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Effect of alveolar (ventilation) hypoxia on conversion of angiotensin I to II and inactivation of bradykinin in the cat lung
Vol. 16, No . 5
Conference Abstracts
82 5
purpose is served by their effects on bronchial muscle?
Handbook of Experimental Pharmacology, 25, Br
1.L.G . ERDOS,
EFFECT OF ALVEOLAR (VENTIIATION) HYPOXIA ON CONVERSION OF ANGIOTENSIN I TO II AND INACTIVATION OF BRADYRININ IN THE CAT LUNG M. Leibawitz, G. Turino, and L .M . Greenbaum Departments of Pharmacology and Medicine, College of Physicians and Surgeons Columbia University, New York There is substantial evidence that the lung is the major Bite for enzymatic conversion of angiotenain I (ang I) to the potent vasoconstrictor and pressor octapeptide, angiotenain II (ang II) . Little is known, however, regarding possible effects of alterations in lung physiologic conditions on the ang I converting process . A change in the normal ability of the lung to metabolize ang I could contribute to or modify disturbances in systemic and/or pulmonary circulatory function occurring in pathophyaiologic states in which ang II may participate, e .g ., renal hypertension, hemorrhagic shock, and perhaps hypoxiainduced pulmonary hypertension . In the present study, alveolar (ventilation) hypoxia was investigated in the _in situ cat lung for its affects on the conversion of ang I to II and inactivation of bradykinin (bk) . Ang I (670 pmol/ml), ang II amide(2gg, pmol/ml), and bk (1 .0 ug/ml)_in Locks solution were each infused via the main pulmonary artery during ventilation with air (control) or hypoxic gee mixtures . Peptide activity in the pulmonary venous effluent was determined by bioassay using the isometric contractions of the isolated rat uterus, and ang II amide or bk as standards . It was found that during air ventilation (n~14), 62 .7+1 .5 percent (x±s .e .) of the ang I was converted to ang II . By contrast, is lungéventilated with 100 percent N20 (n~6) or 5 percent Op in N2 (n~5), conversion was significantly enhanced (p< .001) to 94 .2+2 .5 percent and 91 .6±2 .6 percent, respectively . Inactivation of bk was 90 percent or more under both control and hypoxic conditions . These data indicate that the lung ang I converting process is influenced by ventilatioy conditions . The mechanism for the enhanced conversion during hypoxia is unlmown. Supported by GM-00438 and HL 15832 . ROLE OF RALLIKREIN-KININ SYSTEM IN SflOCK Egil Amundeen Institute for Surgical Research, Rikshospitalet, Oalo 1, Norway Shock is not an entity in itself, but rather an adaptive response to lifethreatening injury of multiple origin . Several types of shock can be recognized and each of them run through several stages . The importance of plasma kinina for pathophyaiological phenomena occurring during : a) cardiogenic, b) vasagenic, c) hypovolemic, and d) anaphylactic shock is discussed . The central role of plasma prekallikrein in activation of the kinin system, fibrinolytic system, extrinsic and intrinsic coagulation systems, and the complement system is discussed in relation to the activation of factor XII that occurs during various types of shock. It is also pointed out that kidney kallikrein excretion via
Conference Abstracts
82 5
purpose is served by their effects on bronchial muscle?
Handbook of Experimental Pharmacology, 25, Br
1.L.G . ERDOS,
EFFECT OF ALVEOLAR (VENTIIATION) HYPOXIA ON CONVERSION OF ANGIOTENSIN I TO II AND INACTIVATION OF BRADYRININ IN THE CAT LUNG M. Leibawitz, G. Turino, and L .M . Greenbaum Departments of Pharmacology and Medicine, College of Physicians and Surgeons Columbia University, New York There is substantial evidence that the lung is the major Bite for enzymatic conversion of angiotenain I (ang I) to the potent vasoconstrictor and pressor octapeptide, angiotenain II (ang II) . Little is known, however, regarding possible effects of alterations in lung physiologic conditions on the ang I converting process . A change in the normal ability of the lung to metabolize ang I could contribute to or modify disturbances in systemic and/or pulmonary circulatory function occurring in pathophyaiologic states in which ang II may participate, e .g ., renal hypertension, hemorrhagic shock, and perhaps hypoxiainduced pulmonary hypertension . In the present study, alveolar (ventilation) hypoxia was investigated in the _in situ cat lung for its affects on the conversion of ang I to II and inactivation of bradykinin (bk) . Ang I (670 pmol/ml), ang II amide(2gg, pmol/ml), and bk (1 .0 ug/ml)_in Locks solution were each infused via the main pulmonary artery during ventilation with air (control) or hypoxic gee mixtures . Peptide activity in the pulmonary venous effluent was determined by bioassay using the isometric contractions of the isolated rat uterus, and ang II amide or bk as standards . It was found that during air ventilation (n~14), 62 .7+1 .5 percent (x±s .e .) of the ang I was converted to ang II . By contrast, is lungéventilated with 100 percent N20 (n~6) or 5 percent Op in N2 (n~5), conversion was significantly enhanced (p< .001) to 94 .2+2 .5 percent and 91 .6±2 .6 percent, respectively . Inactivation of bk was 90 percent or more under both control and hypoxic conditions . These data indicate that the lung ang I converting process is influenced by ventilatioy conditions . The mechanism for the enhanced conversion during hypoxia is unlmown. Supported by GM-00438 and HL 15832 . ROLE OF RALLIKREIN-KININ SYSTEM IN SflOCK Egil Amundeen Institute for Surgical Research, Rikshospitalet, Oalo 1, Norway Shock is not an entity in itself, but rather an adaptive response to lifethreatening injury of multiple origin . Several types of shock can be recognized and each of them run through several stages . The importance of plasma kinina for pathophyaiological phenomena occurring during : a) cardiogenic, b) vasagenic, c) hypovolemic, and d) anaphylactic shock is discussed . The central role of plasma prekallikrein in activation of the kinin system, fibrinolytic system, extrinsic and intrinsic coagulation systems, and the complement system is discussed in relation to the activation of factor XII that occurs during various types of shock. It is also pointed out that kidney kallikrein excretion via