| pubmed-article:2429075 | pubmed:abstractText | The effects of indoramin on sympathetic neuroeffector transmission in rabbit isolated blood vessels were examined. Indoramin reduced the contractions of pulmonary artery evoked by electrical-field stimulation. The IC50 was 7.4 X 10(-8) M. In the presence of cocaine + corticosterone + propranolol, the IC50 was 5 X 10(-7) M. Amphetamine did not antagonize the steady-state inhibition caused by indoramin. Indoramin caused a slight enhancement of the field-stimulation-evoked 3H-overflow from pulmonary artery preloaded with 3H-noradrenaline. In the presence of cocaine + corticosterone + propranolol, indoramin also enhanced the stimulation-evoked 3H-overflow slightly. The effect of indoramin on stimulation-evoked 3H-overflow depended only slightly on stimulation frequencies (1-30 Hz): small enhancement at 1 Hz and nonsignificant changes at 3-30 Hz. Pretreatment with indoramin did not attenuate the inhibitory effect of clonidine on the stimulation-evoked 3H-overflow seen with bretylium. Indoramin and desmethylimipramine reduced the 3H-accumulation by aorta preloaded with 3H-noradrenaline. The IC50 was 3 X 10(-5)M (indoramin) and 10(-8)M (desmethylimipramine). Indoramin inhibited the contractions of aorta evoked by noradrenaline, phenylephrine, histamine and serotonin in a competitive manner. The corresponding pA2 values were 7.54, 7.98, 7.45, and 6.61. Indoramin decreased the maximal contractions of rabbit aorta evoked by potassium. These results suggest that indoramin is a potent competitive antagonist of postsynaptic alpha 1-adrenoceptors, while it may only have a slight inhibitory effect on presynaptic alpha 2-adrenoceptors. Indoramin is devoid of bretylium-like adrenergic neurone blocking activity, while it may act as reserpine. It is a weak inhibitor of the uptake-1 mechanism.(ABSTRACT TRUNCATED AT 250 WORDS) | lld:pubmed |
