On the Existence of Renal Vasodilator Nerves

The renal vasoconstrictor responses to graded frequencies of direct electrical renal nerve stimulation and renal arterial norepinephrine injections were evaluated before and during renal alpha-1 adrenoceptor blockade in anesthetized dogs. Renal alpha-1 adrenoceptor blockade was achieved by infusing increasing doses (1, 10, 20, 40 micrograms/kg/min) of prazosin, a selective postsynaptic alpha-1 adrenoceptor antagonist, into the renal artery. The renal vasoconstrictor response to norepinephrine (1.5 micrograms) was completely abolished by 10 micrograms/kg/min prazosin. However, the renal vasoconstrictor response to a frequency of renal nerve stimulation which produced less renal vasoconstriction than norepinephrine (1.5 micrograms) in the absence of prazosin was not abolished by either 10, 20, or 40 micrograms/kg/min prazosin. During prazosin administration, neither renal nerve stimulation nor norepinephrine produced renal vasodilatation. Therefore, at prazosin doses two- and fourfold greater than that demonstrated to produce complete renal alpha-1 adrenoceptor blockade, no renal vasodilator responses to graded renal nerve stimulation were observed. These studies provide no evidence in support of a neural renal vasodilator mechanism in the dog.