INVESTIGADORES
ALVAREZ Silvina Monica
artículos
Título:
RHO KINASE ATTENUATES CALCIUM-INDUCED CONTRACTION IN B-ESCIN BUT NOT TRITON X-100 PERMEABILIZED RABBIT FEMORAL ARTERY
Autor/es:
CLELLAND L; BROWNE B; MINER AS; ALVAREZ SM; RATZ PH
Revista:
JOURNAL OF MUSCLE RESEARCH AND CELL MOTILITY
Editorial:
SPRINGER
Referencias:
Año: 2011
ISSN:
0142-4319
Resumen:
K?-depolarization (KCl) of smooth muscle has
long been known to cause Ca2?-dependent contraction, but
only recently has this G protein-coupled receptor (GPCR)-
independent stimulus been associated with rhoA kinase
(ROCK)-dependent myosin light chain (MLC) phosphatase
inhibition and Ca2? sensitization. This study examined
effects of ROCK inhibition on the concentrationresponse
curves (CRCs) generated in femoral artery by incrementally
adding increasing concentrations of KCl to intact
tissues, and Ca2? to tissues permeabilized with Triton
X-100, b-escin and a-toxin. For a comparison, tissue
responses were assessed also in the presence of protein
kinase C (PKC) and MLC kinase inhibition. The ROCK
inhibitor H-1152 induced a strong concentration-dependent
inhibition of a KCl CRC. A relatively low GF-109203X
concentration (1 lM) sufficient to inhibit conventional
PKC isotypes also inhibited the KCl CRC but did not affect
the maximum tension. ROCK inhibitors had no effect on
the Ca2? CRC induced in Triton X-100 or a-toxin permeabilized
tissues, but depressed the maximum contraction
induced in b-escin permeabilized tissue. GF-109203X at
1 lM depressed the maximum Ca2?-dependent contraction
induced in a-toxin permeabilized tissue and had no effect
on the Ca2? CRC induced in Triton X-100 permeabilized
tissue. The MLC kinase inhibitor wortmannin (1 lM)
strongly depression the Ca2? CRCs in tissues permeabilized
with Triton X-100, a-toxin and b-escin. H-1152
inhibited contractions induced by a single exposure to a
submaximum [Ca2?] (pCa 6) in both rabbit and mouse
femoral arteries. These data indicate that b-escin permeabilized
muscle preserves GPCR-independent, Ca2?- and
ROCK-dependent, Ca2? sensitization.