Abstract

ADH (synthetic lysine-vasopressin) was administered to conscious rats undergoing steady, sustained water diuresis. The magnitude and duration of the transient antidiuresis induced by single i. v. ADH injection (0.5–8 mU/100 g body weight) increased with the dose to a maximum urinary osmolality of 630 μ-osmole/g H2O (returning towards control values within 1 hr). Both the magnitude of, and the time to attain, a stable antidiuretic effect with continuous i.v. ADH infusion (2.5–30 μU/min/100 g body weight) varied with the dose. The maximal osmolality with 15 was almost as high as that with 30 μU/min/100 g body weight (1815 and 1928 μ-osmole/g H2O), but took longer to attain (4 $${\raise0.7ex\hbox{$1$} \!\mathord{\left/ {\vphantom {1 2}}\right.\kern-\nulldelimiterspace}\!\lower0.7ex\hbox{$2$}}$$ and 2 $${\raise0.7ex\hbox{$1$} \!\mathord{\left/ {\vphantom {1 2}}\right.\kern-\nulldelimiterspace}\!\lower0.7ex\hbox{$2$}}$$ hr, respectively). With both single and continuous ADH injection, a variable, inconsistent natriuresis and kaluresis occurred; the peak natriuresis preceded the time of maximal urinary osmolal and Na concentrations. The data are discussed in relation to (a) physiological rate of secretion of endogenous ADH and (b) the mechanisms responsible for the natriuresis. It is concluded that the natriuretic effect of ADH has little physiological significance in salt regulation.

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