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Slow Force Response After
Myocardialstretch: Increase
in Ca2+ Transient, Myofilament
Responsiveness or Both?

Cingolani,Horacio E; Pérez,Néstor G;
Camilión de Hurtado, María C

Centro de Investigaciones Cardiovasculares, La Plata, Argentina

The slow force response (SFR) to stretch is an increase in the developed force (DF) that results from a chain of events beginning with the release of angiotensin II (Ang II) and followed by Na+/H+ exchanger (NHE) activation by endothelin (ET). This autocrine/paracrine activation of the NHE causes an increase in intracellular Na+ ([Na+]i) and, consequently, an increase in calcium transients (Ca2+T) through the Na+/Ca2+ exchanger (NCX). The activation of the NHE by Ang II and/or ET increases pHi only in the absence of bicarbonate because of the simultaneous activation of the Na+-independent, Cl-/HCO3- exchanger (AE). Since nominally bicarbonate-free (HEPES)-buffered solutions are oftenly used, the SFR of cat papillary muscles bathed with HEPES- or CO2/HCO3- buffers were compared. In HEPES, pHi went up and the SFR almost doubled that in bicarbonate. A negative lusitropic effect, probably reflecting an increase in myofilament responsiveness, was detected only in HEPES buffer. [Na+]i increased similarly under both buffers. KB-R7943, a selective inhibitor of the NCX in reverse mode, completely suppressed the SFR in bicarbonate and reduced it to the half in HEPES. In conclusion, whereas in HEPES the SFR appears to result from an increase

 

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2nd Virtual Congress of Cardiology

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