Considerable research indicates that intracellular calcium, through both transmembrane influx and release from intracellular stores, is necessary for stretch-mediated vasoconstriction. Stretch has also been shown to induce protein synthesis in systemic and pulmonary vascular smooth muscle cells. The purpose of this study was to determine if inhibition of transmembrane calcium influx and intracellular calcium release abolishes stretch-mediated protein synthesis in systemic and pulmonary arteries in vitro. Methods: We applied stretch equal to 100 and 150 mm Hg (aorta), and 12 and 45 mm Hg(pulmonary artery) to intact, 4mm rings (in vitro) for 24hrs. Aortic rings were stretched in tissue culture media containing serum ± nifedipine, verapamil, diltiazem, or ryanodine (all 10uM). Pulmonary artery rings were subjected to stretch in the presence of nifedipine or verapamil (10uM) only.3 H-Leucine (3uC/ml) was added to the culture media 4hrs prior to the conclusion of stretch and the relative rate of protein synthesis was determined using TCA precipitated counts normalized to tissue wet weight.Results: Table Conclusions: 1) Both transmembrane calcium influx and release of intracellular calcium stores are necessary for stretch-mediated growth in aorta, 2) At least transmembrane calcium influx is necessary for stretch-mediated growth in pulmonary arteries, and 3) Calcium-channel blockers may be useful in preventing the pathologic remodeling associated with systemic and pulmonary hypertension.

Table 1
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