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Acute hypotension/hypertension in vitro causes temporary post‐receptor up/down regulation of subsequent arterial contractions
Author(s) -
Bednarek Melissa Lynn,
Miner Amy S,
Alvarez Silvina M,
Speich John E,
Ratz Paul H
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.781.7
Subject(s) - crossbridge , isometric exercise , contraction (grammar) , myosin , vascular smooth muscle , muscle contraction , myosin light chain kinase , chemistry , calcium , medicine , femoral artery , fold (higher order function) , smooth muscle , endocrinology , anatomy , biophysics , biology , mechanical engineering , engineering
Recent studies suggest that smooth muscle length (L)‐tension (T) curves are dynamic. Using in vitro rabbit femoral artery rings we determined whether vascular smooth muscle (VSM) displays L‐history adaptation. The 2 nd of 2 sequential isometric contractions induced after release from the optimum L for muscle contraction (Lo) to 0.8‐fold Lo was 1.1‐fold that of the 1 st . If the muscle was stretched briefly from 0.8‐ to 1.2‐ and 1.4‐fold Lo between the 1 st and 2 nd contractions at 0.8‐fold Lo, the 2 nd contraction was 0.9‐fold and 0.4‐fold, respectively, of the 1 st . This down‐regulation was not due to tissue damage. The generation of two full L‐T curves, one produced by incrementally increasing muscle L (0.4 ‐ 1.2‐fold Lo UP) , the other by incrementally decreasing muscle L (1.2 ‐ 0.4‐fold Lo DN), revealed that active T and passive T were stronger when starting from a shorter muscle L. The maximum difference between active T UP and active T DN was at 0.6‐fold Lo and between passive T UP and passive T DN was at 1.2‐fold Lo. Preliminary data suggest that this L‐history adaptation was not caused by alterations in cell calcium nor myosin light chain phosphorylation. Together, these data support the hypothesis that numbers of crossbridges rather than crossbridge (thick filament) regulation may play the predominant role in VSM L‐history adaptation. Support: R01HL061320