F VIII coagulant, F VHI-related antigen and F VIII ristocetin cofactor activity were significantly increased in 68 patients with various chronic renal diseases. All three F VIII functions correlated generally well with each other. A striking relationship between some F VIII activities and serum creatinine was detectable in patients with glomerulonephritis and kidney transplants, with mild or moderate renal insufficiency. This correlation was no longer present in terminal renal failure. The results suggest that in initial stages of renal disease elevated F VIII levels may be attributable to glomerular endothelial damage. In terminal renal failure, however, increased F VIII concentrations seem to result from nonspecific causes related to uremia such as acute phase reactions.

In seven patients with uncomplicated essential hypertension the effects of an acute alpha-adrenergic blockade, alone and combined with a chronic beta-adrenergic blockade, on blood pressure, renal function as measured by standard clearance methods, plasma renin activity, and plasma aldosterone were evaluated. Acute alpha-adrenergic blockade with phentolamine (20 mg by intravenous infusion) significantly enhanced the antihypertensive effect of chronic beta-adrenergic blockade with slow-oxprenolol (160 mg/ day X 14 days) (- 14.5% verus - 7.4% for pulse pressure, - 12.4% versus - 6.0% for diastolic pressure, 2 alpha less than 0.05). Under combined adrenergic blockade renal plasma flow increased, glomerular filtration rate and filtration fraction decreased (2 alpha less than 0.05 each), whereas the fractional clearances of sodium, potassium, free water, and solute load remained unchanged. The activation of the renin-angiotensin-axis, elicited by alpha-adrenergic blockade alone, was suppressed by the preceding beta-adrenergic blockade. These findings demonstrate a favourable antihypertensive action of a combined blockade of alpha- und beta-adrenergic receptor sites without untoward side effects on renal function or the renin-angiotensin-axis.

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