Angiogenesis is known to be triggered by various stimuli including hyperten
sion. It was previously found that NO-deficient hypertension is accompanied
by structural remodeling of the cardiac muscle and large coronary arteries
. This study was aimed to examine the qualitative subcellular alterations o
f capillaries in the heart of the rats treated with L-NAME (40 mg/kg/day fo
r 4 weeks). The results showed that long-lasting inhibition of NO productio
n induced an apparent activation of fibroblast function. This was associate
d with enhancement of fibrotization as well as with the induction of angiog
enesis. Accordingly, fibroblasts were frequently located in the vicinity of
capillary pericytes. which was followed bi their detachment and migration.
Moreover, besides inactive or, even injured capillaries. the other ones ex
hibited extensive proteosynthetic activity linked to capillary growth, prol
iferation and migration of endothelial cells. The results strongly indicate
enhanced triggering of the angiogenesis ill L-NAME-induced NO-deficient hy
per-tension.