Abstract
In an ex vivo canine tibial preparation, an alpha-1-adrenergic antagonist (prazosin, 212 ng.ml-1.minute-1) markedly attenuated the effect of high intraluminal doses (greater than 0.5 mg) of norepinephrine but was less effective at lower doses. An alpha-2-adrenergic antagonist (rauwolscine, 198 ng/ml/minute) was more effective than prazosin in blocking the vascular smooth muscle contraction evoked by low doses of norepinephrine (greater than 0.125 mg). Cirazoline, an alpha-1-adrenergic agonist, had a potent contractile effect on smooth muscle at high concentrations (5 x 10(-6) M), whereas the alpha-2-adrenergic agonist UK14304 was more effective at low concentrations (1 x 10(-7) M). Thus, in the vascular smooth muscle of canine tibia there is a mixed population of postjunctional alpha-1 and alpha-2-adrenergic receptors that exhibits a dose-dependent responsiveness. Adrenergic receptor mechanisms may contribute to alterations in bone blood flow. This may be relevant to impaired reperfusion after microvascular bone transfer. Furthermore, adrenergic receptor mechanisms may help explain variations in bone blood flow related to systemic, regional humoral, or metabolic factors.
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