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