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Effect of acute footshock stress on the responsiveness of the isolated rat tail artery to phenylephrine and epinephrine.

Angelina Zanesco, S. De-Moraes

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Abstract

The effects of acute footshock stress on the sensitivity of the isolated rat tail artery were studied. Footshock stress applied to male Wistar rats (200-300 g) causes subsensitivity to the vasoconstrictor effects of phenylephrine and epinephrine. No significant changes in the pA2 values of prazosin were detected, using epinephrine as the agonist. Footshock stress-induced subsensitivity to epinephrine was not affected by the calcium entry blocker nifedipine. However, nifedipine significantly depressed the maximum response to epinephrine in tail arteries isolated from acute footshock-stressed rats. The present results suggest that acute footshock stress-induced reduced sensitivity to phenylephrine and epinephrine may not be only related to events at the alpha-adrenoceptor level. The nifedipine-induced depression of the maximum response to epinephrine suggests a role for the calcium mobilization processes in the vascular responsiveness during acute stress.

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The effects of acute footshock stress on the sensitivity of the isolated rat tail artery were studied. Footshock stress applied to male Wistar rats (200-300 g) causes subsensitivity to the vasoconstrictor effects of phenylephrine and epinephrine. No significant changes in the pA2 values of prazosin were detected, using epinephrine as the agonist. Footshock stress-induced subsensitivity to epinephrine was not affected by the calcium entry blocker nifedipine. However, nifedipine significantly depressed the maximum response to epinephrine in tail arteries isolated from acute footshock-stressed rats. The present results suggest that acute footshock stress-induced reduced sensitivity to phenylephrine and epinephrine may not be only related to events at the alpha-adrenoceptor level. The nifedipine-induced depression of the maximum response to epinephrine suggests a role for the calcium mobilization processes in the vascular responsiveness during acute stress.

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Available abstract

The effects of acute footshock stress on the sensitivity of the isolated rat tail artery were studied. Footshock stress applied to male Wistar rats (200-300 g) causes subsensitivity to the vasoconstrictor effects of phenylephrine and epinephrine. No significant changes in the pA2 values of prazosin were detected, using epinephrine as the agonist. Footshock stress-induced subsensitivity to epinephrine was not affected by the calcium entry blocker nifedipine. However, nifedipine significantly depressed the maximum response to epinephrine in tail arteries isolated from acute footshock-stressed rats. The present results suggest that acute footshock stress-induced reduced sensitivity to phenylephrine and epinephrine may not be only related to events at the alpha-adrenoceptor level. The nifedipine-induced depression of the maximum response to epinephrine suggests a role for the calcium mobilization processes in the vascular responsiveness during acute stress.

Key concepts: Epinephrine, Phenylephrine, Prazosin, Nifedipine, Internal medicine, Medicine, Endocrinology, Norepinephrine

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Effect of acute footshock stress on the responsiveness of the isolated rat tail artery to phenylephrine and epinephrine. — Research Paper | ScholarLens