Beta-Receptor Mechanisms in the Superficial Limb Veins of the Dog

perfused at constant flow with autologous arterial blood, and perfusion and femoral vein pressures were monitored; changes in the difference between these pressures were due to changes in venomotor activity. Injection of isoproterenol into the perfusate caused the vein to dilate. The amount of dilatation depended on smooth muscle tension in the wall of the vein before injection. When this was minimal (after sympathectomy), isoproterenol had no effect. During venoconstriction produced by electrical stimulation of the lumbar sympathetic chain or by the infusion of venoconstrictor drugs, the dilating action of 0.1 mg of isoproterenol was measured. Expressed as a percentage of the initial constriction caused by sympathetic stimulation, 5-hydroxytryptamine, or 1 M potassium chloride, the extent of the dilatation was 86.7 ±4.3 (SE of mean), 79.7 ±4.2, and 87.7 +3.2, respectively. With norepinephrine and epinephrine infusions, the isoproterenol dilatations were less (65.1 ±9.0 and 55.2 +7.2, respectively), consistent with the stimulant action of these agents on both alpha and beta receptors; such action was confirmed by comparing the responses to nerve stimulation and infusions of norepinephrine and epinephrine before and after betareceptor blockade. The venoconstriction caused by sympathetic stimulation and by infusions of norepinephrine and epinephrine was greatly enhanced by cooling the vein (decreasing perfusate temperature), but the dilating action of isoproterenol appeared to be insensitive to changes in temperature. The data suggest that beta receptors are specific entities and, when maximally stimulated, are capable of causing a venous relaxation that is proportional to the initial degree of tension in the vein wall