Enhancement and prolongation of vascular smooth muscle contraction by aldosterone

Isolated rings of rabbit thoracic aorta were mounted in tissue baths for the measurement of isometric tension development and desipramine was added to all baths to block neuronal uptake of catecholamines. When these vessels were contracted to a steady-state of 1.5-3.5 g with norepinephrine, the addition of 1, 10 and 100 microM aldosterone caused a further contraction of 0.09, 0.47 and 0.8 g, respectively. Vessels contracted with norepinephrine and exposed to aldosterone were also immersed in mineral oil to trap a finite amount of norepinephrine within the receptor compartment of the tissue and the rate of relaxation was measured. The time to relax 50% (t1/2) in the presence of 100 microM aldosterone was approximately 18 min, while that in the presence of either ethanol diluent or 10 microM aldosterone was 7 min. When maximally effective concentrations of aldosterone and deoxycorticosterone acetate were used, the increases in norepinephrine-induced contractions and relaxation t1/2 values caused by these agents were identical. Combining these agents did not produce additive effects. Aldosterone also increased contractions and t1/2 values in tissues contracted with epinephrine but not in those contracted with methoxamine or 5-hydroxytryptamine. These findings support the conclusion that aldosterone enhances and prolongs contraction by inhibiting the removal of catecholamines from the receptor compartment of vascular smooth muscle.