Research Article| Volume 86, ISSUE 1, P21-26, January 1992

Transpulmonary angiotensin II formation and pulmonary haemodynamics in stable hypoxic lung disease: the effect of captopril

  • A.J. Peacock
    To whom correspondence should be addressed at: Department of Respiratory Medicine, Western Infirmary, Glasgow G11 6NT, U.K.
    Wessex Right Heart Group, Southampton General Hospital, Southampton and Queen Alexandra Hospital, Portsmouth, U.K.
    Search for articles by this author
  • A. Matthews
    Wessex Right Heart Group, Southampton General Hospital, Southampton and Queen Alexandra Hospital, Portsmouth, U.K.
    Search for articles by this author
      This paper is only available as a PDF. To read, Please Download here.
      The effect of chronic hypoxic lung disease on the activity of the renin-angiotensin (RA) system and the role the RA system plays in the pulmonary vascular changes that accompany hypoxia remain controversial. We have measured transpulmonary generation of angiotensin II (A II) and pulmonary haemodynamics in nine patients with airflow obstruction (mean FEV1=0.741) and arterial hypoxaemia (mean PaO2 = 8.4Pa) before and after captopril. In each patient pulmonary artery pressure, cardiac output, systemic arterial pressure, arterial and mixed venous blood gas tensions and arterial and mixedvenous A II were measured at rest and at intervals for a total of 3 h after 25 mg captopril orally. The patients had moderate pulmonary hypertension (mean = 29 mmHg) and slightly raised A II levels (mean = 47.2 pg ml) but no step-up in AII levels across the lung. After captopril, both arterial and mixed venous All levels fell by, on average 80% (sem 2%), but the transpulmonary gradient for A II remained unchanged for each subject. The systemic arterial pressure fell by an average 18% (sem 5%). In seven patients pulmonary vascular resistance fell (mean = 31 %, sem 6%) and in two patients it rose. Therewas no significant change in blood gas tensions. These findings suggest that patients with chronic hypoxic lung disease have decreased conversion of A I to A II in the lung but stimulation of the extra- pulmonary renin-angiotensin system. ACE inhibition appears to cause a fall in PVR in most patients with severe chronic airflow obstruction without deterioration in gas exchange.
      To read this article in full you will need to make a payment

      Purchase one-time access:

      Academic & Personal: 24 hour online accessCorporate R&D Professionals: 24 hour online access
      One-time access price info
      • For academic or personal research use, select 'Academic and Personal'
      • For corporate R&D use, select 'Corporate R&D Professionals'


      Subscribe to Respiratory Medicine
      Already a print subscriber? Claim online access
      Already an online subscriber? Sign in
      Institutional Access: Sign in to ScienceDirect


        • Berkov S
        Hypoxic pulmonary vasoconstriction in the rat: the necessary role of angiotensin II.
        Circ Res. 1974; 35: 256-261
        • Farber MO
        • Roberts LR
        • Weinberger MH
        • Robertson GL
        • Fineberg NS
        • Manfredi F
        Abnormalities of sodium and H2O handling in chronic obstructive lung disease.
        Arch Intern Med. 1982; 142: 1326-1330
        • Milledge JS
        • Catley DM
        • Ward MP
        • Williams ES
        • Clark CRA
        Renin-aldosterone and angiotensin converting enzyme during prolonged altitude exposure.
        J Appl Physiol. 1983; 55: 699-702
        • Jederlini P
        • Hill NS
        • Chang Ou L
        • Fanburg BL
        Lung angiotensin converting enzyme activity in rats with differing susceptibilities to chronic hypoxia.
        Thorax. 1988; 43: 703-707
        • Stalcup SA
        • Lipset JS
        • Woan JM
        • Leuenberger PJ
        • Mellins RB
        Inhibition of angiotensin converting enzyme activity in cultured endothelial cells by hypoxia.
        J Clin Invest. 1979; 63: 966-976
        • Shepard JM
        • Joyner WL
        • Gilmore JP
        Hypoxia does not alter angiotensin converting enzyme activity in hamster pulmonary microvessels.
        Circ Res. 1987; 61: 228-235
        • Krulewitz AH
        • Fanburg BL
        The effect of oxygen tension on the in vivo production and release of angiotensin converting enzyme by bovine pulmonary artery endothelial cells.
        AmRev Resp Dis. 1984; 130: 866-869
        • Dusterdieck G
        • McElwee G
        Estimation of Angiotensin II concentration in human plasma by radio- immunoassay. Some applications to physiological and clinical states.
        Eur J Clin Invest. 1971; 2: 32-38