A mutation in the zebrafish Na,K-ATPase subunitatp1a1a.1provides genetic evidence that the sodium potassium pump contributes to left-right asymmetry downstream or in parallel to nodal flow

2006 ◽  
Vol 235 (7) ◽  
pp. 1794-1808 ◽  
Author(s):  
Elin Ellertsdottir ◽  
Julia Ganz ◽  
Katrin Dürr ◽  
Niki Loges ◽  
Frederic Biemar ◽  
...  
Keyword(s):  
Genetic Evidence ◽  
Sodium Potassium ◽  
Nodal Flow ◽  
Sodium Potassium Pump ◽  
Left Right Asymmetry

Effect of palytoxin on the sodium–potassium pump: model and simulation

2008 ◽  
Vol 5 (3) ◽  
pp. 036005 ◽  
Author(s):  
Antônio M Rodrigues ◽  
Antônio-Carlos G Almeida ◽  
Antonio F C Infantosi
Keyword(s):  
Sodium Potassium ◽  
Model And Simulation ◽  
Sodium Potassium Pump

Abstract 90: Inimitable Ouabain: The Endogenous Circulating Cardiotonic Steroid that Singularly Stimulates Sodium Potassium Pump Activity at Low Doses

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Yeon Jae Kim ◽  
Elisha Hamilton ◽  
William Hannam ◽  
Chia-Chi Liu ◽  
Rachel Teh ◽  
...  
Keyword(s):  
Low Dose ◽  
Lactone Ring ◽  
Cardiac Contractility ◽  
Cancer Cell Line ◽  
Structural Components ◽  
Sodium Potassium ◽  
Sugar Moiety ◽  
Unsaturated Lactone ◽  
Sodium Potassium Pump ◽  
The Difference

Rationale: Cardiotonic steroids (CTS), such as digoxin, have been used to treat heart failure (HF) for over 200 years. They inhibit the sodium-potassium pump (NKP), and increase cardiac contractility by inhibiting efflux of sodium through the pump (“digitalis hypothesis”). CTS possess three structural components: a saturated/unsaturated lactone ring, steroid core, and sugar moiety, each of which may be involved in NKP inhibition/stimulation. It is now known that inhibition of the NKP in patients with HF increases mortality, and all major beneficial treatments increase its activity. Endogenous circulating CTS such as ouabain are generally thought to inhibit the NKP, despite studies sporadically reporting ouabain-induced pump stimulation. This study aims to identify whether ouabain-induced pump stimulation occurs, and if so, which structural components are involved in causing pump stimulation. Methods & Results: Cardiac myocytes were isolated from male New Zealand White rabbits, placed in a Tyrode’s solution, and whole-cell patch clamped. They were exposed to 0-30nM ouabain, 0-50nM dihydroouabain (ouabain with a saturated lactone ring) or 0-500nM ouabagenin (ouabain lacking a sugar moiety) for 1 min, followed by a potassium-free solution, with the difference in current yielding the NKP current. Compared to the 0.47±0.05 pA/pF Tyrode’s solution control (n=11), 5nM ouabain significantly increased NKP current to 0.69±0.09 pA/pF ( P <0.05, n=6). Exposure to dihydroouabain or ouabagenin did not significantly change NKP current in the studied concentration range. Cell viability assays carried out on the breast cancer cell line MCF7, which have an NKP structure extremely similar to that of cardiomyocytes, showed significantly elevated viability above control values (n=2) following 24h treatment with 0-9nM ouabain; maximum viability was 116±5% at 0.28nM ( P <0.05, n=4). A significant change in viability was not observed for ouabagenin or digoxin in the same concentration range. Conclusion: Low-dose ouabain uniquely stimulates NKP activity. Low-dose dihydroouabain and ouabagenin do not, suggesting that a sugar moiety and unsaturated lactone ring are required for pump stimulation. Ouabain in its unaltered form may be a potential treatment for HF.

Effects of hyperkalemia and glycoside on thallium exchange in rabbit ventricle

1981 ◽  
Vol 240 (4) ◽  
pp. H612-H619 ◽  
Author(s):  
J. Krivokapich ◽  
K. I. Shine
Keyword(s):  
Exchange Rate ◽  
Exchange Rates ◽  
Interventricular Septum ◽  
Thallium 201 ◽  
Myocardial Tissue ◽  
Sodium Potassium ◽  
Sodium Potassium Pump ◽  
Insight Into

The exchange characteristics of thallium-201 (201Tl) were studied using the isolated arterially perfused rabbit interventricular septum to gain insight into the mechanisms that govern its uptake and subsequent washout from myocardial tissue. The results were compared to potassium-42 (42K) exchange. Unlike 42K, the uptake and tissue washout exchange rates for 201Tl were not equal. The 201Tl washout exchange rate was slower than that for the uptake. Hyperkalemia increased the efflux of both 42K and 201Tl, but the increase in 201Tl efflux was not due to an increase in permeability, as was true for 42K, but to a hyperkalemia, induced increase in compartment size of exchangeable 201Tl. Acetylstrophanthidin (ACS) resulted in an increase in 201 Tl efflux similar to the increase in 42K efflux seen with ACS. However, ACS did not inhibit 201Tl influx, in contrast to the known inhibition of 42K influx. This indicated that influx of tracer amounts of 201Tl was not dependent on the sodium-potassium pump. A model of Tl exchange in rabbit ventricles is proposed.

Crystal structure of the sodium–potassium pump at 2.4 Å resolution

Nature ◽  
2009 ◽  
Vol 459 (7245) ◽  
pp. 446-450 ◽  
Author(s):  
Takehiro Shinoda ◽  
Haruo Ogawa ◽  
Flemming Cornelius ◽  
Chikashi Toyoshima
Keyword(s):  
Crystal Structure ◽  
Sodium Potassium ◽  
Sodium Potassium Pump
Sign in / Sign up

Export Citation Format

Share Document