Impact of nitric oxide deficiency on blood pressure and glomerular hemodynamic adaptations to pregnancy in the rat. Studies were conducted to investigate the impact of nitric oxide synthesis inhibition on blood pressure and glomerular hemodynamic adaptations to pregnancy in the rat. In normal pregnancy, urinary excretion of NO₂ + NO₃ (NO_x), reflecting increased nitric oxide (NO) production, progressively increased. Blockade of NO production in virgin and late pregnant Sprague-Dawley rats caused systemic hypertension, increased renal vascular resistance (RVR), reductions in RPF but GFR remained unchanged. In cortical nephrons, preglomerular and efferent arteriolar resistance (R_A and R_E) were elevated and glomerular capillary blood pressure (P_GC) increased markedly. Glomerular plasma flow (Q_A) and the glomerular capillary ultrafiltration coefficient, K_f, were reduced without change in single nephron glomerular filtration rate (SNGFR) because of the large elevation in P_GC. The pressor and glomerular hemodynamic responses to NO blockade were similar in virgins and pregnancy. Urinary NO_x excretion was markedly reduced in all groups with chronic NO blockade. Inhibition was incomplete in pregnancy, however, and a level of NO production that was adequate for normal BP and renal function in virgins, led to severe vasoconstriction in pregnancy. The present studies suggest that chronic NO deficiency leads to derangement of the hemodynamic adaptations of pregnancy.