Autonomic and renal effects of intravenous diazoxide. A study of the mechanisms of its hypotensive action in man

The Use of Diazoxide in Hypertensive Crises with Particular Reference to the Control of Hypertension in Severe Renal Failure

“…As indicated above, in contrast to other thiazides, diazoxide has a sodium retaining effect on the renal tubule and can, while effectively controlling the blood pressure, lead to oedema (Leonetti et al,'1970) particularly during prolonged administration.…”

Diazoxide

“…This is thought to be the result of increased tubular reabsorption, since it has been shown to persist in spite of an increase in glomerular filtration rate and therefore in the filtered load of sodium (Hamby et al, 1968).· Free water clearance and total urine flow are also significantly decreased (Johnson, 1968). Leonetti et al (1970) have shown that water excretion was more than halved and that sodium excretion was reduced to about 60 % of control values, within 30 minutes of the intravenous administration of 300 mg diazoxide, and that these changes remained over a period of 2 hours.…”

“…In hypertensive water loaded subjects, Johnson (1968), noted that intravenous injections of diazoxide (4 mg/kg) were associated with immediate reductions in the clearance rates of p-aminohippurate (PAH) and inulin, i.e, decreases in renal plasma flow (RPF) and glomerular filtration rate (GFR), Leonetti et al (1970) in hypertensive subjects obtained a significant reduction in the creatinine clearance rate (occurring within 30 minutes of the intravenous injection of 300 mg diazoxide) which remained approximately of the same magnitude over a 2 hour period. The clearance rate of PAH was variable (increasing in a few subjects), but overall being slightly, though not significantly, decreased.…”

“…In association with these changes, diazoxide causes an immediate and marked decrease in urinary sodium excretion (Hamby et al, 1968;Kakaviatos et al, 1967Kakaviatos et al, , 1968Leonetti et al, 1970;Thompson et al, 1966). This is thought to be the result of increased tubular reabsorption, since it has been shown to persist in spite of an increase in glomerular filtration rate and therefore in the filtered load of sodium (Hamby et al, 1968).· Free water clearance and total urine flow are also significantly decreased (Johnson, 1968).…”