Studies on sodium-potassium-activated adenosinetriphosphatase. IV. Correlation with cation transport sensitive to cardiac glycosides

Bonting, S.L.; Caravaggio, Leo L.; Hawkins, Naomi M.

doi:10.1016/0003-9861(62)90206-0

Cited by 220 publications

(33 citation statements)

References 39 publications

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“…Thus, removal of sodium or its replacement by lithium or choline in the external medium would indirectly depress the activity of the sodiumpotassium pump (Skou, 1957) as the sodium concentration inside the cell is reduced. Since the demonstration by Schatzmann (1953) that cardiac glycosides specifically inhibit cation transport, several investigators have shown their effectiveness against ATPase in a number of organ systems (Skou, 1957;Dunham & Glynn, 1961;Bonting, Caravaggio & Hawkins, 1962). NEM and p-hydroxymercuribenzoate also inhibit ATPase (Skou, 1963;Rendi, 1965;Banerjee, Wong, Khanna & Sen, 1972).…”

Section: Bmentioning

confidence: 99%

Release of noradrenaline from the cat spleen by sodium deprivation

Garcı́a

Kirpekar

1973

British J Pharmacology

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Section: Bmentioning

confidence: 99%

Release of noradrenaline from the cat spleen by sodium deprivation

Garcı́a

Kirpekar

1973

British J Pharmacology

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“…expected in any tissue containing cells and particularly in tissues having nervous or secretory function (Bonting, Caravaggio and Hawkins, 1962). Treatment of the microsomal material with a low concentration of sodium deoxyeholate (0-1 p.c.)…”

Section: Specificity Towards Substratementioning

confidence: 99%

Studies of the Mechanism of Cation Transport

Charnock¹,

Post²

1963

Aust J Exp Biol Med

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SUMMARY.The distribution und activity of adenosine-triphosphatase in homogenates and subfractions of guinea pig kidney cortex has bt-en examined. A portion of the activity associated with particulate fractions could IH; furlhtr stimulated, in the presence of magnesium ions, by the combined addition of sodium and potassium ions but not by the addition of either cation alone or in combination with choline.Treatment of the heavy microsome subfraction with deoxycholate resulted in a large increase in the specific activity of this enzyme, which now re(|uired sodium and potassium ions in a ratio of 4 : 1 for over 85 p.c. of its total activity. Under such conditions of cation stimulation, optimum pH was found to be between 7-5 and 8-0, and the enzyme also exhibited considerable temperature dependence and was stable up to 55° C.The cardiac glycoside Ouabain completely inhibited that portion of enzyme activity stimulated by monovalent cittions but was without effect on the activity observed in the presence of niiiKnesium ions alone.The effect of other reagents and hormones on the cation stimulated adenosine-triphosphatase activity was also examined, with a discussion of the possible significance of this enzyme in active cation transport.INTRODUCTION.

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“…RBC[Na]i has been used for many studies of hypertension, because RBC is a specimen that can easily be obtained and has the lowest quantity of Na + /K + ATPase activity in per tissue weight. 26 Meanwhile, in vascular smooth muscles, isolation of the abdominal aorta needs a close technique. Furthermore, the reduction of Na + /Ca 2+ exchanger activity, the increase of Na + influx and Na + /K + ATPase activity have been reported in experimental hypertension with a high salt diet.…”

Section: Discussionmentioning

confidence: 99%

An ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein

et al. 2009

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It is suggested that an ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein. We reported that glibenclamide, an ATP-sensitive potassium channel blocker, accelerated dose-dependent secretion of renal kallikrein in sliced kidney cortex and in vivo in rats. In vehicle-treated normal BrownNorway-Kitasato (nBN-Ki) rats, the administration of glibenclamide increased urinary kallikrein secretion, but changed neither the systolic blood pressure nor the urinary sodium on low (0.3%) NaCl diets. Although on high (8%) NaCl diets, the systolic blood pressure of the nBN-Ki rats administrated glibenclamide was significantly lower (Po0.05). The urinary levels of kallikrein and sodium of the nBN-Ki rats administrated glibenclamide were significantly increased (Po0.05, glibenclamide vs. vehicle). A similar result was obtained with a kidney-selective ATP-sensitive potassium blocker, N,N¢-dicyclohexyl-4-morpholinecarboxamidine (U18177), in SD rats. Mutant kininogen-deficient Brown-Norway Katholiek (muBN-Ka) rats fed high (8%) NaCl diets showed an increase in urinary kallikrein levels, but showed neither hypotensive nor natriuretic actions by glibenclamide. A bradykinin B 2 receptor antagonist,-dichlorobenzyloxy]-2-methylquinoline (FR173657), which was administrated to SD rats, together with glibenclamide, abolished the hypotensive and natriuretic effects of glibenclamide in high-sodium (8%NaCl) hypertension, despite an accelerated secretion of urinary kallikrein. Therefore, these results indicate that glibenclamide, an ATP-sensitive potassium channel blocker suppressed sodium-induced hypertension through sodium excretion from the kidney resulting from accelerated secretion of urinary kallikrein.

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Studies on sodium-potassium-activated adenosinetriphosphatase. IV. Correlation with cation transport sensitive to cardiac glycosides

Cited by 220 publications

References 39 publications

Release of noradrenaline from the cat spleen by sodium deprivation

Release of noradrenaline from the cat spleen by sodium deprivation

Studies of the Mechanism of Cation Transport

An ATP-sensitive potassium channel blocker suppresses sodium-induced hypertension through increased secretion of urinary kallikrein

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