Previous studies from our laboratory have demonstrated enhanced arterial, but not venous, vasodilatory responses to endothelium-derived nitric oxide (EDNO)-dependent agonists in lungs from chronically hypoxic (CH) rats. Others have provided evidence that pulmonary constitutive NO synthase (cNOS) may be upregulated following CH and in other forms of pulmonary hypertension. We hypothesized that if pulmonary hypertension is responsible for the augmented arterial reactivity to EDNO-dependent dilators following CH, then similar responses should be observed in lungs from rats with monocrotaline (MC)-induced pulmonary hypertension. We examined responses to the EDNO-dependent pulmonary vasodilator arginine vasopressin (AVP) in isolated, saline-perfused lungs from male Sprague-Dawley rats 3 wk following administration of MC (105 mg/kg s.c.) or saline vehicle. AVP (2.5 nM) was administered to lungs preconstricted with the thromboxane mimetic U-46619. Microvascular pressure was assessed by the double occlusion technique allowing calculation of segmental resistances. Total and arterial baseline resistances were significantly greater in lungs from MC-treated rats compared to controls. Arterial, but not venous, dilation to AVP was augmented in lungs from MC-treated vs. control rats. We conclude that the enhanced arterial dilation to AVP in lungs from both CH and MC-trealed rats may reflect a common response to pulmonary hypertension. Further, these data suggest that pulmonary arterial hypertension may selectively upregulate cNOS within the pulmonary arterial vasculature.
|Original language||English (US)|
|State||Published - 1996|
ASJC Scopus subject areas
- Molecular Biology