Effect of infusion of pharmacologic amounts of vasopressin on renal electrolyte excretion

Abstract

Aqueous vasopressin was infused to bicarbonate- and glucose-loaded dogs and to nonloaded antidiuretic dogs in doses of 50 mU/kg per min or 50 mU/kg per h. Both doses caused a marked increase in sodium, chloride, and water excretion. The larger dose raised the fractional excretion (sodium clearance (C-Na)/glomerular filtration rate (GFR) times 100) of these ions from 2% or less to in excess of 20%. Blocking the pressor effects of these doses of vasopressin with sodium nitroprusside did not alter the marked natriuretic and chloriuretic effect. The maximal rate of bicarbonate and glucose reabsorption was not depressed by vasopressin infusion; fractional phosphate excretion, however, was markedly increased. Inhibiting distal hydrogen ion secretion by inducing selective aldosterone deficiency failed to uncover a vasopressin-induced inhibition of proximal bicarbonate reabsorption that might have been masked by increased distal bicarbonate reabsorption. There was no significant change in GFR, renal plasma flow, or filtration fraction. The distribution of cortical renal blood flow (measured by the radioactive microsphere technique) shifted toward the inner cortex after vasopressin administration. Vasopressin, in pharmacologic doses, is a potent diuretic that most likely exerts this effect by directly inhibiting sodium reabsorption at a point in the nephron distal to the proximal tubule.

Effect of Prolactin on Glomerular Filtration Rate

“…It is unlikely that the results in this study are explained by ADH contamination (Bond, Pasley, Koike & Llerena, 1976) as ADH, in anaesthetized dogs, did not result in an increase in GFR, as demonstrated by Mason & Ledsome (197 1) and Kurtzman, Rogers, Boonjarern & Arruda (1975). Further, Wen (1974) also reported no increase in GFR after ADH administration in dogs whose blood pressure did not increase.…”

Natriuretic response of the rat to plasma concentrations of arginine vasopressin within the physiological range.

“…In addition to its antidiuretic effects, arginine vasopressin is known to have a natriuretic action (Jacobson & Kellog, 1956; Kurtzman, Rogers, Boonjarern & Arruda, 1975;Buckalew & Dimond, 1976). It is usually considered that a natriuretic response is seen only when supraphysiological levels of the hormone are present (Dicker, 1957;Atherton, Hai & Thomas, 1969;Kurtzman et al 1975). In other studies, however, increases in electrolyte excretion have been observed in response to low rates of administration of lysine vasopressin (Atherton, Green & Thomas, 1971) and arginine vasopressin (Chan & du Vigneaud, 1970;Fejes-Toth & Szenasi, 1981); however, plasma vasopressin concentrations were not measured.…”

Increased Urinary Kallikrein-Like Activity in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

“…With short-term administration of ADH in animals urinary sodium excretion increases briskly [Ali, 1958;Brooks and Bickford, 1958;Chan and Sawyer, 1962;A therton et al, 1969;Kurtzman et al, 1975;Buckalew and Dia mond, 1976]. In SIADH and in experiments with chronic administration of ADH, however, increased urinary sodi um excretion can be prevented by strict water restriction [Leaf el al., 1953;Wrong, 1956;Jaenike and Waterhouse, 1961;Cooke et al, 1979].…”