Comparison of beta-adrenoceptors mediating vasodilatation in canine subcutaneous adipose tissue and skeletal muscle.
Blood flow changes in response to various drugs in simulataneously autoperfused canine subcutaneous adipose tissue and gracilis muscle were compared to study the vascular beta-adrenoceptors. Compared to isoprenaline the beta 2-selective agonist salbutamol was 4--6 times more potent as a vasodilator in the muscle than in adipose tissue. Furthermore two beta 1-selective agonists (Tazolol and H80/62) caused vasodilatation in adipose tissue but not in the gracilis muscle. When given by close i.a. injection after beta-adrenoceptor blockade, adrenaline was a more potent vasoconstrictor than noradrenaline in both tissues. Before beta-blockade, however, noradrenaline was the more potent vasoconstrictor in the gracilis muscle whereas adrenaline was more potent in adipose tissue. Intravenous infusion of adrenaline in doses causing vasodilatation in the muscle caused vasoconstriction in adipose tissue whereas intravenous infusion of noradrenaline caused vasoconstriction in both tissues. The present findings suggest that the beta-adrenoceptors mediating vasodilatation in skeletal muscle are mainly ose tissue. Since adrenaline is a much more potent beta2- than beta1-agonist, these differences point to different roles of intravascular adrenaline in the two sites. In skeletal muscle circulating adrenaline is mainly a vasodilator whereas in subcutaneous adipose tissue it mainly acts as a vasoconstrictor.
Comparison of beta-adrenoceptors mediating vasodilatation in canine subcutaneous adipose tissue and skeletal muscle. Blood flow changes in response to various drugs in simulataneously autoperfused canine subcutaneous adipose tissue and gracilis muscle were compared to study the vascular beta-adrenoceptors. Compared to isoprenaline the beta 2-selective agonist salbutamol was 4--6 times more potent as a vasodilator in the muscle than in adipose tissue. Furthermore two beta 1-selective agonists (Tazolol and H80/62) caused vasodilatation in adipose tissue but not in the gracilis muscle. When given by close i.a. injection after beta-adrenoceptor blockade, adrenaline was a more potent vasoconstrictor than noradrenaline in both tissues. Before beta-blockade, however, noradrenaline was the more potent vasoconstrictor in the gracilis muscle whereas adrenaline was more potent in adipose tissue. Intravenous infusion of adrenaline in doses causing vasodilatation in the muscle caused vasoconstriction in adipose tissue whereas intravenous infusion of noradrenaline caused vasoconstriction in both tissues. The present findings suggest that the beta-adrenoceptors mediating vasodilatation in skeletal muscle are mainly ose tissue. Since adrenaline is a much more potent beta2- than beta1-agonist, these differences point to different roles of intravascular adrenaline in the two sites. In skeletal muscle circulating adrenaline is mainly a vasodilator whereas in subcutaneous adipose tissue it mainly acts as a vasoconstrictor.