Adrenal component to pulmonary hypertension caused by nicotine administration in the dog.
In this study, we investigated the possibility that the adrenal gland contributes to nicotine-induced pulmonary hypertension using a canine left lower lung lobe (LLL) preparation that was pump-perfused with mixed venous blood at constant flow and outflow pressure. Main pulmonary artery, left atrial, and LLL arterial pressures were monitored to assess the responses of the animal's intact right lung and isolated LLL. With the adrenal venous return intact, injection of 10-26 micrograms/kg nicotine into the left ventricle or ascending aorta resulted in a 42% increase in LLL arterial pressure and a 70% increase in the pulmonary arterial-left atrial pressure gradient (Ppa-Pla). When the adrenal venous return was interrupted, the increases in LLL arterial pressure and Ppa-Pla were reduced to 6 and 10%, respectively. The LLL response could be eliminated by alpha-adrenergic receptor blockade, suggesting that adrenal catecholamines may contribute to the pulmonary hypertension induced by nicotine infusion.
D000311:Adrenal Glands / Q000187:drug effects / Q000502:physiology*; D000818:Animals; D003714:Denervation; D004285:Dogs; D006439:Hemodynamics / Q000187:drug effects; D006976:Hypertension, Pulmonary / Q000139:chemically induced*; D008168:Lung / Q000294:innervation; D009538:Nicotine / Q000494:pharmacology*; D011652:Pulmonary Circulation / Q000187:drug effects*; D013233:Stellate Ganglion / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects
D009538:Nicotine