The purpose of the present study was to determine if acute and chronic increases in sodium intake by isotonic saline infusion are accompanied by changes in plasma concentrations of atrial natriuretic peptide (P(ANP)). Acute saline loading (5% body wt) over a 30-min period in seven conscious chronically instrumented dogs produced a significant increase in P(ANP) (48 ± 5 to 119 ± 24 pg/ml, P < 0.05). However, chronic and progressive increments of sodium intake from 5 to 75 to 300 meq/day for 7 days, each by isotonic saline infusion, were examined in the same group of dogs and had no significant effect on P(ANP), P(ANP)'s were 37 ± 7, 39 ± 8, and 33 ± 5 pg/ml when sodium intake was changed from 5 to 75 to 300 meq/day, respectively. The increase of sodium intake from 5 to 75 meq/day produced decreases of plasma renin activity (PRA) (2.5 ± 0.5 to 1.5 ± 0.4 ng angiotensin I·ml-1·h-1, P < 0.05), plasma aldosterone concentration (PAC) (19.3 ± 5.4 to 2.9 ± 0.4 pg/ml, P < 0.05), and urinary excretion of prostaglandin E2 (760 ± 131 to 320 ± 58 pg/min, P < 0.05). Further increase of sodium intake to 300 meq/day induced decreases of PRA and PAC to undetectable levels and an increase of urinary excretion of 6-ketoprostaglandin F(1α) (649 ± 95 to 1,056 ± 148 pg/min, P < 0.05). Before the completion of the study, sodium intake was decreased from 300 to 75 meq/day. The reduction did not alter P(ANP) but did return PRA, PAC, and urinary excretion of prostaglandin F(1α) to values comparable to those seen before sodium intake was increased from 75 to 300 meq/day. In summary, acute sodium loading significantly increased P(ANP). However, despite marked alterations in PRA, PAC, and urinary excretion of prostaglandins, chronic sodium loading had no long-term effect on P(ANP).
|Original language||English (US)|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|State||Published - 1986|
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