INVESTIGADORES
ENNIS Irene Lucia
artículos
Título:
Mechanisms underlying the increase in force and Ca(2+) transient that follow stretch of cardiac muscle: a possible explanation of the Anrep effect.
Autor/es:
ALVAREZ BV; PÉREZ NG; ENNIS IL; CAMILIÓN DE HURTADO MC; CINGOLANI HE
Revista:
CIRCULATION RESEARCH
Editorial:
LIPPINCOTT WILLIAMS & WILKINS
Referencias:
Lugar: Philadelphia; Año: 1999 p. 716 - 722
ISSN:
0009-7330
Resumen:
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 approximately 88% to
approximately 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
approximately 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.