Mechanisms Underlying the Increase in Force and Ca 2+ Transient That Follow Stretch of Cardiac Muscle

Author:

Alvarez Bernardo V.1,Pérez Néstor G.1,Ennis Irene L.1,Camilión de Hurtado María C.1,Cingolani Horacio E.1

Affiliation:

1. From Centro de Investigaciones Cardiovasculares, Facultad de Ciencias Médicas, Universidad Nacional de La Plata, Argentina.

Abstract

Abstract —Myocardial stretch produces an increase in developed force (DF) that occurs in two phases: the first (rapidly occurring) is generally attributed to an increase in myofilament calcium responsiveness and the second (gradually developing) to an increase in [Ca 2+ ] i . Rat ventricular trabeculae were stretched from ≈88% to ≈98% of L max , and the second force phase was analyzed. Intracellular pH, [Na + ] i , and Ca 2+ transients were measured by epifluorescence with BCECF-AM, SBFI-AM, and fura-2, respectively. After stretch, DF increased by 1.94±0.2 g/mm 2 ( P <0.01, n=4), with the second phase accounting for 28±2% of the total increase ( P <0.001, n=4). During this phase, SBFI 340/380 ratio increased from 0.73±0.01 to 0.76±0.01 ( P <0.05, n=5) with an estimated [Na + ] i rise of ≈6 mmol/L. [Ca 2+ ] i transient, expressed as fura-2 340/380 ratio, increased by 9.2±3.6% ( P <0.05, n=5). The increase in [Na + ] i was blocked by 5-( N -ethyl- N -isopropyl)-amiloride (EIPA). The second phase in force and the increases in [Na + ] i and [Ca 2+ ] i transient were blunted by AT 1 or ET A blockade. Our data indicate that the second force phase and the increase in [Ca 2+ ] i transient after stretch result from activation of the Na + /H + exchanger (NHE) increasing [Na + ] i and leading to a secondary increase in [Ca 2+ ] i transient. This reflects an autocrine-paracrine mechanism whereby stretch triggers the release of angiotensin II, which in turn releases endothelin and activates the NHE through ET A receptors.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Cardiology and Cardiovascular Medicine,Physiology

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