, L-NA (1 mM) did not attenuate the increases in CBF elicited by topical application of papaverine (10-1,000 microM; n = 8).(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				K. Ide, M. Worthley, T. Anderson, and M. J. Poulin Effects of the nitric oxide synthase inhibitor L-NMMA on cerebrovascular and cardiovascular responses to hypoxia and hypercapnia in humans J. Physiol., October 1, 2007; 584(1): 321 - 332. [Abstract] [Full Text] [PDF]

				G. Zoccoli, D. A. Grant, J. Wild, and A. M. Walker Nitric oxide inhibition abolishes sleep-wake differences in cerebral circulation Am J Physiol Heart Circ Physiol, June 1, 2001; 280(6): H2598 - H2606. [Abstract] [Full Text] [PDF]

				K. Niwa, L. Younkin, C. Ebeling, S. K. Turner, D. Westaway, S. Younkin, K. H. Ashe, G. A. Carlson, and C. Iadecola Abeta 1-40-related reduction in functional hyperemia in mouse neocortex during somatosensory activation PNAS, August 15, 2000; 97(17): 9735 - 9740. [Abstract] [Full Text] [PDF]

				K. Niwa, E. Araki, S. G. Morham, M. E. Ross, and C. Iadecola Cyclooxygenase-2 Contributes to Functional Hyperemia in Whisker-Barrel Cortex J. Neurosci., January 15, 2000; 20(2): 763 - 770. [Abstract] [Full Text] [PDF]

				U. Lindauer, D. Megow, H. Matsuda, and U. Dirnagl Nitric oxide: a modulator, but not a mediator, of neurovascular coupling in rat somatosensory cortex Am J Physiol Heart Circ Physiol, August 1, 1999; 277(2): H799 - H811. [Abstract] [Full Text] [PDF]

				F. M. FARACI and D. D. HEISTAD Regulation of the Cerebral Circulation: Role of Endothelium and Potassium Channels Physiol Rev, January 1, 1998; 78(1): 53 - 97. [Abstract] [Full Text] [PDF]

				S. S. L. Tsui, P. M. Kirshbom, M. J. Davies, M. T. Jacobs, W. J. Greeley, F. H. Kern, J. W. Gaynor, and R. M. Ungerleider Nitric Oxide Production Affects Cerebral Perfusion and Metabolism After Deep Hypothermic Circulatory Arrest Ann. Thorac. Surg., June 1, 1996; 61(6): 1699 - 1707. [Abstract] [Full Text]

				R. W. McPherson, J. R. Kirsch, R. F. Ghaly, and R. J. Traystman Effect of Nitric Oxide Synthase Inhibition on the Cerebral Vascular Response to Hypercapnia in Primates Stroke, April 1, 1995; 26(4): 682 - 687. [Abstract] [Full Text]