Spontaneous and pharmacologically-induced vasoconstrictive responses of rat aortic rings are attenuated by balloon angioplasty.

The effects of arterial dilatation with differently sized PTCA catheters on prestretch-induced, receptor-induced and voltage-induced vasoconstriction was investigated. Rat aortic rings were kept incubated in HEPES buffer for 0,3,6, and 12 hours before mounting in the experimental set-up for contraction measurements. Balloon dilation (BD) was applied prior to incubation or directly before measurement following a period of incubation. Isometric force was measured after applying a prestretch to the vascular rings. The ring then contracted spontaneously or, if not, was brought to contraction by norepinephrine (NE, 50 microM) or potassium ions (K+, 30 mM). Prestretch-induced vasoconstriction reached maximum values after 6 hours of incubation. NE-induced vasoconstriction was maximal at 6 hours of incubation and K(+)-induced vasoconstriction kept rising up to 12 hours of incubation. The addition of enoximone resulted in vasodilatation (ED50 = 0.1 microM) of prestretch-induced vasoconstriction, but was less potent (ED50 = 168 microM) if added to NE-induced or K(+)-induced vasoconstricted rings. BD applied before the incubation period reduced prestretch-induced, receptor-induced and voltage-induced contractions (the effectivity decreasing in that order) and did not elicit vasospastic activity. BD applied after the incubation period and immediately before the contraction measurements prevented the occurrence of prestretch-induced spontaneous contractions, caused a nonsignificant (p = 0.08) decrease of NE-induced vasoconstriction, and had no effect on K(+)-induced vasoconstriction. It is concluded that this model to study spontaneous and induced vasoactivity elucidates the consequences of the application of balloon dilatation in nonatherosclerotic vascular rings.