It is suggested that vasoconstriction mediated by angiotensin II cleaved from angiotensin I by angiotensin converting enzyme (ACE) is counterbalanced by concomitant formation of vasodilator angiotensin (1-7) by neutral endopeptidase (NEP). Here, we tested this hypothesis using as a bioassay the isolated rat lung perfused with Krebs-Henseleit (KH) solution and ventilated with negative pressures. Addition of angiotensin I (100 nM) into the isolated lung resulted in an immediate increase in pulmonary arterial pressure (Delta PAP) which was not accompanied by a significant change in respiratory lung function or weight of the lung.
View Article and Find Full Text PDFRecent evidence suggests that hypoxic pulmonary vasoconstriction (HPV) is mediated by hypoxia-induced closure of voltage-gated potassium channels in pulmonary vascular smooth muscle cells. It is also claimed that various vasoconstrictor mediators such as thromboxane A2 (TXA2), platelet activating factor (PAF), cysteinyl leukotrienes (cys-LTs) or endothelin-1 (ET-1) contribute to HPV. Their role, however, has not been unequivocally accepted.
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