Evidence is presented that glucocorticoids (GC) and mineralocorticoids (MC) control contractility of vascular smooth muscle (VSM). This control is effected through the in situ mechanism for the action of these steroids in the arterial and arteriolar wall. This action is mediated through GC and MC receptors in the VSM cell. Acting through these receptors, MC and GC increase transport capacities of different transmembrane transport systems for Na+ and/or Ca2+ through induction of synthesis of proteins constituting the transport systems. Colocalization of enzymes deactivating cortisol in VSM, with VSM receptors for GC and MC further strengthens the concept that the arterial network houses an in situ molecular mechanism for the control of VSM contractility, thus peripheral vascular resistance.