抄録
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<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<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<, 0.01). Furthermore, ANP brought about a recovery in NE-induced falls in renal blood flow (+40%) and glomerular filtration rate (+38%, both p<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<0.05). thus, increased sympathetic nervous activity seems to augment the renal effects of ANP, and the antagonistic effects of ANP to NE-induced pregllomerular vasoconstriction may counteract Na retention caused by excessive sympathetic tone.
