Abstract |
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.
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Authors | Amanda L Jagolino, William M Armstead |
Journal | American journal of physiology. Heart and circulatory physiology
(Am J Physiol Heart Circ Physiol)
Vol. 284
Issue 1
Pg. H101-7
(Jan 2003)
ISSN: 0363-6135 [Print] United States |
PMID | 12485817
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Opioid Peptides
- nociceptin
- Protein-Tyrosine Kinases
- Mitogen-Activated Protein Kinases
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Topics |
- Animals
- Arteries
(physiopathology)
- Cerebrovascular Circulation
- Female
- Hypercapnia
(physiopathology)
- Hypoxia
(physiopathology)
- Ischemia
(physiopathology)
- Male
- Mitogen-Activated Protein Kinases
(physiology)
- Opioid Peptides
(physiology)
- Pia Mater
(blood supply)
- Protein-Tyrosine Kinases
(physiology)
- Swine
- Vasodilation
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