Methyclothiazide is an orally active antihypertensive agent and a diuretic agent. Methyclothiazide leads to a reduction of the vascular response to the action of endogenous vasoconstricting stimuli, such as Norepinephrine (HY-13715). Methyclothiazide is against voltage-dependent Ca-channel (VDCC) activity in vitro.

Methyclothiazide (0-100 μM) induces endothelium-dependent inhibition of the vasoconstrictor responses to NE and AVP only in aortas from SHR, and the maximal vasoconstrictive effect of Norepinephrine (HY-13715) and arginine vasopressin (AVP) is decreased by 59% and 32.3 %, respectively.
Methyclothiazide (0-100 μM) induces inhibitory effect on the contractile response to Norepinephrine (HY-13715) is abolished by N-nitro-L-arginine (NOLA) but not indomethacin.
Methyclothiazide (100 μM) affects the vascular responses to extracellular Ca²⁺ under high-K⁺ depolarizing conditions. It can reduce Ca²⁺ contracture in a high-K⁺, Ca²⁺-free solution. The maximal contracture is reduced by 90.4%.

西域 has not independently confirmed the accuracy of these methods. They are for reference only.

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