ENDOGENOUS NITRIC-OXIDE MODULATES VASOPRESSOR RESPONSES, BUT NOT DEPRESSOR RESPONSES, TO SPINAL SYMPATHETIC-NERVE STIMULATION IN PITHED RATS

The effects of N-omega-nitro-L-arginine methylester (L-NAME), an inhib itor of nitric oxide (NO) synthase (1,5, and 10 mg/kg) on vasopressor and depressor responses to segmental sympathetic nerve stimulation wer e studied in the pithed rat preparation. Vasopressor responses were ev oked by stimulation of the spinal sympathetic outflow at T6-T8 (30 V, 0.05 ms at 5 Hz with 10 pulses). This presser response was biphasic: A n initial transient response (to nerve stimulation) was followed by a later prolonged response (to adrenal catecholamine release). L-NAME 1, 5, and 10 mg/kg increased mean arterial blood pressure (MAP); this ef fect was maximal at 1 mg/kg L-NAME, but had no effect on heart rate (H R). L-NAME 1, 5, and 10 mg/kg potentiated both phases of the presser r esponse; the effect was maximal at 10 mg/kg. Vasodepressor responses w ere evoked by stimulation of the spinal sympathetic outflow at S2-L6 ( 30 V, 0.05 ms at 5 Hz with 10 pulses). L-NAME 1, 5, and 10 mg/kg did n ot inhibit these depressor responses. We conclude that inhibition of t he synthesis of endogenous NO causes a hypertension in pithed rats tha t is associated with increased vasoconstriction in response to sympath etic nerve stimulation and adrenal catecholamine release. Systemic vas cular depressor responses to segmental sympathetic nerve stimulation a re not affected, however; therefore, NO cannot be the major mediator o f these responses.