AJP - Heart and Circulatory Physiology, Vol 270, Issue 2 423-H426, Copyright © 1996 by American Physiological Society

ARTICLES

Role of ATP-sensitive K+ channels in cGMP-mediated pial artery vasodilation

W. M. Armstead
Department of Anesthesia, University of Pennsylvania, Philadelphia, USA.

The present study was designed to investigate the role of ATP-sensitive K+ channels in guanosine 3',5'-cyclic monophosphate (cGMP)-mediated pial artery vasodilation in newborn pigs equipped with a closed cranial window. Sodium nitroprusside (SNP) (10(-8), 10(-6) M), a nitrovasodilator, elicited pial artery dilation that was attenuated by the ATP-sensitive K+ channel antagonist glibenclamide (10(-6) M). On a percentage basis, these responses were 25 +/- 1% for the presence of SNP (10(-6) M) alone, whereas 15 +/- 1% dilation was observed for SNP (10(-6) M) in the presence of glibenclamide (n = 5 pigs). Dilation produced by the cGMP analogue, 8-BrcGMP (10(-8), 10(-6) M), was similarly attenuated by glibenclamide. SNP-induced pial dilation was accompanied by increased cortical periarachnoid cerebrospinal fluid (CSF) cGMP levels, and these biochemical changes were blocked by the soluble guanylate cyclase inhibitor, LY-83583 (10(-5) M). SNP (10(-6) M) alone increased CSF cGMP concentration from 407 +/- 14 to 956 +/- 41 fmol/ml, whereas SNP in the presence of LY-83583 yielded a CSF cGMP concentration of 340 +/- 13, which was no different from the control value of 335 +/- 23 fmol/ml (n = 5 pigs). SNP-induced pial dilation was blunted by LY-83583, whereas 8-BrcGMP-induced dilation was unchanged. Cromakalim (10(-8), 10(-6) M), an ATP-sensitive K+ channel agonist, produced dilation that was blocked by glibenclamide (24 +/- 1 vs. 5 +/- 1% for cromakalim 10(-6) M, in the absence and presence of glibenclamide, respectively, n = 5). These data indicate that activation of ATP-sensitive K+ channels contribute to cGMP-mediated pial artery dilation.

This article has been cited by other articles:

				B. L. Jennings and J. A. Donald Neurally-derived nitric oxide regulates vascular tone in pulmonary and cutaneous arteries of the toad, Bufo marinus Am J Physiol Regulatory Integrative Comp Physiol, November 1, 2008; 295(5): R1640 - R1646. [Abstract] [Full Text] [PDF]

				W. M. Armstead and J. G. Hecker Heat shock protein modulation of KATP and KCa channel cerebrovasodilation after brain injury Am J Physiol Heart Circ Physiol, September 1, 2005; 289(3): H1184 - H1190. [Abstract] [Full Text] [PDF]

				J. Ross and W. M. Armstead Differential role of PTK and ERK MAPK in superoxide impairment of KATP and KCa channel cerebrovasodilation Am J Physiol Regulatory Integrative Comp Physiol, July 1, 2003; 285(1): R149 - R154. [Abstract] [Full Text] [PDF]

				W. M. Armstead Role of Nociceptin/Orphanin FQ in the Physiologic and Pathologic Control of the Cerebral Circulation Experimental Biology and Medicine, December 1, 2002; 227(11): 957 - 968. [Abstract] [Full Text]

				W. M. Armstead Vasopressin-Induced Protein Kinase C-Dependent Superoxide Generation Contributes to ATP-Sensitive Potassium Channel but Not Calcium-Sensitive Potassium Channel Function Impairment After Brain Injury Stroke, June 1, 2001; 32(6): 1408 - 1414. [Abstract] [Full Text] [PDF]

				Y. Takahashi, M. De Vroomen, C. Roman, and M. A. Heymann Mechanisms of calcitonin gene-related peptide-induced increases of pulmonary blood flow in fetal sheep Am J Physiol Heart Circ Physiol, October 1, 2000; 279(4): H1654 - H1660. [Abstract] [Full Text] [PDF]

				W. M. Armstead Role of endothelin-1 in age-dependent cerebrovascular hypotensive responses after brain injury Am J Physiol Heart Circ Physiol, November 1, 1999; 277(5): H1884 - H1894. [Abstract] [Full Text] [PDF]

				T. W. Hein and L. Kuo cAMP-Independent Dilation of Coronary Arterioles to Adenosine : Role of Nitric Oxide, G Proteins, and KATP Channels Circ. Res., October 1, 1999; 85(7): 634 - 642. [Abstract] [Full Text] [PDF]

				W. M. Armstead and W. G. Mayhan Superoxide Generation Links Protein Kinase C Activation to Impaired ATP-Sensitive K+ Channel Function After Brain Injury • Editorial Comment Stroke, January 1, 1999; 30(1): 153 - 159. [Abstract] [Full Text] [PDF]

				W. M. Armstead Relationship among NO, the KATP channel, and opioids in hypoxic pial artery dilation Am J Physiol Heart Circ Physiol, September 1, 1998; 275(3): H988 - H994. [Abstract] [Full Text] [PDF]

				W. M. Armstead ATP-dependent K+ channel activation reduces loss of opioid dilation after brain injury Am J Physiol Heart Circ Physiol, May 1, 1998; 274(5): H1674 - H1683. [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]

				T. Kasemsri and W. M. Armstead Endothelin impairs ATP-sensitive K+ channel function after brain injury Am J Physiol Heart Circ Physiol, December 1, 1997; 273(6): H2639 - H2647. [Abstract] [Full Text] [PDF]

				W. M. Armstead Brain Injury Impairs ATP-Sensitive K+ Channel Function in Piglet Cerebral Arteries Stroke, November 1, 1997; 28(11): 2273 - 2280. [Abstract] [Full Text]

				M. J. Wilderman and W. M. Armstead Role of neuronal NO synthase in relationship between NO and opioids in hypoxia-induced pial artery dilation Am J Physiol Heart Circ Physiol, October 1, 1997; 273(4): H1807 - H1815. [Abstract] [Full Text] [PDF]