Vasoconstrictor effects of aldosterone in isolated vascular tissue.

Isolated rings of rabbit ear artery or thoracic aorta were prepared for the measurement of isometric contraction. Treatment of ear artery with 1 X 10(-4)M aldosterone had no effect. However, in ear artery pretreated with 1 X 10(-7)M desipramine to block the catecholamine neuronal uptake process, 1 X 10(-6), 1 X 10(-5) and 1 X 10(-4)M aldosterone elicited contractions of 0.16, 0.48 and 1.31 g, respectively. Phentolamine, 1 X 10(-7)M, an alpha adrenoceptor antagonist, both prevented and reversed the aldosterone-induced contractions. Desipramine-pretreated thoracic aortas were contracted to a steady-state of 1-2 g with norepinephrine and immersed in mineral oil to prevent diffusion of drugs from the tissue. Relaxation, which reflects the rate of tissue inactivation of norepinephrine, was markedly slowed by exposure of these tissues to either aldosterone, deoxycorticosterone acetate (an inhibitor of the catecholamine-extraneuronal uptake process) or the combination of these steroids prior to oil immersion. It is concluded that in the ear artery, endogenous norepinephrine was spontaneously released from intramural nerves and that aldosterone blocked the catecholamine extraneuronal uptake process within the muscle coat allowing the concentration of norepinephrine to increase well above the threshold for contraction.