Effects of Cardiac Glycosides on Kidneys

Heidenreich, O.; Oßwald, Hartmut

doi:10.1007/978-3-642-68163-9_25

Cited by 3 publications

(2 citation statements)

References 107 publications

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“…This BP-independent natriuresis and diuresis is probably due to decreased renal tubular Na + reabsorption subsequent to the inhibition of renal Na+.K^-ATPase. 36 Admittedly, some of the natriuresis and diuresis that we observed during cumulative infusions of bufalin must have resulted from the large increase in BP. Perhaps the massive natriuresis and diuresis immediately following the end of bufalin infusion is due to additive factors such as 1) increased BP, 2) inhibited tubular , and 7, respectively) at six different rates for total of 30 minutes on blood pressure, heart rate, and rate of ventricular pressure change (dp/dt) in rats.…”

Section: Discussionmentioning

confidence: 83%

“…Therefore, effective doses of cardiac glycosides in rats initially are more likely to produce extrarenal electrolyte disturbances, leading to hyperkalemia and hyponatremia. 36 Despite the hyponatremia, high doses of cardiac glycoside cause increased U Nl V due to inhibition of tubular Na + reabsorption. The significantly increased U K V that we observed after ouabain infusion may be in part due to hyperkalemia.…”

Section: Discussionmentioning

confidence: 99%

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Effects of three sodium-potassium adenosine triphosphatase inhibitors.

et al. 1991

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Reports from several laboratories suggest the presence of an ouabainlike compound in plasma and various animal tissues, particularly during acute volume expansion and in low-renin hypertension. It has been hypothesized that this compound, through inhibition of the Na + -K + pump, can constrict blood vessels, enhance vasoconstriction in response to agonists, increase cardiac contractility, raise blood pressure, and cause natriuresis/diuresis and therefore is implicated in the pathophysiology of the low-renin, volume-expanded type of hypertension. However, so far, only two steroid Na + -K + pump inhibitors (namely, a bufodienolide derivative [resibufogenin], obtained from toad skin and plasma and a factor with the same carbon, oxygen, and hydrogen content as ouabain obtained from the plasma of volume-expanded humans) have been purified and structurally characterized. To determine whether such endogenous Na + -K + pump inhibitors can in fact produce the above effects on the cardiovascular and renal systems, we infused commercially available bufalin (aglycone, identical to resibufogenin except for one H + ), ouabain, and ouabagenin (aglycone) at equimolar doses in normotensive rats. Relative to ouabain, bufalin produced significantly greater dose-dependent increases in blood pressure, left ventricular rate of pressure change, heart rate, and excretion of urinary volume and sodium. Ouabagenin was without effect on any of these parameters. These data indicate that a Na + -K + pump inhibitor can cause an increase in blood pressure despite potent diuretic and natriuretic effects and that, in rats, bufalin is much more potent in this respect than ouabain or ouabagenin. {Hypertension 1991;18:316-324)

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Effects of three sodium-potassium adenosine triphosphatase inhibitors.

et al. 1991

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A study of androgen-stimulated l-leucine transport by the intestine of rainbow trout (Salmo gairdneri Richardson) in vitro

Habibi

Ince

1984

Comparative Biochemistry and Physiology Part A: Physiology

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Long-term ouabain administration produces hypertension in rats.

et al. 1993

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Ouabain has recently been identified as an endogenous Na + -K + pump inhibitor. We administered ouabain chronically to normotensive rats with varying degrees of reduced renal mass (RRM) and to normal two-kidney rats to see whether hypertension could be produced. Normal male Wistar rats and rats with 25%, 60%, and 70% RRM received ouabain (13.9 Mg/kg per day IP) in normal saline for 4 weeks followed by ouabain (27.8 figJkg per day IP) for 3 to 4 more weeks. Respective control animals received vehicle only. Blood pressure was recorded weekly by tail plethysmography. Animals received tap water and standard rat chow, except for 70% RRM rats, which received distilled water and sodium-free chow. After 6 to 8 weeks of treatment, with rats under thiobutabarbital anesthesia, direct blood pressure was determined. Plasma, tissue, and urinary ouabain levels were measured with a specific radioimmunoassay. Animals receiving ouabain developed significant increases in mean blood pressure compared with control animals (70% RRM, 147±4 vs 116±4 mm Hg; 60% RRM, 140±4 vs 107±3 mm Hg; 25% RRM, 131 ±5 vs 100±2 mm Hg; no RRM, 116±4 vs 98±5 mm Hg). Plasma ouabain levels measured 24 hours after the last ouabain dose were not different in animals receiving ouabain vs those receiving vehicle. However, kidney tissue ouabain levels were significantly greater (6J9±1.17 vs 2.36±0. 52 fig/kg, P<.05) in animals receiving ouabain. In conclusion, ouabain, given chronically, is associated with the development of hypertension in RRM rats as well as in normal rats. Blood pressure was greater in animals with greater degrees of RRM for a given ouabain dose. (Hypertension 1993^2:178-187)

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Effects of Cardiac Glycosides on Kidneys

Cited by 3 publications

References 107 publications

Effects of three sodium-potassium adenosine triphosphatase inhibitors.

Effects of three sodium-potassium adenosine triphosphatase inhibitors.

A study of androgen-stimulated l-leucine transport by the intestine of rainbow trout (Salmo gairdneri Richardson) in vitro

Long-term ouabain administration produces hypertension in rats.

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