Relationship between Cytosolic Ca2+ Level and Contractile Tension in Canine Basilar Artery of Chronic Vasospasm

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Abstract
IN ORDER TO study the role of the Ca2+/calmodulin/myosin light chain kinase system in the development of chronic vasospasm caused by subarachnoid hemorrhage, the cytosolic Ca2+ level ([Ca2+]i), measured with fura-2, a fluorescent Ca2+ indicator, and contractile tension were measured simultaneously, and their quantitive correlation was examined in basilar arterial tissue obtained from the canine “two-hemorrhage” model. Sixteen adult mongrel dogs were divided into two groups, control (n = 8) and vasospasm (n = 8), and were killed 7 days after the first experimental subarachnoid hemorrhage. In basilar arterial tissue loaded with fura-2, 1) [Ca2+]i in the resting condition was not significantly different between the two groups; 2) the increment in [Ca2+]i induced by 40 mmol/L K+ stimulation was significantly smaller in vasospastic tissue (P < 0.01); and 3) 40 mmol/L K+-induced tension development per cross-sectional area for a fixed increment in [Ca2+]i was significantly greater in vasospastic tissue (P < 0.01). In tissue not loaded with fura-2, active myogenic tone, which was tentatively represented by the ratio of tonus relaxed with 10−4 mol/L papaverine to initial resting tone, was significantly greater in vasospastic tissue (P < 0.05). These findings, coupled with recent reports concerning the ratio of phosphorylated myosin light chain, indicate the following about vasospastic arterial tissue in vitro: 1) in the resting condition, augmented myogenic tone, which is not accompanied by [Ca2+]i elevation, is probably not attributable to the Ca2+/calmodulin/myosin light chain kinase system, and by contrast, 2) at a higher level of [Ca2+]i, a stronger contraction for a fixed increment in [Ca2+]i is induced by Ca2+ sensitization mechanisms of the calmodulin/myosin light chain kinase system.