| 15105296 |
von Lewinski D, Stumme B, Fialka F, Luers C, Pieske B: Functional relevance of the stretch-dependent slow force response in failing human myocardium. Circ Res. 2004 May 28;94(10):1392-8. Epub 2004 Apr 22.
The resulting immediate and delayed (ie, slow force response [SFR]) increases in twitch force were assessed without and after blockade of the sarcoplasmic reticulum (SR; cyclopiazonic acid and ryanodine), stretch-activated ion channels (SACs; gadolinium, streptomycin), L-type Ca2+-channels (diltiazem), angiotensin II type-1 (AT1) receptors (candesartan), endothelin (ET) receptors (PD145065 or BQ123), Na+/H+ exchange (NHE1; HOE642), or reverse-mode Na+/Ca+ exchange (NCX; KB-R7493). |
31(0,1,1,1) |
Details |
| 18503051 |
Kockskamper J, Khafaga M, Grimm M, Elgner A, Walther S, Kockskamper A, von Lewinski D, Post H, Grossmann M, Dorge H, Gottlieb PA, Sachs F, Eschenhagen T, Schondube FA, Pieske B: Angiotensin II and myosin light-chain phosphorylation contribute to the stretch-induced slow force response in human atrial myocardium. Cardiovasc Res. 2008 Sep 1;79(4):642-51. Epub 2008 May 24.
Inhibition of Na (+)/H (+)-exchange (3 microM HOE642), Na (+)/Ca (2+)-exchange (5 microM KB-R7943), or stretch-activated channels (0.5 microM GsMtx-4 and 80 microM streptomycin) did not reduce the SFR. |
2(0,0,0,2) |
Details |