title: Impairment in biochemical level of arterial dilative capability of a cyclic nucleotides-dependent pathway by induced vasospasm in the canine basilar artery.
abstract: The authors investigated the changes and the potential of cyclic nucleotide-dependent signal transduction, which induces smooth muscle relaxation, in the basilar artery with severe vasospasm in dogs with double experimental subarachnoid hemorrhage (SAH) to explore at which biochemical level the arterial dilative capability was impaired. The amount of cyclic adenosine and guanosine monophosphates (cAMP and cGMP) decreased 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 addition to the failure of the pathways to produce cyclic nucleotides, the activities of cAMP- and cGMP-dependent protein kinases, which are representative actual enzymes that amplify the signal for vascular dilation, also significantly decreased together with the almost total loss of activation by cyclic nucleotides in the same basilar artery after SAH. It was revealed that the system for smooth muscle relaxation was impaired severely in the cerebral arteries with severe vasospasm after SAH, on the biochemical basis of significantly less vasodilative capability and in several of the steps to produce the cyclic nucleotides of intracellular signal transduction.
authors.affiliation: Department of Neurological Surgery, Ehime University School of Medicine, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Todo
authors.forename: S
authors.initials: S
authors.lastname: Ohta
authors.forename: J
authors.initials: J
authors.lastname: Wang
authors.forename: H
authors.initials: H
authors.lastname: Ichikawa
authors.forename: S
authors.initials: S
authors.lastname: Ohue
authors.forename: Y
authors.initials: Y
authors.lastname: Kumon
authors.forename: S
authors.initials: S
authors.lastname: Sakaki
mesh_terms: D000262:Adenylyl Cyclases / Q000378:metabolism; D000818:Animals; D001488:Basilar Artery / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D000242:Cyclic AMP / Q000378:metabolism*; D017868:Cyclic AMP-Dependent Protein Kinases / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism*; D017869:Cyclic GMP-Dependent Protein Kinases / Q000378:metabolism; D004285:Dogs; D005260:Female; D006162:Guanylate Cyclase / Q000378:metabolism; D002546:Ischemic Attack, Transient / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology*; D007700:Kinetics; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D015398:Signal Transduction; D013345:Subarachnoid Hemorrhage / Q000503:physiopathology*; D014664:Vasodilation
chemical_list: D000242:Cyclic AMP; D017868:Cyclic AMP-Dependent Protein Kinases; D017869:Cyclic GMP-Dependent Protein Kinases; D000262:Adenylyl Cyclases; D006162:Guanylate Cyclase; D006152:Cyclic GMP