ISSN:
1432-2013
Keywords:
Medullary Na−K-ATPase
;
Suprarenal caval ligation
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract To assess the effects of altered renal function on Na−K-ATPase, the following groups of rats were studied: 1. rats with suprarenal vena cava ligation (SVCL), la. DOCA-treated rats with SVCL, 2. rats with infrarenal vena cava ligation (IVCL), 3. rats with glycerol-induced acute renal failure, 4. rats with bilateral ureteric ligation, and 5. K-exalate-treated rats with SVCL. In group 1, acute renal failure with hyperkalemia developed and medullary Na−K-ATPase increased from 95±5 in control to 155±7 μmol Pi/mg prot//h,P〈0.001, DOCA did not prevent the increase of Na−K-ATPase. In group 2, medullary Na−K-ATPase decreased from 130±10 in control to 88±7,P〈0.01, in rats with IVCL. In group 3, cortical Na−K-ATPase decreased from 55±5 to 27±6,P〈0.02. In group 4, Na−K-ATPase was unchanged. In group 5, maintenance of normokalemia prevented the rise in Na−K-ATPase. These experiments demonstrated a K-dependent activation of medullary Na−K-ATPase after SVCL but not in other forms of renal failure. Because SVCL diminishes drastically GFR per nephron, the present findings imply that increased loads of Na and K per nephron are not a prerequisite for an increase in medullary Na−K-ATPase. Hyperkalemia in presence of increased renal venous pressure seems to be causually related to the rise in medullary Na−K-ATPase activity.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00582920
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