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We compared the effects of calcium entry blockers on myogenic tone with the effects of these compounds on agonist- and depolarization-induced mechanical responses in isolated rings of the rabbit facial vein. The development of intrinsic tone in response to distension of the vessel wall and its potentiation by increasing the ambient temperature were antagonized by MnCl2 (0.5 mM) but not verapamil, diltiazem, or nifedipine. Similarly, the contractile response to histamine was blocked by MnCl2 but was unaffected by moderate concentrations of the organic calcium entry blockers. The histamine contractile response elicited at 34 degrees C (a condition which abolishes intrinsic tone) was also refractory to verapamil (10(-6) M). Verapamil, diltiazem, and nifedipine antagonized the contractile response to calcium in depolarized facial vein rings. Thus both extrinsic and intrinsic contractile responses in the rabbit facial vein depend on an extracellular source of calcium. The distension-operated channels are unique in exhibiting a marked temperature sensitivity. However, receptor- and distension-operated calcium channels can be distinguished from the voltage-operated channels in their insensitivity to the organic calcium entry blockers.