Desipramine induces relaxation in depolarized rat renal arteries, likely by interfering with calcium-mediated smooth muscle contraction.
Desipramine's effects in isolated rat arteries should not alter clinical practice; leaves open mechanistic and translational studies in human vessels.
Depolarization of the isolated renal artery of the rat by a potassium-rich solution caused a triphasic response. The artery contracted submaximally then relaxed partially, this relaxation being followed by a slowly developing contracture. Desipramine reduced the height of the initial contraction, increased the relaxation and reduced the contracture. The latter action was antagonized by increasing the calcium ion concentration of the depolarizing solution. Calcium caused a contraction of the depolarized artery and the contraction was reduced by the drug. The results suggest that the relaxation of the depolarized artery produced by desipramine may be due to interference with the action of calcium in initiating and maintaining a contraction of the arterial smooth muscle.
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Hrdina et al. (1967) studied this question.
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