In recent years, transgenic mouse models have been developed to examine the underlying cellular and molecular mechanisms of lung disease and pulmonary vascular disease such as asthma, pulmonary thromboembolic disease, and pulmonary hypertension. However, there has not been systematic characterization of the basic physiological pulmonary vascular reactivity in normal and transgenic mice. This represents an intellectual 'gap' since it is important to characterize basic murine pulmonary vascular reactivity in response to various contractile and relaxant factors to which the pulmonary vasculature is exposed under physiological conditions. The current study evaluates excitation- and pharmacomechanical-contraction coupling in pulmonary arteries (PA) isolated from wild-type Balb c mice. We demonstrate that both pharmaco- and electro-mechanical coupling mechanisms exist in mice PA. These arteries are also reactive to stimulation by ₁-adrenergic agonists, serotonin, endothelin-1, vasopressin, and U46619 (a thromboxane A₂ analogue). We conclude that the basic vascular responsiveness of mouse pulmonary arteries is similar to those observed in pulmonary arteries of other species, including rat, pig, and human, albeit on a different scale and to varying amplitudes.