Changes of renal function and blood pressure after nitric oxide synthase inhibition in renal-denervated conscious...

Conscious male Wistar rats with implanted catheters in femoral artery for blood pressure registration, femoral vein for drug infusion and bladder for urine collection were used. Nitric oxide synthase inhibition (NOSI) was performed by intravenous administration of 10 mg/kg b.w. N(omega)-nitro-L-arginine methyl ester (L-NAME) before and one week after bilateral renal denervation. Renal denervation led to a decrease of urine osmolality (p<0.05). NOSI decreased heart rate (p<0.001) and increased systolic, mean and diastolic artery pressure both in the intact and the renal-denervated rats (p<0.001). The P(MF)/P(HF) ratio in the heart rate spectrum, considered a criterion for the sympathovagal balance decreased after NOSI in intact and in renal-denervated rats (p<0.001) indicating a reduction in the sympathetic tone. The baroreflex sensitivity after NOSI increased both in conscious rats with intact renal nerves and in rats with bilateral renal denervation. In intact rats NOSI increased urine flow rate by 48.7% (p<0.05), sodium excretion by 339.7% (p<0.01) and chloride excretion by 272.1% (p<0.01). In contrast to the intact rats, NOSI in the renal denervated rats decreased their urine flow rate by 35.5% (p<0.05) and did not alter sodium and chloride excretion. So, chronic renal denervation inversed the diuretic and clearly attenuated the natriuretic and chloruretic response to acute NOSI without inhibiting the rise in blood pressure. Therefore, the increased urine flow as well as the sodium and chloride excretion observed after NOSI are not exclusively the result of a pressure diuresis but are somewhat dependent on the renal sympathetic nerve activity. Renal denervation did not change the pattern of sympathovagal balance and baroreflex sensitivity modified by NO-synthase inhibition.