NEURONAL CELL-BODIES IN PARAVENTRICULAR NUCLEUS AFFECT RENAL HEMODYNAMICS AND EXCRETION VIA THE RENAL NERVES

Several lines of evidence support the existence of an oligosynaptic pr ojection from the paraventricular nucleus of the hypothalamus (PVN) to the kidney in the rat. We sought to provide evidence that this neural pathway is capable of influencing renal function in rats. Bilateral m icroinjections of bicuculline (Bic; 1 nmol) into the PVN decreased glo merular filtration rate (59%), effective renal plasma flow (71%), urin e flow (UV; 57%), and urinary sodium excretion (UNaV; 54%), accompanie d by increased mean arterial pressure (17%) and heart rate (17%). Thes e results were not obtained when Bic was injected outside the PVN or w hen vehicle (0.9% saline) was injected into the PVN. Bilateral renal d enervation (5-7 days before the experiments) significantly reduced the renal vasoconstriction, attenuated the antidiuresis, and abolished th e antinatriuresis evoked by PVN stimulation. On the other hand, both t he antidiuresis and antinatriuresis evoked by PVN stimulation were und iminished after treatment with either of two vasopressin receptor anta gonists amethylenepropionyl(1),O-Et-Tyr(2),Val(4),Arg(8)]- vasopressin , a vasopressin V-1 receptor antagonist, or 1),O-Et-D-Tyr(2),Val(4),am inobutyryl(6),Arg(8,9)]- vasopressin, a Vt receptor antagonist). In re nal-denervated rats treated with the same Vt receptor antagonist, PVN stimulation produced highly variable increases in both UV and UNaV, wh ich overall were not statistically different than zero. We conclude th at the activation of neurons in PVN evokes 1) renal vasoconstriction a ccompanied by antinatriuresis, both of which are attributable to the r enal nerves, and 2) decreased water excretion, which is mediated by th e renal nerves and vasopressin Vt receptors.