Forearm Venous Responses to Stimulation of Adrenergic Receptors*

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Abstract
Systemic administration of isoprotere-nol, a substance which stimulates beta or vasodilator receptors in arteries, causes venoconstriction. These experiments were done to study the direct action of isoproterenol on veins. Venous tone was measured in the left forearm with a plethysmograph and expressed as venous volume existing at a transmural venous pressure of 30 mm Hg (W30). An increase W30 indicates venodilatation; a decrease indicates venoconstriction. Blood flow was estimated from the rate of change in forearm volume. Two doses of isoproterenol were infused into the left brachial artery in each of 13 subjects. Flow increased with each infusion but VV30 remained unchanged (P> 0. 8). Infusions were repeated in four subjects after intrabrachial administration of nethalide, a beta receptor blocker, and phentolamine, an alpha blocker. Nethalide blocked the flow response, but neither antagonist altered W30. In 4 subjects intrabrachial infusion of isoproterenol, in the presence of forearm venoconstriction induced by systemic administration of noreplnephrine, caused increases in flow but no venodilatation. In 5 subjects intrabrachial infusions of eplnephrine decreased VV30. Phentolamine blocked this venoconstriction but nethalide had no effect. Six subjects received isoproterenol, 5. 8 [mu]g/minutes, systemically. This caused venoconstriction which was blocked by intrabrachial administration of phentolamine. Stimulation of beta receptors in the forearm has no significant effect on venous tone while stimulation of alpha receptors causes venoconstriction. Forearm venous constriction occurring with systemic infusions of isoproterenol must be of reflex origin and midiated through alpha receptors.