Details of Drug Interaction | MecDDI

Drug General Information (ID: DDITDB89FX)
Drug Name			Diazoxide		Drug Info		Chloral hydrate		Drug Info
Drug Type		Small molecule				Small molecule
Therapeutic Class		Antihypertensive Agents				Anxiolytics/Sedatives/Hypnotics
Structure

Mechanism of Diazoxide-Chloral hydrate Interaction (Severity Level: Moderate)
Additive hypotensive effects Click to Show/Hide Mechanism Graph

Drug Name		Diazoxide				Chloral hydrate
Mechanism 1		Hypotensive effects ATP-sensitive inward rectifier potassium channel Inducer				Antihypertensive agent
Key Mechanism Factor 1
		Factor Name		Inward rectifier potassium channel				Structure Sequence
		Protein Family		Inward rectifier-type potassium channel (TC 1.A.2.1) family
		Protein Function		This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium (By similarity). Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with ABCC9. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation. Click to Show/Hide
Mechanism Description		Additive hypotensive effects by the combination of Diazoxide and Chloral hydrate
Mechanism 2		Hypotensive effects ATP-sensitive inward rectifier potassium channel Inducer				Hypotensive effects
Key Mechanism Factor 2
		Factor Name		Inward rectifier potassium channel				Structure Sequence
		Protein Family		Inward rectifier-type potassium channel (TC 1.A.2.1) family
		Protein Function		This receptor is controlled by G proteins. Inward rectifier potassium channels are characterized by a greater tendency to allow potassium to flow into the cell rather than out of it. Their voltage dependence is regulated by the concentration of extracellular potassium; as external potassium is raised, the voltage range of the channel opening shifts to more positive voltages. The inward rectification is mainly due to the blockage of outward current by internal magnesium. Can be blocked by extracellular barium (By similarity). Subunit of ATP-sensitive potassium channels (KATP). Can form cardiac and smooth muscle-type KATP channels with ABCC9. KCNJ11 forms the channel pore while ABCC9 is required for activation and regulation. Click to Show/Hide
Mechanism Description		Additive hypotensive effects by the combination of Diazoxide and Chloral hydrate

Recommended Action
Management		Caution and close monitoring for development of hypotension is advised during coadministration of these agents. Avoid alcohol in patients receiving vasodilating antihypertensive drugs. Patients should be advised to avoid rising abruptly from a sitting or recumbent position and to notify their physician if they experience dizziness, lightheadedness, syncope, orthostasis, or tachycardia.

References
1	Ellison JM, Milofsky JE, Ely E "Fluoxetine-induced bradycardia and syncope in two patients." J Clin Psychiatry 51 (1990): 385-6. [PMID: 2211552]
2	Feder R "Bradycardia and syncope induced by fluoxetine." J Clin Psychiatry 52 (1991): 139. [PMID: 2005082]
3	Sternbach H "Fluoxetine-associated potentiation of calcium-channel blockers." J Clin Psychopharmacol 11 (1991): 390-1. [PMID: 1770159]