Abstract
NO-mediated vasodilatation can be realized via two pathways: dependent and independent on soluble guanylate cyclase; the latter is implemented through NO interaction with ionic channels. We evaluated the contribution of these pathways into NO-induced relaxation of isolated pulmonary arteries in rats. In pulmonary arteries, in contrast to systemic vessels, soluble guanylate cyclase-independent mechanisms is more important, because it mediates relaxation in response to low concentrations of NO donor. The role of soluble guanylate cyclase-dependent mechanisms in the mechanisms of vasodilatation increases with increasing NO donor concentrations.
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