To determine the possible role of Ca²⁺‐activated K⁺ (K_Ca) channels in the regulation of resting tone of arteries from spontaneously hypertensive rats (SHR), the effects of agents which interact with these channels on tension and ⁸⁶Rb efflux were compared in endothelium‐denuded strips of carotid, femoral and mesenteric arteries from SHR and normotensive Wistar‐Kyoto rats (WKY). Strips of carotid, femoral and mesenteric arteries from SHR exhibited a myogenic tone; that is, the resting tone decreased when either the Krebs solution was changed to a 0‐Ca²⁺ solution or 10⁻⁷ m nifedipine was added. The addition of charybdotoxin (ChTX, 10⁻⁹−10⁻⁷ m), a blocker of large conductance K_Ca channels, to the resting strips of these arteries produced a concentration‐dependent contraction, which was significantly greater in SHR than in WKY. Relatively low concentrations of tetraethylammonium (0.05–5 mm) produced a concentration‐dependent contraction which was similar to the ChTX‐induced contraction in these strips. The ChTX‐induced contractions in SHR were greatly attenuated by 10⁻⁷ m nifedipine and by 3 × 10⁻⁶ m cromakalim, a K⁺ channel opener. Cromakalim alone abolished the myogenic tone in SHR. The addition of apamin (a blocker of small conductance K_Ca channels, up to 10⁻⁶ m), or of glibenclamide (a blocker of ATP‐sensitive K⁺ channels, up to 5 × 10⁻⁶ m), to the resting strips failed to produce a contraction. In resting strips of carotid, femoral and mesenteric arteries preloaded with ⁸⁶Rb, the basal ⁸⁶Rb efflux rate constants were significantly greater in SHR than in WKY. The addition of 10⁻⁷ m nifedipine to the resting strips decreased the basal ⁸⁶Rb efflux rate constants only in SHR. The cellular Ca²⁺ uptake in the resting state of carotid and femoral arteries from SHR was significantly increased when compared to WKY, and this increase in SHR was significantly reduced by 10⁻⁷ m nifedipine. These results suggest that the ChTX‐sensitive K_Ca channels were highly activated to regulate the myogenic tone in the resting state of carotid, femoral and mesenteric arteries from SHR. The increased K_Ca channel functions in SHR arteries appeared to be secondary to the increased Ca²⁺ influx via L‐type voltage‐dependent Ca²⁺ channels in the resting state of these arteries.

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