IMPAIRMENT IN BIOCHEMICAL LEVEL OF ARTERIAL DILATIVE CAPABILITY OF A CYCLIC NUCLEOTIDES-DEPENDENT PATHWAY BY INDUCED VASOSPASM IN THE CANINE BASILAR ARTERY

Citation
H. Todo et al., IMPAIRMENT IN BIOCHEMICAL LEVEL OF ARTERIAL DILATIVE CAPABILITY OF A CYCLIC NUCLEOTIDES-DEPENDENT PATHWAY BY INDUCED VASOSPASM IN THE CANINE BASILAR ARTERY, Journal of cerebral blood flow and metabolism, 18(7), 1998, pp. 808-817
Citations number
41
Categorie Soggetti
Neurosciences,"Endocrynology & Metabolism",Hematology
ISSN journal
0271678X
Volume
18
Issue
7
Year of publication
1998
Pages
808 - 817
Database
ISI
SICI code
0271-678X(1998)18:7<808:IIBLOA>2.0.ZU;2-5
Abstract
The authors investigated the changes and the potential of cyclic nucle otide-dependent signal transduction, which induces smooth muscle relax ation, in the basilar artery with severe vasospasm in dogs with double experimental subarachnoid hemorrhage (SAH) to explore at which bioche mical level the arterial dilative capability was impaired. The amount of cyclic adenosine and guanosine monophosphates (cAMP and cGMP) decre ased significantly in the basilar artery after SAH. The activities of adenylate and guanylate cyclases also were decreased significantly in the smooth muscle cells of the basilar artery 4 days after SAH. In add ition to the failure of the pathways to produce cyclic nucleotides, th e activities of cAMP- and cGMP-dependent protein kinases, which are re presentative actual enzymes that amplify the signal for vascular dilat ion, also significantly decreased together with the almost total loss of activation by cyclic nucleotides in the same basilar artery after S AH. It was revealed that the system for smooth muscle relaxation was i mpaired severely in the cerebral arteries with severe vasospasm after SAH, on the biochemical basis of significantly less vasodilative capab ility and in several of the steps to produce the cyclic nucleotides of intracellular signal transduction.