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Thapsigargin does not affect phenylephrine-induced contractions in the anococcygeus muscle of rats

C da Silva1, L M Bendhack

  • 1Laboratory of Pharmacology, College of Pharmaceutical Sciences, University of Sao Paulo, Ribeirao Preto, Brazil.

General Pharmacology
|August 1, 1997
PubMed

Insights

Intracellular calcium significantly contributes to phenylephrine-stimulated contractions in rat anococcygeus smooth muscle. However, the calcium store activated by phenylephrine is not sensitive to thapsigargin.

Area of Science:

  • Pharmacology
  • Physiology
  • Smooth Muscle Biology

Background:

  • Intracellular calcium stores play a critical role in smooth muscle contraction.
  • Understanding the specific calcium pathways involved in phenylephrine-induced contractions is essential for elucidating smooth muscle function.

Purpose of the Study:

  • To investigate the role of intracellular calcium in phenylephrine-stimulated contractions of rat anococcygeus smooth muscle.
  • To evaluate the effects of thapsigargin and TMB-8, antagonists of intracellular calcium stores, on these contractions.

Main Methods:

  • Functional studies were employed to assess smooth muscle contractions.
  • Phenylephrine-induced contractions were measured in calcium-free media.
  • The effects of thapsigargin and 8-(Diethylamino)-octyl-3,4,5-trimethoxybenzoate, HC1 (TMB-8) were evaluated.

Main Results:

  • Phenylephrine induced concentration-related contractions in calcium-free media, persisting for approximately 26 stimulations.
  • TMB-8 (10 microM) rightward shifted phenylephrine concentration-response curves, reducing maximum contraction by 39.2% without altering EC50.
  • Thapsigargin (1 microM) did not affect phenylephrine-stimulated contractions in calcium-free media.

Conclusions:

  • Intracellular calcium is crucial for phenylephrine-stimulated contractions in rat anococcygeus smooth muscle.
  • The phenylephrine-sensitive intracellular calcium store is not sensitive to thapsigargin, suggesting a distinct calcium release mechanism.

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