Interaction between sympathetic nerve activity and atrial natriuretic peptide with respect to the effects on renal hemodynamics in patients with cardiovascular diseases.

Since it is still controversial as to whether or not atrial natriuretic peptide (ANP) antagonizes norepinephrine (NE)-induced vasoconstriction, we examined the interactions of ANP and NE with respect to renal circulation. (I) Although ANP infusion at 25 ng/kg/min for 40 min caused a decrease in total peripheral resistance (-11%, p less than 0.01) in 34 patients with cardiovascular disease and 15 normotensives (NTs), renal vascular resistance (RVR) was not reduced consistently by ANP. However, there was a negative correlation between changes in RVR and the preinfusion plasma NE level (r = -0.51, p less than 0.001). (II) When NE infusion into 6 NTs at 100 ng/kg/min was followed by ANP infusion, urinary Na excretion was increased to a greater degree than that by ANP infusion alone (+234% vs +34%, p less than 0.01). Furthermore, ANP brought about a recovery in NE-induced falls in renal blood flow (+40%) and glomerular filtration rate (+38%, both p less than 0.05). These effects were attributed to both a decrease in calculated renal afferent resistance and an increase in efferent resistance (-43% and +17%, respectively, p less than 0.05). Thus, increased sympathetic nervous activity seems to augment the renal effects of ANP, and the antagonistic effects of ANP to NE-induced preglomerular vasoconstriction may counteract Na retention caused by excessive sympathetic tone.