Activator of ATP-dependent K⁺ channels; antihypertensive.

<B>Diazoxide</B> increases K<SUP>+</SUP> efflux: like Cromakalim, it opens 86 Rb<SUP>+</SUP>-permeable K<SUP>+</SUP> channels in vascular smooth muscle (aorta and portal vein). In the insulin-secreting cell line RINm5F, in the continued presence of ATP, <B>Diazoxide</B> 200 &mu;M evokes a marked and sustained activation of ATP-inhibited channels. <B>Diazoxide</B> mediates its effects through the activation of ATP-sensitive K<SUP>+</SUP> channels.<BR><br>Used as an antihypertensive agent because of its arterial smooth muscles vasodilator activity. It has vascular effects on embryo and foetus. Perifusion of 10 &mu;M decreases integrated spontaneous contractions of the rat portal vein to 22 %. In the rabbit aorta, inhibited vasoconstrictor responses to Angiotensin II, Noradrenaline and low concentrations (<=30 mM) of KCl, the antivasoconstrictor activities being abolished in vessels depolarized with >= 35 mM K<SUP>+</SUP>. <br><br>Its hyperglycaemic effect is correlated with its ability to induce the opening of the ATP-regulated K<SUP>+</SUP> channels in mouse pancreatic beta-cells. 30 mg/kg caused a more than 2-fold increase in plasma glucose in rats and prevented any return toward base line within 1.5 hour after a glucose load.<br><br>
<B>Diazoxide </B>has the opposite effect to glucose: hyperpolarizing the cell membrane, it abolishes the glucose-induced release of insulin.<BR><br>It is also an antidiuretic agent.

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