Diabetic nephropaty, in the initial stages, is characterized by hyperf
iltration and proteinuria. The mechanism underlying this hyperfiltrati
on is not fully understood, but it is possible that it could be due, a
t least partially, to a decreased response of glomerular structures to
some vasoconstrictor mediators. It has been suggested that captopril
can decrease the diabetes-related proteinuria by lowering the hyperfil
tration. In our experiments, we tried to assess the contractile respon
se of glomeruli from control rats, diabetic rats and diabetic rats rec
eiving captopril, in the presence of some vasoconstrictor agonists (An
giotensin II, Platelet Activating Factor, Epidermal Cell Growth Factor
and Phorbol Myristate Acetate). In all cases we observed a smaller co
ntractile response in diabetic glomeruli than in controls. Likewise, w
e saw a trend of captopril treatment to normalize this smaller respons
e, but differences did not reach statistical significance in all cases
. In summary, our results show that the smaller contractile response o
f diabetic glomeruli, seems to be due to an alteration in the intracel
lular mechanisms of contraction. At least partially, the beneficial ef
fect of captopril under these circumstances, could lie in a partial im
provement of this defect.