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Published on: October 20, 2013
Pulmonary PKG-1 is upregulated following chronic hypoxia
Nikki L Jernigan1, Benjimen R Walker, Thomas C Resta
1Dept. of Cell Biology and Physiology, Univ. of New Mexico Health Sciences Center, 915 Camino de Salud NE, Albuquerque, NM 87131-5218, USA. njernigan@salud.unm.edu
Summary
Chronic hypoxia attenuates pulmonary vasodilation. This study found that while protein kinase G-1 (PKG-1) is involved, its increased expression and activity in chronic hypoxia do not explain the reduced vasodilation to 8-bromoguanosine 3
Area of Science:
- Physiology
- Cardiovascular Research
- Pulmonary Hypertension
Background:
- Pulmonary vasodilation mediated by nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) is attenuated following chronic hypoxia (CH).
- Previous studies demonstrated reduced vasodilatory responses to exogenous NO and cGMP analogs in CH.
- The role of protein kinase G-1 (PKG-1) in this attenuated response remains unclear.
Purpose of the Study:
- To investigate the hypothesis that decreased protein kinase G-1 (PKG-1) expression or activity mediates attenuated pulmonary vasodilation to 8-bromoguanosine 3',5'-cyclic monophosphate (8-BrcGMP) following chronic hypoxia (CH).
Main Methods:
- Isolated, saline-perfused rat lungs from control and CH groups were used.
- Vasodilatory responses to 8-BrcGMP were assessed with and without PKG inhibitors (Rp-8-Br-PET-cGMPS and KT-5823).
- PKG-1 expression and activity were quantified in lung homogenates and vasculature via Western blot and immunohistochemistry.
Main Results:
- PKG inhibition attenuated 8-BrcGMP vasodilation in both control and CH lungs, confirming PKG's role.
- Contrary to the hypothesis, PKG-1 expression was approximately twofold greater in CH lungs compared to controls.
- This PKG-1 upregulation was localized to the vasculature and correlated with increased PKG activity in CH.
Conclusions:
- Protein kinase G-1 (PKG-1) plays a role in mediating 8-BrcGMP-induced vasodilation.
- Attenuated pulmonary vasodilation following chronic hypoxia (CH) is not due to decreased PKG-1 expression or activity.
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