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Departments of Cell Biology and Physiology, Pediatrics, and Biochemistry and Molecular Biology, University of New Mexico Health Sciences Center, Albuquerque, New Mexico 87131
We previously demonstrated augmented
endothelium-derived nitric oxide (EDNO)-dependent pulmonary arterial
dilation and increased arterial endothelial nitric oxide synthase
(eNOS) levels in chronic hypoxic (CH) and monocrotaline (nonhypoxic)
models of pulmonary arterial hypertension. Therefore, we hypothesized
that the long-term elevation of arterial eNOS levels associated with CH
is related to pulmonary hypertension or some factor(s) associated with
hypertension and not directly to hypoxia. To test this hypothesis, we
examined responses to the EDNO-dependent dilator ionomycin in
U-46619-constricted, isolated, saline-perfused lungs from control rats,
CH (4 wk at 380 mmHg) rats, and rats previously exposed to CH but
returned to normoxia for 4 days or 2 wk. Microvascular pressure was
assessed by double-occlusion technique, allowing calculation of
segmental resistances. In addition, vascular eNOS immunoreactivity was
assessed by quantitative immunohistochemistry, and eNOS mRNA abundance was determined by RT-PCR assays. Our findings indicate that 4-day and
2-wk posthypoxic rats exhibit persistent pulmonary hypertension, likely
due to maintained arterial remodeling and polycythemia associated with
prior exposure to CH. Furthermore, arterial dilation to ionomycin was
augmented in lungs from each experimental group compared with controls.
Finally, arterial eNOS immunoreactivity and whole lung eNOS mRNA levels
remained elevated in posthypoxic animals. These findings suggest that
altered vascular mechanical forces or vascular remodeling contributes
to enhanced EDNO-dependent arterial dilation and upregulation of
arterial eNOS in various models of established pulmonary hypertension.
quantitative immunohistochemistry; reverse transcription-polymerase chain reaction; endothelial nitric oxide synthase; pulmonary hypertension; vascular remodeling
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