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In this study, we ascertained which voltage-gated Ca<jats:sup>2+<\/jats:sup>channels are expressed in rat cerebral arterial smooth muscle and determined their contribution to the myogenic response. mRNA analysis revealed that the \u03b1<jats:sub>1<\/jats:sub>-subunit of L-type (Ca<jats:sub>v<\/jats:sub>1.2) and T-type (Ca<jats:sub>v<\/jats:sub>3.1 and Ca<jats:sub>v<\/jats:sub>3.2) Ca<jats:sup>2+<\/jats:sup>channels are present in isolated smooth muscle cells. Western blot analysis subsequently confirmed protein expression in whole arteries. With the use of patch clamp electrophysiology, nifedipine-sensitive and -insensitive Ba<jats:sup>2+<\/jats:sup>currents were isolated and each were shown to retain electrical characteristics consistent with L- and T-type Ca<jats:sup>2+<\/jats:sup>channels. The nifedipine-insensitive Ba<jats:sup>2+<\/jats:sup>current was blocked by mibefradil, kurtoxin, and efonidpine, T-type Ca<jats:sup>2+<\/jats:sup>channel inhibitors. Pressure myography revealed that L-type Ca<jats:sup>2+<\/jats:sup>channel inhibition reduced tone at 20 and 80 mmHg, with the greatest effect at high pressure when the vessel is depolarized. In comparison, the effect of T-type Ca<jats:sup>2+<\/jats:sup>channel blockade on myogenic tone was more limited, with their greatest effect at low pressure where vessels are hyperpolarized. Blood flow modeling revealed that the vasomotor responses induced by T-type Ca<jats:sup>2+<\/jats:sup>blockade could alter arterial flow by \u223c20\u201350%. Overall, our findings indicate that L- and T-type Ca<jats:sup>2+<\/jats:sup>channels are expressed in cerebral arterial smooth muscle and can be electrically isolated from one another. 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