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The bioluminescent calcium indicator aequorin was chemically loaded into isolated strips of ferret portal vein and ferret aorta. Aequorin light emission (a function of [Ca2+]i) was recorded simultaneously with tension. Assuming an [Mg2+]i of 0.5 mM, [Ca2+]i was 1.8 X 10(-7) M in the unstimulated portal vein at 22 degrees C where there was negligible resting tone. In contrast, in the unstimulated aorta at 22 degrees C where there was significant basal tone, the [Ca2+]i was 2.7 X 10(-7) M. In both portal vein and aorta, potassium depolarization caused a monophasic rise in intracellular Ca2+ in parallel with the rise in tension, whereas phenylephrine caused an initial spike of light during the period of the force development which then fell to a much lower plateau level during the period of force maintenance. Calcium-force curves were generated by plotting calibrated aequorin light against force while intracellular [Ca2+] was made to change either by increasing degrees of potassium depolarization or decreasing extracellular [Ca2+]. The steady-state calcium-force curve in the presence of phenylephrine was shifted to the left of the curve in the presence of potassium depolarization in both the portal vein and aorta. In the aorta there was a counter-clockwise hysteresis in the calcium-force relationship. In contrast, in the portal vein there was no demonstrable hysteresis, indicating that the apparent change in calcium sensitivity of the contractile apparatus in the presence of phenylephrine must be caused by a second messenger other than calcium.

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