Abstract
Vasomotor tone is largely maintained by norepinephrine (NE) released by sympathetic nerves and activating mainly alpha adrenergic receptors (α‐ARs). We investigated the relative contributions of α‐ARs to NE contractile responses in rat mesenteric vessels. Pressure myography was used to study isolated third order mesenteric small veins (6 or 12 mmHg) and arteries (60 or 120 mmHg). NE and phenylephrine (PE) concentration response curves (CRC) were constructed at normal and high transmural pressures in the absence and presence of α‐AR antagonists. Clonidine CRC were obtained at normal transmural pressures. All agonists evoked concentration dependent contractions with NE and PE being more potent in veins compared with arteries. In veins, NE was a more potent agonist than PE. Phentolamine (α‐AR antagonist, 10 μM) and prazosin (α1‐AR antagonist, 100 nM) completely abolished NE responses in all vessels. Yohimbine (α2‐AR antagonist, 100 nM) significantly reduced NE CRC in veins at 6 mmHg. Clonidine responses in veins were significantly reduced by yohimbine. These results indicate the predominant involvement of α1‐ARs in NE‐induced contractions of pressurized mesenteric vessels with no change in the contribution of α1‐ARs as pressure increased. In addition to α1‐ARs, α2‐ARs mediate NE responses in veins at 6 mmHg. This work was supported by grants from the Natural Sciences and Engineering Research Council of Canada.
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