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Nitric oxide inhibition causes an exaggerated pressor response in Yucatan miniature swine.

The involvement to nitric oxide (NO) in cardiovascular and renal function was evaluated in 12 anesthetized Yucatan miniature swine. The effect of NO blockade on blood pressure was measured in six additional conscious swine. In the anesthetized swine, mean arterial pressure (MAP), heart rate, glomerular filtration rate (GFR), and urinary excretion of water, sodium, and potassium were measured after systemic inhibition of NO synthesis by NG-nitro-L-arginine methyl ester (L-NAME), and were compared with values for a control period. After NO synthesis blockade, MAP increased by 63 +/- 5 mm Hg, a far greater increase than those observed in rats, dogs, domestic swine, or humans. The changes in GFR, urine flow rate (UFR), and sodium excretion (UNaV) were time-dependent. The GFR decreased to 50 +/- 6% of control values immediately after L-NAME administration, but returned to control values within 1 h. Significant increases in UFR and UNaV were observed only during the third experimental period, 40 to 60 min after drug infusion. In the conscious swine, L-NAME administration increased MAP by 24 +/- 4 mm Hg. Administration of the sympatholytic hexamethonium bromide fully reversed the increase of MAP in anesthetized and conscious swine. These findings indicate that NO has an important role in the maintenance of cardiovascular and renal function in Yucatan miniature swine. The exaggerated pressor response to NO blockade in miniature swine appears to involve the sympathetic nervous system.