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J Appl Physiol 85: 1070-1078, 1998;
8750-7587/98 $5.00
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Vol. 85, Issue 3, 1070-1078, September 1998

Regulation of the endogenous NO pathway by prolonged inhaled NO in rats

Deborah U. Frank1, Damian J. Horstman1, Geoffrey N. Morris2, Roger A. Johns2, and George F. Rich2

Departments of 1 Biomedical Engineering and 2 Anesthesiology, University of Virginia Health System, Charlottesville, Virginia 22906-0010

Nitric oxide (NO) modulates the endogenous NO-cGMP pathway. We determined whether prolonged inhaled NO downregulates the NO-cGMP pathway, which may explain clinically observed rebound pulmonary hypertension. Rats were placed in a normoxic (N; 21% O2) or hypoxic (H; 10% O2) environment with and without inhaled NO (20 parts/million) for 1 or 3 wk. Subsequently, nitric oxide synthase (NOS) and soluble guanylate cyclase (GC) activity and endothelial NOS (eNOS) protein levels were measured. Perfusate cGMP levels and endothelium-dependent and -independent vasodilation were determined in isolated lungs. eNOS protein levels and NOS activity were not altered by inhaled NO in N or H rats. GC activity was decreased by 60 ± 10 and 55 ± 11% in N and H rats, respectively, after 1 wk of inhaled NO but was not affected after 3 wk. Inhaled NO had no effect on perfusate cGMP in N lungs. Inhaled NO attenuated the increase in cGMP levels caused by 3 wk of H by 57 ± 11%, but there was no rebound in cGMP after 24 h of recovery. Endothelium-dependent vasodilation was not altered, and endothelium-independent vasodilation was not altered (N) or slightly increased (H, 10 ± 3%) by prolonged inhaled NO. In conclusion, inhaled NO did not alter the endogenous NO-cGMP pathway as determined by eNOS protein levels, NOS activity, or endothelium-dependent vasodilation under N and H conditions. GC activity was decreased after 1 wk; however, GC activity was not altered by 3 wk of inhaled NO and endothelium-independent vasodilation was not decreased.

nitric oxide; pulmonary hypertension; chronic hypoxia; nitric oxide synthase; guanylate cyclase; cyclic 3',5'-guanosine monophosphate; pulmonary vasodilation


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