Failure to demonstrate a humoral mechanism in the antinatriuresis of acute caval constriction

Kaloyanides, George J.; Azer, Maher

doi:10.1172/jci106925

Cited by 4 publications

(2 citation statements)

References 7 publications

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“…This is due to avid sodium resorption in the proximal tubule (Cirkensa et al, 1966) as well as to enhanced sodium absorption in the diluting segment of Henle's loop and the distal site of Na-K exchange (Kaloyanides et al, 1969). Under comparable experimental conditions, Kaloyanides and Azer (1972) and Buckalew and Lancaster (1971) also failed to demonstrate a humoral activity previously observed in ECV expansion (Buckalew et al, 1970). A similar effect was demonstrated during constriction of the superior vena cava ) but was not achieved following abdominal cava constriction although leading to an equal rise in renal venous pressure (Cirkensa et al, 1966).…”

Section: Discussionmentioning

confidence: 99%

Natriuretic hormone—its possible role in fluid and electrolyte disturbances in chronic liver disease

Kramer

1975

Postgraduate Medical Journal

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SummaryBesides intrarenal physical factors and aldosterone, a natriuretic hormone has been postulated to modulate renal tubular sodium resorption in order to maintain body fluid homeostasis. To investigate the possible role of a natriuretic activity in sodium retention of chronic liver disease, the effects of plasma and plasma fraction IV from patients with cirrhosis of the liver and ascites on sodium transport of the isolated frog skin and on renal sodium excretion in the rat were compared to the antinatriferic and natriuretic effects of plasma from healthy subjects. While plasma from healthy individuals obtained following acute expansion of the extracellular fluid volume (ECV) significantly inhibited potential difference (PD) by -43-8 ± 5.5%o and short circuit current (SCC) by -41-3 ± 1F7% when applied to the inner skin surface, control plasma and plasma from patients with liver cirrhosis and ascites affected PD by -3-8 i 4-7y and -5 2 4± 3 7 % and SCC by -73 ± 4Y6% and -11 7 + 2.5% respectively.Similar effects on PD and SCC were observed with plasma fractions IV.In contrast to fraction IV from ECV-expanded individuals, which caused marked diuresis and natriuresis when injected in the rat, fraction IV of plasma from cirrhotic patients failed to affect urinary flow rate, free-water clearance or renal sodium excretion. The results suggest that at least some patients with cirrhosis of the liver and sodium retention may lack an adequate humoral natriuretic activity sufficiently to promote renal sodium excretion.

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Section: Discussionmentioning

confidence: 99%

Natriuretic hormone—its possible role in fluid and electrolyte disturbances in chronic liver disease

Kramer

1975

Postgraduate Medical Journal

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“…Acute constriction of the thoracic vena cava in the dog is associated with a decrease in the natriuretic response to extracellular fluid volume expansion (ECVE) [1][2][3][4][5]. The mechanisms responsible for this phenomenon are not entirely evident but several factors have been considered.…”

Section: Introductionmentioning

confidence: 99%

Effect of Volume Expansion on Nephrogenous Cyclic AMP during Vena Cava Constriction in the Dog

Friedler¹,

Klein²,

Tuma³

et al. 1980

Nephron

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Previous studies in our laboratory support the notion that an increase in the production of cyclic AMP (cAMP) by the kidney may play a role in the natriuresis of extracellular fluid volume expansion (ECVE). The present study was designed to evaluate whether a suppression in the rise in nephrogenous cAMP is involved in the blunted natriuretic response to ECVE during acute caval constriction. ECVE was produced by saline infusion in 8 thyropara-thyroidectomized dogs during acute constriction of the thoracic inferior vena cava and after its release. Arterial pressure decreased during caval constriction and ECVE and returned to values not different from control after the release of the constriction. There were no significant changes in renal plasma flow, glomerular filtration rate (GFR), fraction of filtered sodium excreted, or nephrogenous cAMP during the caval constriction. The release of the constriction in 4 dogs was followed by no significant changes in renal plasma flow and GFR, while the fraction of filtered sodium excreted increased significantly together with a significant rise in total nephrogenous cAMP by 1,682 ± 409 pmol/min (p < 0.05). The data are consistent with the hypothesis that the blunted natriuresis during ECVE in caval dogs is at least partly due to lack of increment in nephrogenous cAMP. The results provide further support for the role of renal cAMP in modulating renal handling of sodium.

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Methodology for Study of Isolated Perfused Dog Kidney in Situ

Kaloyanides¹

1978

Renal Pharmacology

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Failure to demonstrate a humoral mechanism in the antinatriuresis of acute caval constriction

Cited by 4 publications

References 7 publications

Natriuretic hormone—its possible role in fluid and electrolyte disturbances in chronic liver disease

Natriuretic hormone—its possible role in fluid and electrolyte disturbances in chronic liver disease

Effect of Volume Expansion on Nephrogenous Cyclic AMP during Vena Cava Constriction in the Dog

Methodology for Study of Isolated Perfused Dog Kidney in Situ

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