1978 年 20 巻 8 号 p. 921-930
In order to elucidate the intrarenal role of angiotensin II, we studied the relations among mean blood pressure (MBP), glomerular filtration rate (GFR), urinary sodium excretion (UNaV), urinary potassium excretion (UKV), urinary chlorine excretion (UCIV), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) after the infusion of a specific competitive antagonist of angiotensin II, 1-Sarcosine-8-Isoleucine-Angiotensin II into patients with essential hypertension on normal sodium diet (15-20g/day) and low sodium diet (2g/day). Antagonistic action of this drug appeared more frequently in the subjects on low sodium diet than in those on normal sodium diet. Consequently the number of subjects showing vasodepressor response increased after sodium restriction. A significant negative correlation was recognized between PRA and %change of MBP in patients on normal sodium diet (P<0.05). This correlation was more remarkable in sodium depleted status (P<0.02). A positive correlation was recognized between PRA and %change of GFR on normal sodium diet (P<0.001), as well as on low sodium diet (P<0.005). Positive correlations were recognized between %change of GFR and that of UNaV (P<0.05), %change of GFR and that of UKV (P< 0.001), %change of GFR and that of UC1V (P<0.001) on normal sodium diet, as well as on low sodium diet. A negative correlation was recognized between %change of GFR and that of MBP on normal sodium diet (P<0.01). In high PRA patients, this drug lowered blood pressure, but tended to increase GFR, UNaV, UKV and UC1V. No correlation was recognized between %change of PRA and that of PAC. In conclusion, (a) the present results indicate that endogenous angiotensin II seems to reduce GFR in patients with abnormally high PRA and (b) the observed changes in UNaV, UKV and UC1V following angiotensin II antagonist can be explained by alteration in GFR.