C Delaey1, J Van de Voorde. 1. Department of Physiology and Pathophysiology, Ghent University, Belgium.
Abstract
PURPOSE: To investigate whether a pressure-induced myogenic vasoconstriction can be demonstrated in isolated bovine retinal arteries and to determine the cellular mechanisms involved. METHODS: Isolated bovine retinal arteries were mounted on a pressure myograph without flow and exposed to stepwise increases in intraluminal pressure. Changes in internal diameter were monitored continuously using an inverted microscope video system. RESULTS: Bovine retinal arteries showed myogenic tone at pressures higher than 10 mm Hg. This pressure-induced contraction was absent in calcium-free Krebs-Ringer bicarbonate solution. Inhibition of L-type voltage-operated calcium channels with nifedipine (1 microM) suppressed the myogenic contraction. After depolarization of the vascular smooth muscle cells with a K+ 120 mM solution, a pressure-induced contraction was still observed, indicating that besides stimulation of voltage-operated calcium channels, depolarization-independent mechanisms contribute to the pressure-induced myogenic vasoconstriction. CONCLUSIONS: Isolated bovine retinal arteries spontaneously contract when exposed to raised intraluminal pressure. This response depends on extracellular calcium and is blocked by nifedipine. In addition, depolarization-independent mechanisms seem to be involved.
PURPOSE: To investigate whether a pressure-induced myogenic vasoconstriction can be demonstrated in isolated bovine retinal arteries and to determine the cellular mechanisms involved. METHODS: Isolated bovine retinal arteries were mounted on a pressure myograph without flow and exposed to stepwise increases in intraluminal pressure. Changes in internal diameter were monitored continuously using an inverted microscope video system. RESULTS:Bovine retinal arteries showed myogenic tone at pressures higher than 10 mm Hg. This pressure-induced contraction was absent in calcium-free Krebs-Ringer bicarbonate solution. Inhibition of L-type voltage-operated calcium channels with nifedipine (1 microM) suppressed the myogenic contraction. After depolarization of the vascular smooth muscle cells with a K+ 120 mM solution, a pressure-induced contraction was still observed, indicating that besides stimulation of voltage-operated calcium channels, depolarization-independent mechanisms contribute to the pressure-induced myogenic vasoconstriction. CONCLUSIONS: Isolated bovine retinal arteries spontaneously contract when exposed to raised intraluminal pressure. This response depends on extracellular calcium and is blocked by nifedipine. In addition, depolarization-independent mechanisms seem to be involved.
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