The spontaneous tone of vascular smooth muscle is augmented in hypertension. The present study examined the role played by nitric oxide (NO), cyclooxygenase (COX), TP and EP-1 receptors, reactive oxygen species and large-conductance Ca²⁺-activated K⁺ channels (BK_Ca) in the regulation of spontaneous tone in renal arteries of young or mature Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Rings of arteries, with and without endothelium, were suspended in a myograph for isometric force recording. Spontaneous tone (increase above initial tension) was observed only in arteries of mature SHR and was larger in the absence of endothelium. L-NAME (inhibitor of NO synthases) induced contractions which were larger in arteries of SHR than those of WKY. Indomethacin (COX inhibitor), SC19220 (EP-1 receptor antagonist), or terutroban (TP receptor antagonist) reduced the L-NAME-evoked contractions. Tiron (superoxide anion scavenger), catalase (enzyme that degrades H₂O₂) and deferoxamine (hydroxyl radical scavenger) augmented the L-NAME-induced contractions in arteries of mature SHR. Charybdotoxin (BK_Ca blocker) caused contractions in arteries of mature SHR without endothelium and in rings with endothelium incubated with L-NAME. A decreased protein level of eNOS, an increased release of prostacyclin, and an increased expression of EP-1 receptors were observed in arteries of mature SHR. The present study suggests that the occurrence of spontaneous tone is precipitated by age and hypertension. The reduced production of NO, leading to decreased activation of BK_Ca, may leave the actions of endogenous vasoconstrictors unopposed. COX products that activate EP-1 and TP receptors are involved in the development of spontaneous tone.