Attenuation of the pressor activity of endogenous vasoconstrictors by sodium nitroprusside in the pithed rat.

The present study characterized the effects of sodium nitroprusside (SNP) on the responsiveness of pithed rats to pressor stimuli. Intravenous infusions of SNP produced a dose-related inhibition of the pressor responses to stimulation of sympathetic preganglionic neurons in the thoracolumbar region of the spinal cord. The site at which SNP affected the vasoconstrictor response appeared to be post-junctional because norepinephrine responses were also attenuated, as were blood pressure increases to angiotensin II and vasopressin. Responsiveness to all of the pressor stimuli was restored when the infusion of SNP was terminated. The effects of SNP could not be attributed simply to observed reductions in baseline blood pressure because pretreatment of the pithed rats with captopril, which produced an initial hypotensive effect equivalent to that seen after SNP, did not alter the pressor responses to angiotensin II or vasopressin. However, like SNP, captopril did attenuate the blood pressure increments to spinal cord stimulation and norepinephrine. These results suggest that a part of the hypotensive potency of SNP may result from its ability to antagonize vasoconstriction mediated by norepinephrine, angiotensin II and vasopressin.