EFFECTS OF ^|^ldquo;LIVING HIGH AND TRAINING LOW^|^rdquo; ON PULMONARY CIRCULATION HEMODYNAMICS AND ENDOTHELIAL NITRIC OXIDE SYNTHASE PROTEIN EXPRESSION IN PULMONARY ARTERY OF RATS

2009 ◽  
Vol 58 (2) ◽  
pp. 285-294
Author(s):  
TOMOYA KASHIWAGI ◽  
TOMONOBU SAKURAI ◽  
KAZUHIRO MINAMI ◽  
KENTA SUZUKI ◽  
OSAMU KASHIMURA
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pulmonary Artery ◽  
Protein Expression ◽  
Pulmonary Circulation ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
And Training

Estrogen Upregulates Endothelial Nitric Oxide Synthase Gene Expression in Fetal Pulmonary Artery Endothelium

1997 ◽  
Vol 81 (3) ◽  
pp. 355-362 ◽  
Author(s):  
Amy N. MacRitchie ◽  
Sandy S. Jun ◽  
Zhong Chen ◽  
Zohre German ◽  
Ivan S. Yuhanna ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pulmonary Artery ◽  
Endothelial Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Heat shock protein 90 modulates endothelial nitric oxide synthase activity and vascular reactivity in the newborn piglet pulmonary circulation

2007 ◽  
Vol 292 (6) ◽  
pp. L1515-L1525 ◽  
Author(s):  
Judy L. Aschner ◽  
Susan L. Foster ◽  
Mark Kaplowitz ◽  
Yongmei Zhang ◽  
Heng Zeng ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Heat Shock ◽  
Nitric Oxide Synthase ◽  
Heat Shock Protein ◽  
Pulmonary Circulation ◽  
Endothelial Nitric Oxide Synthase ◽  
Vascular Reactivity ◽  
Heat Shock Protein 90 ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Heat shock protein 90 (Hsp90) binding to endothelial nitric oxide synthase (eNOS) is an important step in eNOS activation. The conformational state of bound Hsp90 determines whether eNOS produces nitric oxide (NO) or superoxide (O2•−). We determined the effects of the Hsp90 antagonists geldanamycin (GA) and radicicol (RA) on basal and ACh-stimulated changes in vessel diameter, cGMP production, and Hsp90:eNOS coimmunoprecipitation in piglet resistance level pulmonary arteries (PRA). In perfused piglet lungs, we evaluated the effects of GA and RA on ACh-stimulated changes in pulmonary arterial pressure (Ppa) and perfusate accumulation of stable NO metabolites (NOx−). The effects of GA and RA on ACh-stimulated O2•− generation was investigated in cultured pulmonary microvascular endothelial cells (PMVEC) by dihydroethidine (DHE) oxidation and confocal microscopy. Hsp90 inhibition with GA or RA reduced ACh-mediated dilation, abolished the ACh-stimulated increase in cGMP, and reduced eNOS:Hsp90 coprecipitation. GA and RA also inhibited the ACh-mediated changes in Ppa and NOx− accumulation rates in perfused lungs. ACh increased the rate of DHE oxidation in PMVEC pretreated with GA and RA but not in untreated cells. The cell-permeable superoxide dismutase mimetic M40401 reversed GA-mediated inhibition of ACh-induced dilation in PRA. We conclude that Hsp90 is a modulator of eNOS activity and vascular reactivity in the newborn piglet pulmonary circulation. Uncoupling of eNOS with GA or RA inhibits ACh-mediated dilation by a mechanism that involves O2•− generation.

Maturation-related changes in endothelial nitric oxide synthase immunolocalization in developing ovine lung

1994 ◽  
Vol 267 (5) ◽  
pp. L585-L591 ◽  
Author(s):  
A. C. Halbower ◽  
R. M. Tuder ◽  
W. A. Franklin ◽  
J. S. Pollock ◽  
U. Forstermann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Pulmonary Circulation ◽  
Endothelial Nitric Oxide Synthase ◽  
Vascular Tone ◽  
Pulmonary Arteries ◽  
Fetal Lung ◽  
Fetal Life ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

It is unknown whether high fetal pulmonary vascular tone is due in part to absent or decreased endothelial nitric oxide synthase (eNOS), the enzyme that produces nitric oxide in the vascular endothelium. To determine the timing of appearance and maturational changes of eNOS in the developing pulmonary circulation, we performed immunohistochemistry in lungs from fetal, neonatal, and adult sheep. Using a mouse monoclonal antibody against bovine aortic eNOS, we found immunoreactive eNOS selectively in the endothelium and it was present at all fetal ages. Immunoreactivity was seen as early as 29% gestation in the developing capillaries coursing through fetal mesenchyme. By 6 days after birth, immunoreactivity was decreased in most vessels and nearly absent in the distal pulmonary arteries of adult animals. We conclude that immunoreactive eNOS is present very early in fetal life and appears to decrease postnatally. We speculate that the early presence of eNOS in the fetal lung supports a possible role for endogenous nitric oxide activity in the regulation of vascular tone or angiogenesis in the developing pulmonary circulation.

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