Objektive: Voltage gated calcium channels (Ca_v) are involved in the excitation- contraction mechanism of renal resistance vessels and play an essential role in regulation of renal blood flow and glomerular filtration rate. T-type Ca_v (Ca_v3.2) has recently been shown to be involved in relaxation of coronary arteries. We investigated the involvement of T-type channels in dilatation of efferent arterioles. Methods: Microdissected perfused mouse efferent arterioles, PCR on microdissected vessels and immunohistochemistry. Results: In efferent arterioles a transient vasoconstriction was observed in response to depolarization with potassium (7.9 mm ± 0.3 to 0.1 mm ± 0.1) lasting for 16.2 ± 7.0 seconds. A T type antagonist, nickel 10^-6M blocking Ca_v3.2, changed the postassium elicited constriction to a sustained response lasting 48.2 ± 1.1 seconds. Inhibition of eNOS by L-NAME (5·10^-5M) or deletion of eNOS had similar effect on the vasoconstrictor response. PCR analysis showed expression of T-type subtypes Ca_v3.1 and Ca_v3.2 in microdissected efferent arterioles and immunohistochemistry revealed Ca_v3.1 in mouse efferent arterioles. Furthermore, Ca_v3.2 protein was observed in endothelia and vascular smooth muscle cells in rat renal vasculature. Whether Ca_v3.2 was involved in dilator responses in general was tested using acetylcholine. U46619 (10^-6M) resulted in a luminal diameter of 1.4 ± 1.4mm and acetylcholine (10^-6M) increased the luminal diameter to 7.6 ± 0.2mm. L-NAME abolished the acetylcholine induced dilation whereas Ca_v3.2 inhibition by nickel had no effect. Conclusion: T-type channels Ca_v3.2 are involved in the spontaneous dilatation occurring in renal efferent arterioles after the initial constriction that follows a depolarization.