The Relationship Between Calcium and Increased Sensitivity of Rabbit Aortae Four Hours After Reserpine

Abstract

Four hours after reserpine, rabbit aortic strips were supersensitive to acetylcholine, isoprenaline and noradrenaline. The threshold concentration of the drugs necessary to induce a response was less and the maximum tension developed by the tissues was greater than in control strips. Reserpine‐treatment potentiated the contractile responses to CaCl2. Reserpine‐treatment resulted in an increase in calcium uptake and an increase in the slow component of 45Ca2+ efflux. After resperine‐treatment, the rate of relaxation from a potassium‐induced contraction was decreased. It is concluded that reserpine‐induced supersensitivity is related to an enhanced ability of the tissue to retain and utilize calcium.

Effects of short‐ and long‐term sympathectomy on vasoconstrictor responses of the rat mesenteric arterial bed

“…Potentiation of responses of the mesenteric vasculature to 5-HT, methoxamine and NA by ouabain is consistent with a role for membrane depolarization and a decrease in the activity ofthe Na + /K + pump in denervation supersensitivity; however, absent or weak augmentation by ouabain of responses to ATP, vasopressin and endothelin is in contrast to the marked denervation supersensitivity to these agents, suggesting that other factors may be involved. Changes in permeability or binding of calcium have been suggested to occur after denervation (Carrier & Hester, 1976;Fleming, 1987).…”

“…De-nervation supersensitivity can be prejunctional, resulting from an increase in the concentration of transmitter at the postjunctional site due to a loss of uptake of neurotransmitter into the nerve terminal (Trendelenburg, 1966). Partial depolarization of the smooth muscle has been suggested to account for non-specific postjunctional denervation supersensitivity (Aprigliano & Hermsmeyer, 1977;Abel et al, 1981) and may be related to a decrease in Na+/K+ pump activity as well as to a change in permeability or binding to calcium (Carrier & Hester, 1976;Fleming, 1987). In the guinea-pig vas deferens (Fleming, 1987) and rabbit ear artery (Bevan, 1989) inhibition of the Na+/K+ pump with ouabain in vitro caused depolarization of the cell membrane and was able to mimic the effects Bridsh Joumal of Phamacology (1996) 119, 1347 1354 of denervation.…”

MECHANISM OF NORADRENALINE POTENTIATION BY PROSTAGLANDIN E2 IN RAT MESENTERIC ARTERY

“…The mechanism by which reserpine and bretylium quantitatively affected prostaglandin enhancement of NA vasoconstriction is not yet known, but an additive effect with reserpine might be expected if PGE2 was acting in a similar way to reserpine. Reserpine-induced supersensitivity has been attributed to an enhanced ability of the reserpine-treated tissue to retain and utilise Ca2 + (Carrier & Hester, 1976 Couper & Mclennan 1978).…”

Effects of 6-Hydroxydopamine Pretreatment on in vivo Femoral Arterial Responses to Vasodilator Agents

“…Reserpine has been reported to alter calcium content [Carrier and Shibata, 1967;Hudgins and Harris, 1970;Carrier et al. 1970] and transport [Carrier and Hester. 1976;Garrett and Carrier, 1971;De Felice and Joiner, 1976;Kaiman and Shibata, 1978] in vascular preparations.…”