Stroke/Cerebral Vasospasm

R. M. Wadsworth
r.m.wadsworth@strath.ac.uk

>You may have seen the following article which is relevant to your
>interesting work:

> Neuronal nitric oxide synthase activation by vasoactive intestinal peptide in bovine cerebral arteries.  Gonzalez et al. Journal of Cerebral Blood Flow and Metabolism 17: 977-984, 1997.

>Carmen Gonzalez

Thanks for your message.

Yes I have read your paper. I am particularly interested in the VIP tachyphyllaxis procedure that you use. In your Fig 2C, the VIP desensitisation gives approximately 40% reduction in the VIP-induced relaxation in the bovine anterior cerebral artery. Clearly it is hard to get complete desensitisation. Could that explain why this desensitisation protocol did not affect the neurally-meduated relaxation ? In our experiments, we used a VIP antiserum, and this did reduce neurally-mediated relaxation. Thus we have concluded that VIP is a neurotransmitter in these nerves.

I am also interested in your data showing that VIP is partly inhibited by L-NAME (your Fig 4A). Have you tried higher concentrations of L-NAME, since 100 miroM may not be maximal ? I think your data agrees with our data on this point: VIP appears to exert is cerebral vasodilator action through the NO-cyclic-GMP pathway.

With best wishes,

Roger Wadsworth