Sodium-potassium pump inhibitor in the mechanism of one-kidney, one wrap hypertension in dogs.
Using ouabain sensitive 86Rb uptake by the vessel wall, we previously showed that sodium-potassium pump activity is decreased in the arteries and veins, and that the sodium-potassium pump inhibitor (SPI) is increased in the plasma of dogs with one-kidney, one wrap (1-K, 1W) hypertension, a low renin model of hypertension. We also showed in rats with a similar type of hypertension that the membrane potential of vascular smooth muscle cells in arteries is decreased, and that this decrease can be reproduced in arterial cells in arteries from normal rats by applying plasma from the hypertensive animals. One endogenous SPI in human plasma has been reported to be ouabain or its isomer. In this study, we used a newly available Dupont ouabain enzyme immunoassay kit to examine plasma and kidneys for SPI in dogs with 1-K, 1W hypertension. We also examined 1) the inhibiting activity of plasma of Na+, K(+)-ATPase obtained from normal kidneys, and 2) the Na+, K(+)-ATPase activity of the kidneys from these hypertensive animals. 1-K, 1W hypertension was produced in dogs by wrapping the left kidney in a silk bag and removing the right kidney. The removed kidney was kept at -70 degrees C till assayed. After 4 weeks of hypertension, the remaining kidney was removed and stored at -70 degrees C till assayed. Blood samples were drawn before and at weeks 3 and 4 of hypertension. Plasma levels of "ouabain" and Na+, K(+)-ATPase inhibitory activity were increased at weeks 3 and 4 of hypertension, compared to pre-hypertension levels. Renal tissue "ouabain" levels were also increased at week 4 of hypertension. However, renal Na+, K(+)-ATPase activity was unchanged. These findings, using two different assays, confirm our 1980 conclusion that SPI is elevated in the plasma of dogs with 1-K, 1W hypertension. The absence of renal Na+, K(+)-ATPase inhibition, despite increased plasma and renal SPI in these animals, may have important implications for the development of this type of hypertension.
Pamnani
M B
MB
Department of Physiology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA. MPAMNANI@USUHS.MIL
Swindall
B T
BT
Schooley
J F
JF
Ghai
R
R
Haddy
F J
FJ
D000818:Animals; D004195:Disease Models, Animal; D004285:Dogs; D006977:Hypertension, Renal / Q000378:metabolism*; D007668:Kidney; D007672:Kidney Cortex / Q000378:metabolism; D007679:Kidney Medulla / Q000378:metabolism; D008274:Magnesium / Q000378:metabolism; D008297:Male; D010042:Ouabain / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D013997:Time Factors
D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D008274:Magnesium