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Expression of eNOS in kidneys from hypertensive patients.

Gu X, Herrera GA - Int J Nephrol Renovasc Dis (2010)

Bottom Line: In contrast, the expression of eNOS was significantly decreased in the glomeruli and arterioles/small arteries of patients with malignant hypertension, particularly in those with significant intimal edema and myxoid degeneration or thrombi.Endothelial dysfunction is an important pathogenetic factor for chronic primary hypertension and eNOS plays a major role in the regulation of vascular tone and function.In patients with malignant hypertension, the expression of eNOS protein was diminished in the injured vasculature.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Louisiana State University Health Sciences Center, Shreveport, LA, USA. xgu@lsuhsc.edu

ABSTRACT
Endothelium-derived nitric oxide (NO) is essential for maintenance and regulation of blood pressure. In animal models, altered endothelium-derived nitric oxide synthase (eNOS) expression and impaired NO generation are important factors for renal injury. However, the pattern of eNOS expression in the kidneys from hypertensive patients has not been well established. We have studied the eNOS immuno-expression in kidney biopsies from hypertensive patients. Compared to kidneys from normotensive individuals, there were no significant alterations of eNOS immuno-expression in the vasculature of patients with chronic essential hypertension. In contrast, the expression of eNOS was significantly decreased in the glomeruli and arterioles/small arteries of patients with malignant hypertension, particularly in those with significant intimal edema and myxoid degeneration or thrombi. Endothelial dysfunction is an important pathogenetic factor for chronic primary hypertension and eNOS plays a major role in the regulation of vascular tone and function. Unchanged eNOS in the kidney vasculature in chronic primary hypertension indicates that these patients have an ability to compensate. In patients with malignant hypertension, the expression of eNOS protein was diminished in the injured vasculature. Loss of the compensatory mechanism via continued release of NO to prevent vascular injury may be responsible for morphological changes typically seen in the renal vasculature in patients with accelerated hypertension.

No MeSH data available.


Related in: MedlinePlus

Expression of eNOS in the arteries. A) Control. B) Chronic hypertension. C) Malignant hypertension. The marker was in the center of the artery that revealed myxoid degeneration of intima and injured endothelial cells.
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f4-ijnrd-3-011: Expression of eNOS in the arteries. A) Control. B) Chronic hypertension. C) Malignant hypertension. The marker was in the center of the artery that revealed myxoid degeneration of intima and injured endothelial cells.

Mentions: In the control group (Figure 3A), moderate to strong (3+) expression of eNOS was present in the cytoplasm of endothelial cells in glomeruli, arterioles, interlobular arteries, veins and peritubular capillaries (Figure 4A). In the glomeruli, there was no immunoreaction in mesangial cells. The visceral epithelial cells that were also negative for eNOS. Weak staining along tubular basement membranes and cytoplasm of some tubular epithelial cells (0 to 1+) was noted in focal areas. The interstitial cells and inflammatory cells were negative for eNOS.


Expression of eNOS in kidneys from hypertensive patients.

Gu X, Herrera GA - Int J Nephrol Renovasc Dis (2010)

Expression of eNOS in the arteries. A) Control. B) Chronic hypertension. C) Malignant hypertension. The marker was in the center of the artery that revealed myxoid degeneration of intima and injured endothelial cells.
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3108783&req=5

f4-ijnrd-3-011: Expression of eNOS in the arteries. A) Control. B) Chronic hypertension. C) Malignant hypertension. The marker was in the center of the artery that revealed myxoid degeneration of intima and injured endothelial cells.
Mentions: In the control group (Figure 3A), moderate to strong (3+) expression of eNOS was present in the cytoplasm of endothelial cells in glomeruli, arterioles, interlobular arteries, veins and peritubular capillaries (Figure 4A). In the glomeruli, there was no immunoreaction in mesangial cells. The visceral epithelial cells that were also negative for eNOS. Weak staining along tubular basement membranes and cytoplasm of some tubular epithelial cells (0 to 1+) was noted in focal areas. The interstitial cells and inflammatory cells were negative for eNOS.

Bottom Line: In contrast, the expression of eNOS was significantly decreased in the glomeruli and arterioles/small arteries of patients with malignant hypertension, particularly in those with significant intimal edema and myxoid degeneration or thrombi.Endothelial dysfunction is an important pathogenetic factor for chronic primary hypertension and eNOS plays a major role in the regulation of vascular tone and function.In patients with malignant hypertension, the expression of eNOS protein was diminished in the injured vasculature.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, Louisiana State University Health Sciences Center, Shreveport, LA, USA. xgu@lsuhsc.edu

ABSTRACT
Endothelium-derived nitric oxide (NO) is essential for maintenance and regulation of blood pressure. In animal models, altered endothelium-derived nitric oxide synthase (eNOS) expression and impaired NO generation are important factors for renal injury. However, the pattern of eNOS expression in the kidneys from hypertensive patients has not been well established. We have studied the eNOS immuno-expression in kidney biopsies from hypertensive patients. Compared to kidneys from normotensive individuals, there were no significant alterations of eNOS immuno-expression in the vasculature of patients with chronic essential hypertension. In contrast, the expression of eNOS was significantly decreased in the glomeruli and arterioles/small arteries of patients with malignant hypertension, particularly in those with significant intimal edema and myxoid degeneration or thrombi. Endothelial dysfunction is an important pathogenetic factor for chronic primary hypertension and eNOS plays a major role in the regulation of vascular tone and function. Unchanged eNOS in the kidney vasculature in chronic primary hypertension indicates that these patients have an ability to compensate. In patients with malignant hypertension, the expression of eNOS protein was diminished in the injured vasculature. Loss of the compensatory mechanism via continued release of NO to prevent vascular injury may be responsible for morphological changes typically seen in the renal vasculature in patients with accelerated hypertension.

No MeSH data available.


Related in: MedlinePlus