Zinc mediated vasoconstriction in the isolated perfused rat lung

Hypoxic pulmonary vasoconstriction (HPV) is a complex multifactorial physiological response resulting in the shunting of blood flow to oxygen rich areas of the lung. Recent data from our laboratory suggest that zinc signaling plays a role in the effects of acute hypoxia mediated nitric oxide biosynthesis, and this pathway contributes to HPV. The objective of this study was to assess the ability of the pulmonary vasculature to constrict in response to exogenous zinc. We used the isolated perfused rat lung to determine the effect of exogenous zinc on pulmonary arterial pressure (PaP). Dose‐dependent constriction was observed in response to zinc supplied in the perfusate. The response to zinc was independent of the oxygen tension of the inspirate, as vasoconstriction was observed under both hypoxic and normoxic conditions. In addition, removing Ca 2+ from the perfusate had no effect on the ability of Zn to induce changes in PaP; suggesting that Zn‐mediated constriction may be Ca 2+ independent. These data provide evidence that Zn induces pulmonary vasoconstriction and suggest that this response may be via a novel mechanism independent of oxygen tension or Ca 2+ . Funded by RHL081421‐01.