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Intravascular Pressure Initiates Cerebral Arterial Constriction by Inducing Voltage‐Independent Calcium Waves
Author(s) -
Karen Bradley,
Brett Suzanne,
Tran Cam Ha,
Hunt Donald,
Jones Peter,
Chen Wayne,
Welsh Donald
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.lb82
Subject(s) - chemistry , biophysics , myogenic contraction , ryanodine receptor , diltiazem , calcium , cerebral arteries , medicine , membrane potential , smooth muscle , biology
The study examined whether elevated intravascular pressure induces asynchronous Ca(2+) waves in cerebral arterial smooth muscle cells and if their generation contributes to myogenic constiction. Rat cerebral arteries mounted in a customized arteriograph were pressurized (20‐100 mmHg) and examined under a variety of experimental conditions. Diameter and membrane potential (Vm) were assessed using conventional techniques whereas Ca(2+)waves were monitored by measuring Fluo‐4 fluorescence with a spinning disk confocal microscope. Elevated pressure increased the proportion of cells firing Ca(2+) waves (30 to 97%) and their frequency (3 to 10 waves/cell). Ryanodine, an agent that depletes the sarcoplasmic reticulum (SR) of Ca(2+) blocked Ca(2+) wave generation. Interestingly, Ca(2+)waves were voltage‐independent as Diltiazem (L‐type Ca(2+) channel blocker) along with changes in Vm had little effect on these pressure‐induced events. Functional experiments also revealed that Ca(2+) waves contribute to myogenic tone development through a mechanism independent of arterial Vm. In summary, this study revealed that like agonists, mechanical stimuli elicit Ca(2+) waves in arterial smooth muscle and that such events facilitate tone development through myosin light chain kinase activation.