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Am J Physiol Heart Circ Physiol 284: H101-H107, 2003; doi:10.1152/ajpheart.00457.2002
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Vol. 284, Issue 1, H101-H107, January 2003

PTK, MAPK, and NOC/oFQ impair hypercapnic cerebrovasodilation after hypoxia/ischemia

Amanda L. Jagolino and William M. Armstead

Departments of Anesthesia and Pharmacology, University of Pennsylvania, Philadelphia, Pennsylvania 19104

This study characterized the contributions of protein tyrosine kinase (PTK) and mitogen-activated protein kinase (MAPK) in nociceptin/orphanin FQ (NOC/oFQ)-induced impairment of hypercapnic pial artery dilation (PAD) after hypoxia/ischemia (H/I) in piglets equipped with a closed cranial window. NOC/oFQ (10-10 M cerebrospinal fluid H/I concentration) impaired hypercapnic PAD (21 ± 2% vs. 13 ± 1%). Coadministration of either of the PTK inhibitors genistein or tyrphostin A23 or the MAPK inhibitors U-0126 or PD-98059 with NOC/oFQ (10-10 M) partially prevented the inhibition of hypercapnic PAD compared with that observed in their absence (21 ± 2% vs. 17 ± 1% for genistein). After exposure to H/I, PAD in response to hypercapnia was impaired, but pretreatment with either genistein, tyrphostin A23, U-0126, or PD-98059 partially protected such impairment (17 ± 1% vs. 4 ± 1% vs. 9 ± 1% for sham control, H/I, and H/I + genistein pretreatment, respectively). These data show that PTK and MAPK activation contribute to NOC/oFQ-induced impairment of hypercapnic PAD. These data suggest that activation of PTK and MAPK is also involved in the mechanism by which NOC/oFQ impairs hypercapnic PAD after H/I.

newborn; cerebral circulation; opioids; signal transduction; protein tyrosine kinase; mitogen-activated protein kinase; nociceptor/orphanin FQ


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