Many of the interactions of hydrochlorothiazide are due to their effects on fluid and electrolyte imbalance. Diuretic-induced hypokalemia may enhance the toxicity of digitalis glycosides, and may also increase the risk of arrhythmias with drugs that prolong the QT interval such as astemizole, terfenadine, halofantrine, pimozide and sotalol. Thiazide may enhance the neuromuscular blocking action of competitive muscle relaxants probably by their hypokalaemic effect. The potassium-depleting effect of diuretics may be enhanced by corticosteroids, corticotropin, β2 agonists such as salbutamol, carbenoxolone, amphotericin B, or reboxetine. Diuretics may enhance the effect of other antihypertensives particularly the first-dose hypotension that occurs with α blockers or ACE inhibitors. Orthostatic hypotension associated with diuretic therapy may be enhanced by concomitant ingestion of alcohol, barbiturates or opioids. The antihypertensive effects of diuretics may be antagonized by drugs that cause fluid retention, such as corticosteroids, NSAIDS, or carbenoxolone. Thiazides have been reported to diminish the response to pressor amines, such as noradrenaline (norepinephrine), but the clinical significance of this effect is uncertain. Thiazide diuretics should not usually be used with lithium salts since the association may lead to toxic blood concentration of lithium. Other drugs which increased toxicity had been reported when given with thiazides include allopurinol and tetracyclines. Thiazide may alter the requirement for hypoglycemic in diabetic patients.