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Vol. 283, Issue 2, 619-624, 1997
Divisions of
Neuroscience and Biomedical Systems (M.R.M., E.D.J.,
K.M.M.) and
Biochemistry and Molecular Biology (L.P., M.D.H.),
Institute of Biomedical and Life Sciences, University of Glasgow,
Glasgow, Scotland
Phosphodiesterase (PDE) activity was determined in pulmonary arteries
removed from control and chronic hypoxia-induced pulmonary hypertensive
rats. The main, first-branch, intrapulmonary and resistance pulmonary
arteries were studied. We measured total cAMP PDE activity and cGMP PDE
activity, as well as that of individual isoforms (PDE1-5). cAMP PDE
activity in chronic hypoxic rats was increased in first-branch and
intrapulmonary arteries from hypoxic rats. No changes were observed in
the main or resistance pulmonary arteries. Similarly, cGMP PDE activity
was increased in the main, first-branch and intra-pulmonary arteries of
the hypoxic rats. No changes in cGMP PDE activity were observed in
resistance arteries. There was evidence for PDE1-5 activity in all
pulmonary arteries. The increased cAMP PDE activity in first-branch and
intrapulmonary vessels was associated with an increase in
cilostimide-inhibited PDE (PDE3) activity. Increased total cGMP PDE in
main pulmonary artery was associated with increases in
Ca++/calmodulin-stimulated (PDE1) activity. An increase in
zaprinast-inhibited (PDE5) activity was observed in first-branch and
intrapulmonary arteries. Our results suggest that decreases in
intracellular cyclic nucleotide levels in pulmonary arteries from
pulmonary hypertensive rats are associated with increased PDE activity. Further, these changes may reflect alterations at the level of specific
types of PDE isoforms.
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