Cyclic nucleotides in stroke and related cerebrovascular disorders

Adenylyl Cyclase/cAMP System Involvement in the Antiangiogenic Effect of Somatostatin in the Retina. Results from Transgenic Mice

“…This topic is also strengthened by the fact that the profile of stimulated AC activity is the same of the enhanced expression of AC VII in the three strains. Since it has been reported that hypoxia increases the release of AC stimulatory agents, such as catecholamines and adenosine, as well as their receptor expression [40][41][42], AC VII isoform may play a central role in the enhancement of cAMP in these conditions. The increased cAMP level in hypoxia is likely to be instrumental to the induction of neoangiogenesis and the increased expression of proangiogenic factors such as VEGF, that we have observed recently in all three strains, in the same experimental model.…”

Effects of naloxone and morphine on cerebral ischemia in gerbils

“…The 6-hr period of focal ischemia was selected because at this time frame, prominent histopathological damage was evident within the affected cerebral cortex along with reduced activities of the synaptic enzymes Na+, K+-ATPase and adenylate cyclase [Christie-Pope et al, 19851. These two enzyme systems have served as models in which to monitor the efficacy of pretreated drugs under various conditions of cerebral ischemia including the bilateral model used herein [Taylor et al, 1984;Christie-Pope et al, 1984, 1985Palmer et al, 19851. Our findings of an inability of naloxone (posttreatment) to reduce mortality and neurological symptoms of cerebral ischemia in gerbils are incompatable with those of Hosobuchi et a1 [1982]. They found that serial injections of naloxone were indeed beneficial after 9 hr of focal ischemia.…”

“…Several investigations have shown that levels of the cyclic nucleotides cyclic AMP and cyclic GMP display dramatic flucuations during primary and secondary (damage attributable to the reperfusion of ischemic tissue) ischemia [see reviews by Palmer, 1985;Lust and Passonneau, 19791. In addition, the activity of two enzymes intimately involved in the maintenance of electrochemical gradients and cyclic-nucleotide-related synaptic events, Na' , K+-ATPase and adenylate cyclase, are markedly altered after an ischemic stroke in the gerbil [Schwartz et al, 1976;Taylor et al, 1984;Christie-Pope et al, 1984;Palmer et al, 19851.…”

“…This laboratory is currently engaged in identifying synaptic enzymes vulnerable to a cerebral ischemic insult. Several investigations have shown that levels of the cyclic nucleotides cyclic AMP and cyclic GMP display dramatic flucuations during primary and secondary (damage attributable to the reperfusion of ischemic tissue) ischemia [see reviews by Palmer, 1985;Lust and Passonneau, 19791. In addition, the activity of two enzymes intimately involved in the maintenance of electrochemical gradients and cyclic-nucleotide-related synaptic events, Na' , K+-ATPase and adenylate cyclase, are markedly altered after an ischemic stroke in the gerbil [Schwartz et al, 1976;Taylor et al, 1984;Christie-Pope et al, 1984;Palmer et al, 19851. Pretreatment of animals with proposed therapeutic agents such as methylprednisolone, indomethacin, thiopental, and allopurinol has shown varying degrees of protection of these enzyme systems [Taylor et al, 1984;Christie-Pope et al, 1984;Palmer et al, 19851. Opioidlike compounds affect cyclic nucleotide-related systems either directly through receptor-mediated influences on the activity of synthesizing enzymes, in particular adenylate cyclase wolleman, 198 1 ; Palmer, 19831, or indirectly through an influence on neurotransmitter release [Iwatsubo, 19771.…”