JPET Celsis microsomes equal better data

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Journal of Pharmacology And Experimental Therapeutics, Vol. 155, Issue 1, 42-49, 1967
Copyright © 1967 by American Society for Pharmacology and Experimental Therapeutics


A POSSIBLE ROLE FOR TISSUE CALCIUM IN RESERPINE SUPERSENSITIVITY

Oliver Carrier Jr. 1, Shoji Shibata 1, and Walter Lee Lewis III 1

1 Department of Pharmacology, University of Mississippi Medical Center, Jackson, Mississippi

Dog femoral artery calcium content decreased from 7.5 ± 0.6 to 5.5 ± 0.1 mEq/kg d.wt. 24 hr after 0.5 mg/kg of reserpine (P <.02), and to 3.5 ±1.0 and 3.9 ± 0.3 mEq/kg d.wt. after 0.2 and 0.1 mg/kg of reserpine respectively 24 and 48 hr prior. Rat aortic calcium fell from 9.4 ± 0.4 to 7.4 ± 0.4 mEq/kg d.wt. 24 hr after 5 mg/kg of reserpine (P <.001). One group of rabbits (2 kg) had no significant drop in aortic calcium 24 hr after 4 mg/kg of reserpine, while another group (1 kg) had a decrease in aortic calcium from 62 ± 0.4 to 2.6 ± 0.4 mEq/kg d.wt. ( P <.01). Aortic calcium of the older rabbits after 2 hr in zero calcium Ringer's solution fell to 2.5 ± 0.5 ( P .01). Aortic strips were tested for supersensitivity to catechol amines. No significant potentiation could be elicited in the older group with 10-10 to 10-5 M epinephrine or norepinephnine. In the young group, significant supersensitivity was obtained at 10-10 to 10-5 M norepinephrine. None of the preparations were supersensitive to KC1. It is suggested from the data that tissue calcium is involved in supersensitivity. This could be due to an increased membrane permeability and an increased excitability due to the calcium deficiency. It could also be due to an increased available pool of ionized calcium.

Submitted on May 16, 1966
Accepted on July 7, 1966







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Copyright © 1967 by the American Society for Pharmacology and Experimental Therapeutics.