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Calcium‐dependent and ‐independent mechanisms in the response to oxygen of the chicken ductus arteriosus
Author(s) -
Cleef Anne NH,
Zoer Bea,
Cogolludo Angel L,
PerezVizcaino Francisco,
Villamor Eduardo
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1027.3
Subject(s) - thapsigargin , nifedipine , bay k8644 , chemistry , cyclopiazonic acid , contraction (grammar) , dihydropyridine , medicine , endocrinology , channel blocker , voltage dependent calcium channel , calcium , verapamil , extracellular , intracellular , biology , biochemistry , organic chemistry
We aimed to investigate the relative contribution of voltage‐ and store‐operated Ca 2+ channels (VOCC and SOCC respectively), intracellular Ca 2+ stores and Ca 2+ sensitization in O 2 ‐induced contraction of chicken ductus arteriosus (DA). Isolated DA rings from 15 and 19‐d chicken fetuses (total incubation 21‐d) were mounted in a myograph and exposed to normoxia. In the 19‐d DA, O 2 ‐induced contraction was reduced by the absence of extracellular Ca 2+ (28.7% of control contraction) or by the presence of the L‐type VOCC antagonist nifedipine (10 μM; 45.0%); the sarcoplasmic reticulum Ca 2+ ATPase inhibitors thapsigargin (0.1 μM; 80.7%) and cyclopiazonic acid (0.1 μM; 22.2%); the SOCC inhibitor SKF 96365 (10 μM; 41.7%); the blocker of Ca 2+ release from IP 3 ‐sensitive stores 2‐APB (0.5 μM; 44.0%); and the Rho‐kinase inhibitor hydroxyfasudil (1 μM; 62.3%). The combination of nifedipine, thapsigargin, SKF 96365 and hydroxyfasudil abolished O 2 ‐induced contraction. The L‐type VOCC agonist BAY K8644 contracted the 19‐d DA in a concentration‐dependent manner. This contraction was not affected by O 2 tension. The 15‐d DA showed a very weak O 2 ‐induced contraction and did not respond to BAY K8644. In conclusion, our results indicate that Ca 2+ entry through VOCC and SOCC, Ca 2+ release from intracellular stores and Rho‐kinase‐mediated Ca 2+ sensitization contribute to O 2 ‐induced contraction of the chicken DA. Functional immaturity of VOCC appears to play a role in the lack of O 2 responsiveness in the immature chicken DA. Supported by "Fundación de Investigación Médica Mutua Madrileña".