Abstract

The effects of intra-arterial infusions of adenosine (ADO) on sympathetic vasconstrictor responses were studied in the gracilis nerve-muscle preparation of the dog under constant flow conditions. Sympathetic nerves to the muscle were activated at a frequency of 1 Hz for 2 min during infusions of ADO, 2-chloroadenosine, nitroglycerine or hydralazine. ADO concentrations of 1, 10 and 50 microM decreased perfusion pressure by 19, 42 and 57 mm Hg, respectively, from a control (saline infusion) perfusion pressure of 110 mm Hg. Sympathetic vasoconstrictor responses were attenuated only at 50 microM ADO. Sympathetic responses during 1 and 10 microM ADO infusion were the same as during infusion of 10 and 100 microM nitroglycerine, which produced the same degree of vasodilation as 1 and 10 microM ADO, respectively. Except for greater vasodilator potency, 2-chloroadenosine infusions produced effects similar to ADO. Infusion of hydralize produced concentration-dependent decreases in control perfusion pressure and sympathetic vasoconstrictor responses. These results indicate that intra-arterial administration of ADO or one of its stable analogs (2-chloroadenosine) does not cause inhibition of sympathetic vasoconstrictor responses except at concentrations that cause nearly maximal vasodilation.