Saluretic activity of blood during carotid occlusion in the cat

108

A B S T R A C T In order to obtain direct evidence for the existence of a natriuretic hormone, dialysates and ultrafiltrates of plasma of dogs expanded with saline were tested for effects on sodium transport by the toad urinary bladder. Dialysate was obtained by dialysis of blood in vivo in a clinical dialyzer and by dialysis in vitro of small volumes of blood using a miniature model of the clinical dialyzer. Ultrafiltrates were prepared using selective molecular filters which permit passage of substances on the basis of molecular weight and three dimensional configuration.Dialysates and ultrafiltrates of hydropenic dogs caused a change in toad bladder potential difference of + 1% and in short circuit current of -5%. In contrast, dialysates and ultrafiltrates from expanded dogs caused a change in potential difference of -23% and in short circuit current of -32%, a highly significant difference. Onset of reduction of short circuit current occurred within 3-5 min, reaching a maximum in 10-20 min. The effect was rapidly reversible, was specific for the serosal surface of the bladder, and could not be explained on the basis of nonspecific alterations in ionic composition or by dilutional effects. Ultrafiltrates of jugular vein plasma caused significantly more reduction of short circuit current than ultrafiltrates of femoral vein plasma. The data indicate the presence in plasma of saline-loaded dogs of a dialyzable inhibitor of toad bladder sodium transport. Ultrafiltrate studies using membranes of appropriate selectivity suggest the factor has a molecular weight of less than 3000.

Section: Methodssupporting

confidence: 89%

The effect of dialysates and ultrafiltrates of plasma of saline-loaded dogs on toad bladder sodium transport

Buckalew¹,

Martínez²,

Green³

1970

108

“…In several studies (8,13,14), the natriuresis paralleled an increase in renal blood flow and glomerular filtration rate suggesting that the factor promoted a natriuresis through a vasodilating effect on the kidney. However, this conclusion is difficult to reconcile with those studies purporting to show a direct effect of this factor on sodium transport in isolated membranes (2,3,5) or tubule fragments (4,7).…”

Section: Introductionmentioning

confidence: 71%

“…laboratories (1)(2)(3)(4)(5)(6)(7) have reported the presence of a factor in blood or urine which exhibits natriuretic activity when tested in various biological assay systems, it remains to be established that this factor plays a physiologic role in regulating sodium excretion in the intact animal.…”

Section: Introductionmentioning

confidence: 99%

Evidence for a Humoral Mechanism in Volume Expansion Natriuresis

Kaloyanides¹,

Azer²

1971

A B S T R A C T The role of a humoral mechanism in the natriuresis induced by volume expansion was evaluated using an isolated dog kidney perfused by a second dog which had been pretreated with desoxycorticosterone acetate (DOCA). Expansion of the perfusion dog with an equilibrated volume of blood from a reservoir, resulted in an increase in UNaV (sodium excretion) from 153.6 +27.9 (SEM) to 345.5 ±57.8 AsEq/min, P < 0.001. FENa (fractional sodium excretion) increased from 3.4 +0.6 to 8.1 ±1.2%, P < 0.01. The natriuresis occurred in the face of a significant decrease in Cim, RBF, and renal arterial pressure, and in the absence of any change in plasma protein concentration or packed cell volume. In a control group of experiments, sodium excretion did not change when the perfusion dog was not volume expanded, although CIN (inulin clearance) and RBF (renal blood flow) decreased to the same degree as in the expanded group. These data support the conclusion that volume expansion of the perfusion dog either stimulated the release of a natriuretic factor or suppressed the release of an antinatriuretic factor which was manifested by an increase in sodium excretion in the isolated kidney.

“…Finally, and most critically, the presence of the inhibitor in the urine of patients and dogs with chronic uremia and of the present dogs with normal renal function appears to correlate with the dictates of maintaining external sodium balance. A number of other investigators have now demonstrated the presence of natriuretic factor(s) or inhibitor(s) of sodium transport in the blood of animals and man using whole animal experiments (13)(14)(15)(16)(17)(18)(19)(20)(21) or in vitro assays (13,18,20,(22)(23)(24)(25)(26)(27)(28)(29). Similarly, extracts of urine have also been shown to contain natriuretic substance(s) (16,17,19,20,(30)(31)(32)(33)(34)(35)(36) or inhibitor(s) of sodium transport (20,37,38).…”

Section: Discussionmentioning

confidence: 99%

An inhibitor of sodium transport in the urine of dogs with normal renal function.

Favre¹,

Hwang²,

Schmidt³

et al. 1975

AB STRA CT The urine and serum of chronically uremic patients and dogs contain an inhibitor of sodium transport that reduces short-circuit current (SCC) in the toad bladder and produces natriuresis in the rat. The present studies represent an effort to determine whether the same inhibitor is detectable in urine of normal dogs maintained on a sodium intake varying from 3 to 258 meq/day. Observations were made with and without fludrocortisone. The same Sephadex G-25 gel filtration fraction previously shown to contain the "uremic" inhibitor was tested in both the isolated toad bladder and rat bioassay systems. The fraction from dogs maintained on 258 meq sodium plus 0.2 mg fludrocortisone/day consistently inhibited SCC in the toad bladder and induced a natriuresis in the rat (P < 0.001). The fraction from dogs on the same sodium intake without fludrocortisone was also natriuretic (P <0.01) but did not inhibit SCC significantly. In contrast, the fraction from dogs fed 3 meq sodium with fludrocortisone or 91 meq sodium without fludrocortisone had no significant effect in either assay system. Thus, an inhibitor of sodium transport has been found in the urine of nonuremic dogs. Both the degree of natriuresis in the rat and the degree of inhibition of SCC in the toad bladder correlated with the state of sodium balance which ensued in the dog.