Contribution of nitric oxide to β2‐adrenoceptor mediated vasodilatation in human forearm arterial vasculature

Publisher Website
Google Scholar
Abstract
Aims β2-adrenoceptor agonists are generally considered to produce endothelium independent vasodilatation through adenylate cyclase. We determined whether nitric oxide contributes to β2-adrenoceptor vasodilatation in human arterial vasculature. Methods Forearm blood flow responses to brachial intra-arterial infusions of ritodrine (2.5–50 μg min−1 ), a selective β2-adrenoceptor agonist, were determined in 24 healthy, normotensive subjects (mean age 22 years, 5F) on two occasions with initial and concomitant administration of l-NMMA (800 μg min−1 ), an NO synthase inhibitor, or noradrenaline (5–30 ng min−1 ), a control constrictor not affecting basal NO activity. Responses to the endothelium dependent vasodilator serotonin (n=6) and an endothelium independent vasodilator GTN (n=9) were also determined. Results Maximal dilatation to ritodrine during l-NMMA infusion (310±32%; mean±s.e.mean) was reduced compared to that during noradrenaline infusion (417±41%, P Conclusions β2-adrenoceptor mediated vasodilatation in the human forearm has an NO mediated component. The underlying mechanism for this effect is unclear, but flow mediated vasodilatation is unlikely to be responsible.