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Polyamines increase Ca2+ sensitivity in permeabilized smooth muscle of guinea pig ileum

Författare

Summary, in English

The effects of polyamines were investigated in strips of smooth muscle from guinea pig ileum permeabilized with beta-escin (0.005%). Spermine (1 mM) inhibited transient contractions induced in Ca(2+)-free medium by carbachol (0.1 mM) and GTP gamma S (0.1 mM) but potentiated responses to caffeine (20 mM) and D-myo-inositol 1,4,5-trisphosphate (40 microM). At high ethylene glycol-bis(beta-amino-ethyl ether)-N,N,N',N'-tetraacetic acid concentration (10 mM) and in the presence of A-23187 (10 microM), force at optimal and suboptimal Ca2+ concentrations was increased both by spermine and by carbachol. Spermine did not potentiate contraction in Ca(2+)-free medium or after full thiophosphorylation of the regulatory 20-kDa myosin light chains but slightly potentiated contractions produced by partial thiophosphorylation. Also, spermidine and putrescine, as well as the aminoglycoside antibiotic neomycin, increased sensitivity to Ca2+, with potency correlating with number of positive charges. After permeabilization by a high concentration (0.1%) of beta-escin, the sensitivity to Ca2+ was increased by spermine but not by GTP gamma S. In preparations permeabilized by Triton X-100, spermine slightly increased Ca2+ sensitivity but not maximal force. Tissue contents of putrescine, spermidine, and spermine in intact ileum muscle were 8, 98, and 184 nmol/g, respectively. Permeabilization by 0.005 and 0.1% beta-escin reduced spermine contents by 40 and 53%, respectively. Effects of added polyamines in permeabilized preparations may thus reflect physiological effects of endogenous polyamines modulating contraction in the intact tissue.

Avdelning/ar

Publiceringsår

1994

Språk

Engelska

Sidor

1754-1763

Publikation/Tidskrift/Serie

American Journal of Physiology: Cell Physiology

Volym

266

Issue

6

Dokumenttyp

Artikel i tidskrift

Förlag

American Physiological Society

Ämne

  • Physiology

Status

Published

Forskningsgrupp

  • Vascular Physiology

ISBN/ISSN/Övrigt

  • ISSN: 1522-1563