The Effect of Progesterone on Spontaneous and Agonist-Evoked Contractions of the Rat Aorta and Portal Vein

The mechanisms underlying the suppression of vasocontractility caused by progesterone were investigated by studying changes in the contractile force of rat isolated aorta and portal vein, induced by altering extracellular concentrations of noradrenaline (NA) potassium ions (K+) and calcium ions (Ca2+). In the aorta, progesterone (10 μM) had a general suppressive effect on NA‐, Ca2+‐ and K+‐induced contractions. In contrast, in the portal vein a more selective suppression of contractions was observed. Both tonic and phasic components of contractions induced by cumulative addition of Ca2+ to tissues equilibrated in Ca2+‐free saline were suppressed. The phasic but not tonic components of contractions induced by NA addition were suppressed. There was no significant effect on tonic contractions induced by elevated (40–120 mM) K+, but a concentration‐dependent suppression of the phasic component of contractions was observed during depolarisation with smaller elevations of K+ concentrations (5–20 mM). These results suggest that on the portal vein the suppressive effect of progesterone is due to a potassium channel opening action, whilst on the aorta a different or additional mechanism of suppression exists.