Renin-angiotensin system has long been thought to be a classic endocrine ne
gative feedback system in the pathophysiology of hypertension. Furthermore,
angiotensin II formation was believed to be regulated by renin secreted fr
om the kidneys. In contrast to these considerations is the identification o
f local angiotensin ZI production in other tissues than pulmonary vasculatu
re. Prorenin, the molecular precursor of renin, has been assumed to be invo
lved in local angiotensin II production because of its renin-like activity.
Prorenin has also been found to be secreted from extrarenal sources, altho
ugh a major part of it is derived from the kidneys. Increased concentration
of total renin in serum has been proposed to be useful in identifying pati
ents with active proliferative retinopathy in insulin-dependent diabetic pa
tients. Renin-angiotensin system is strongly affected by angiotensin-conver
ting enzyme (ACE) inhibitors and therefore the interfering effect of ACE in
hibitor medication on total renin concentration should be known in order to
interpret serum total renin concentrations. Nine hypertensive outpatients,
all men, treated at the department of internal medicine in Turku Universit
y Central Hospital, received randomly 5 mg of ramipril or 95 mg of metoprol
ol once a day for 4 weeks. Ramipril significantly increased the mean value
of total renin (191.9 ng/l vs 312.0 ng/l, p<0.01), but the metoprolol-induc
ed increase in the concentration of serum total renin was insignificant. We
conclude that the negative feedback mechanism in regulating renin and pror
enin secretion was inhibited by ACE inhibitor ramipril but beta(1)-selectiv
e adrenoceptor antagonist metoprolol did not significantly change total ren
in concentration in serum.