All Phenotypes S100a1<tm1Jhh> MGI Mouse

increased lung endothelial cell apoptosis ( J:230300 )

• endothelial cells show increased basal apoptosis

• exposure of endothelial cells to the pro-apoptotic TNF-alpha increases apoptosis to a higher rate than in wild-type endothelial cells

abnormal lung vasculature morphology ( J:230300 )

• decrease in vessel density in the lungs, indicating a reduction in microvascular perfusion with pruning and narrowing in the distal vasculature

• increase in basal vascular remodeling in the lungs

increased heart right ventricle weight ( J:230300 )

• the right ventricle/body weight ratio is higher

increased pulmonary vascular resistance ( J:230300 )

• vascular resistance R(o) is increased in isolated perfused lungs at baseline and 10 min after infusion of angiotensin

decreased cardiac muscle contractility ( J:75781 )

• mice exhibit normal cardiac function under baseline conditions; upon beta-adrenergic stimulation, a reduced contraction and relaxation rate is observed; upon pressure overload following thoracic aorta constriction, a deterioration in left-ventricular contractility was observed

increased left ventricle systolic pressure ( J:230300 )

• left ventricular systolic and mean arterial pressures are elevated

increased right ventricle systolic pressure ( J:230300 )

• mice exhibit a 2-fold elevation in right ventricular systolic pressure

pulmonary hypertension ( J:230300 )

• mild pulmonary hypertension

decreased vasodilation ( J:230300 )

• lungs exhibit an absence of endothelial-dependent vasorelaxation in response to acetylcholine

abnormal nitric oxide homeostasis ( J:230300 )

• endothelial nitric oxide production in microvessels of perfused lungs is reduced

• microvessel nitric oxide production is decreased in response to acetylcholine in perfused lungs