This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Xie, H. Articles by Bevan, J. A. Search for Related Content PubMed PubMed Citation Articles by Xie, H. Articles by Bevan, J. A. Pubmed/NCBI databases Compound via MeSH Substance via MeSH Hazardous Substances DB CAFFEINE CALCIUM COMPOUNDS CALCIUM, ELEMENTAL HISTAMINE POTASSIUM SODIUM CHLORIDE

(Hypertension. 1995;26:1051-1055.)
© 1995 American Heart Association, Inc.

Articles

Intracellular Ca²⁺ Release in Flow-Induced Contraction of Venous Smooth Muscle

Hui Xie; Ismail Laher; John A. Bevan

From the Department of Pharmacology, College of Medicine, The University of Vermont, Burlington.

Correspondence to John A. Bevan, Department of Pharmacology, College of Medicine, The University of Vermont, Burlington, VT 05405-0068.

Abstract We designed the present study to determine whether Ca²⁺ release from intracellular stores contributes to flow-induced contraction. We carried out experiments on segments of rabbit facial vein under isometric conditions. Intraluminal flow by perfusion of physiological salt solution (10 to 80 µL/min) caused contraction in this vessel, which was significantly inhibited by (1) 30-minute pretreatment with 10 µmol/L ryanodine, the sarcoplasmic reticulum Ca²⁺ channel opener, and (2) 30-minute pretreatment with concomitant application of 20 mmol/L caffeine and 1 µmol/L cyclopiazonic acid in Ca²⁺-free medium to deplete the sarcoplasmic reticulum. In comparison, contraction initiated by 300 nmol/L histamine was significantly attenuated by the same interventions. K⁺ (25 mmol/L)–induced contraction was unaffected by ryanodine but was reduced after depletion of the sarcoplasmic reticulum. The phospholipase C inhibitor 2-nitro-4-carboxyphenyl-N,N-diphenylcarbamate (10 µmol/L) inhibited contractions induced by flow and histamine but not by K⁺. These findings indicate that Ca²⁺ release from intracellular stores, presumably via the phosphatidylinositol pathway, contributes to flow- and histamine- but not raised K⁺–induced contractions in this vessel.

Key Words: calcium • potassium • muscle, smooth, vascular • muscle contraction