[RAAS changes due to dysfunction of pulmonary ventilation].

Abstract

OBJECTIVE: RAAS was determined to investigate the relationship between their changes and the dysfunction of pulmonary ventilation for evaluating the pathogenesis of early pulmonary hypertension in chronic bronchitis with or without emphysema. METHODS: Angiotensin II (AT II), plasma renin activity (PRA) and aldosterone (Ald) were determined at 8:00 AM in sitting position for 30 minutes in 12 heathy nonsmokers, 50-60 years old, with normal functions of small airway, normal FEV1 and lung volumes, and in 23 patients with chronic bronchitis with or without emphysema. RESULTS: All patients with chronic bronchitis showed dysfunction of small airway with or without abnormalities of FEV1 and lung volumes. In healthy control group, the plasma PRA, AT II and Ald levels were 0.22 +/- 0.12 microgram.L-1.h-1 (x +/- sx), 52 +/- 7 ng/L and 315 +/- 26 pmol/L respectively comparing with those levels of 0.43 +/- 0.11 microgram.L-1.h-1, 197 +/- 32 ng/L and 388 +/- 59 pmol/L in aged patients with chronic bronchitis. It was found that dysfunction of small airway alone could cause remarkable elevation of PRA and AT II levels. In patients with mild pulmonary emphysema, the levels of PRA and AT II were significantly increased. The moderate pulmonary emphysema induced greatly increase of PRA, AT II and Ald levels. In patients with severe pulmonary emphysema, however, the plasma levels of PRA and AT II were significantly attenuated from the levels in moderate pulmonary emphysema while Ald level was still getting higher. There were no evidence to indicate the relationship between the changes of RAAS and hypoxemia. CONCLUSION: The elevation of AT II and PRA might partly be the pathogenesis of early pulmonary hypertension in COPD.