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Am J Physiol Heart Circ Physiol 273: H2639-H2647, 1997;
0363-6135/97 $5.00
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Vol. 273, Issue 6, H2639-H2647, December 1997

Endothelin impairs ATP-sensitive K+ channel function after brain injury

T. Kasemsri and W. M. Armstead

Departments of Anesthesia and Pharmacology, University of Pennsylvania, and The Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104

In piglets, pial arteries constrict, ATP-sensitive K+ (KATP) channel function is impaired, and cerebrospinal fluid endothelin-1 (ET-1) increases to 10-10 M after brain injury [fluid percussion injury (FPI)]. Nitric oxide (NO) elicits dilation via guanosine 3',5'-cyclic monophosphate (cGMP) and KATP channel activation. This study was designed to characterize the relationship between ET-1 and impaired function of KATP channels after FPI. Injury was produced via the lateral FPI technique in piglets equipped with a closed cranial window. Cromakalim, a KATP agonist, produced dilation that was attenuated by FPI and partially restored by BQ-123, an ET-1 antagonist (11 ± 1 and 23 ± 2 vs. 2 ± 1 and 4 ± 1 vs. 8 ± 1 and 17 ± 2% for responses to 10-8 and 10-6 M cromakalim before FPI, after FPI, and after FPI with BQ-123, respectively). Because ET-1 constriction may antagonize dilation, separate experiments were conducted under conditions of equivalent baseline diameter in the absence and presence of ET-1 (10-10 M). Cromakalim dilation was attenuated by ET-1 and partially restored by the protein kinase C (PKC) inhibitor staurosporine (12 ± 1 and 28 ± 1 vs. 2 ± 1 and 21 ± 3 vs. 9 ± 1 and 29 ± 2% for 10-8 and 10-6 M cromakalim, cromakalim with ET-1, and cromakalim with ET-1+staurosporine, respectively). Similar interactions were observed with calcitonin gene-related peptide, 8-bromoguanosine 3',5'-cyclic monophosphate, and the NO releasers sodium nitroprusside and S-nitroso-N-acetylpenicillamine. These data show that ET-1 blunts KATP channel-, NO-, and cGMP-mediated dilation. These data suggest that ET-1 contributes to altered cerebral hemodynamics after FPI through impairment of KATP channel function via PKC activation.

newborn; cerebral circulation; nitric oxide; cyclic nucleotides


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