Aims: 

The renin angiotensin system plays important roles in pathogenesis of various pulmonary diseases as pulmonary hypertension and lung fibrosis. The contractile effects of angiotensinogen (Aogen) and its metabolisation pathways were studied on rat pulmonary artery (RPA) and vein (RPV) rings with or without endothelium.

Methods: 

We quantified Aogen – induced contractions in the presence or in the absence of pepstatin A (a renin inhibitor, 10 mM), captopril (an ACE inhibitor, 10 mM), chymostatin (a chymase inhibitor, 10 mM), amastatin (an aminopeptidase-A and -M inhibitor) or losartan (a specific AT1 blocker, 10 mM).

Results: 

On all rings, Aogen-induced contractions were only reduced by pepstatin A (with two thirds on RPA and one third on RPV) or captopril (with a half on RPA and at least 35% for RPV), amplified by amastatin (with 27.96 ± 5.86% on RPA and 11,72 ± 7.03% for RPV) and totally prevented by losartan. The Aogen contractile effects were powerfully on bronchi obtained from ovalbumin-sensitized rats (after challenge) but these differences were blocked by chimostatin, which did not significantly modify Aogen-induced contractions on normal rats. The enzymes effects were not influenced by the presence or absence of intact endothelium.

Conclusion: 

It is suggested that pulmonary vessels possess a local renin-angiotensin system and there is the possibility of angiotensin production within the vessel walls using various and physiological circumstances – dependent enzymatic pathways.