| Indication | Used parentally to treat hypertensive emergencies. Also used to treat hypoglycemia secondary to insulinoma. |
| Pharmacodynamics | Diazoxide is a potassium channel activator, which causes local relaxation in smooth muscle by increasing membrane permeability to potassium ions. This switches off voltage-gated calcium ion channels which inhibits the generation of an action potential. |
| Mechanism of action | As a diuretic, diazoxide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like diazoxide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of diazoxide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle. As a antihypoglycemic, diazoxide inhibits insulin release from the pancreas, probably by opening potassium channels in the beta cell membrane. |
| Absorption | Readily absorbed following oral administration. |
| Volume of distribution | Not Available |
| Protein binding | Very high (more than 90%) to serum proteins. |
| Metabolism | Hepatic. |
| Route of elimination | Proglycem is extensively bound (more than 90%) to serum proteins, and is excreted in the kidneys. |
| Half life | 28 ±8.3 hours in normal adults. |
| Clearance | Not Available |
| Toxicity | Oral LD50 in rat and mouse: 980 mg/kg and 444 mg/kg, respectively. |