Membrane imidazoline receptors (I-1) are present in smooth muscles. We used the endogenous I-1 agonist agmatine (1 µM to 10 mM), and the specific antagonist efaroxan (0.1 mM), aorta as a typical tonic muscle and uterus as a phasic one. Aorta rings from male adult Wistar rats and uterine horn fragments from virgin female rats were studied in isometric conditions, in oxygenated saline solution (bicarbonate buffer, pH 7.2Ð7.4), at 37 °C (animals were killed by decapitation; all experiments conformed to local/national guidelines). Submaximal contractions were induced in the aorta by 10^-5 M phenylephrine and in the uterus by 10^-5 M carbachol; results are expressed as % active tension (mean ± S.E.M.; n = 6). Agmatine does not affect aortic relaxation induced by 0.01 M carbachol. It partially relaxes (maximum 58.6 ± 8.3 % at 10 mM agmatine; IC₅₀ ~213 µM) aorta rings precontracted by phenylephrine; there was similar inhibition with agmatine pretreatment; both effects are abolished by efaroxan; contractile force initially (1 min) developed is not significantly influenced by agmatine. Agmatine does not alter the baseline tone of uterine smooth muscle, but inhibits carbachol-induced contraction and reduces mean active force to 62.8 ± 4.9 % (maximal at 10 mM agmatine; IC₅₀ ~460 µM) based upon frequency reduction (maximum 67.4 ± 4.6% IC₅₀ ~423 µM) without significant changes in the amplitude of transient contractions, not altered by efaroxan. In the aorta agmatine inhibits the maintenance of contractile force acting on I-1 receptors endothelium independently. In the uterus agmatine inhibits the phasic contraction by an I-1-independent mechanism apparently absent in the aorta.

All procedures accord with current national guidelines.