Key result
Pretreatment with pertussis toxin attenuated the high-affinity relaxant component of glyceryl trinitrate in bovine mesenteric arteries, suggesting involvement of a regulatory protein.
GTN induces vascular smooth muscle relaxation via two separate pathways, with the high affinity pathway likely involving a receptor-complex interaction with a regulatory protein sensitive to pertussis toxin.
Hypothesis-generating for G-protein involvement in low-dose GTN relaxation; leaves open human vessel relevance and clinical translation.
Low concentrations (less than 1 nM) of glyceryl trinitrate (GTN) induced a considerable relaxation of bovine mesenteric arteries (BMA) brought to sustained contraction by the addition of phenylephrine. The concentration-response curve of GTN showed a biphasic pattern with a high and a low affinity component. Pretreatment with pertussis toxin (IAP) attenuated the high affinity relaxant component, but not the low affinity component or the relaxation induced by NaNO2. A polyclonal antibody to IAP counteracted the effect of the toxin on the GTN-response. Low concentrations of GTN increased the cGMP level in BMA via activation of the high affinity pathway. This effect was also inhibited in preparations pretreated with IAP. It is suggested from the present study that GTN induces relaxation of vascular smooth muscle via two separate pathways, the high affinity pathway might involve a receptor-complex interaction with a regulatory protein.
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Ahlner et al. (1988) studied this question. Glyceryl trinitrate (GTN) and Pertussis toxin (IAP) was evaluated on Relaxation of bovine mesenteric arteries and cGMP levels. Pretreatment with pertussis toxin attenuated the high-affinity relaxant component of glyceryl trinitrate in bovine mesenteric arteries, suggesting involvement of a regulatory protein.
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