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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

Small arteries. A) A small artery in control kidney. B) A small artery in the kidney from patient with chronic hypertension. The artery showed thickening and hyalinosis of vascular wall. C) A small artery in the kidney from patient with malignant hypertension. The artery revealed significant thickening of vascular wall, myxoid degeneration of intima and obliteration of lumen. The endothelial cells showed edema with enlarged nuclei and pale cytoplasm.
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f2-ijnrd-3-011: Small arteries. A) A small artery in control kidney. B) A small artery in the kidney from patient with chronic hypertension. The artery showed thickening and hyalinosis of vascular wall. C) A small artery in the kidney from patient with malignant hypertension. The artery revealed significant thickening of vascular wall, myxoid degeneration of intima and obliteration of lumen. The endothelial cells showed edema with enlarged nuclei and pale cytoplasm.

Mentions: Control kidneys were normal. There was no significant interstitial fibrosis, tubular atrophy or thickening of vascular intima. The glomeruli showed open loops. The capillary walls were thin and smooth (Figure 1A). There was no fibrinoid thickening of the intima of arteriole and interlobular arteries (Figure 2A). The kidneys from patients in the chronic primary hypertensive group showed patchily distributed interstitial fibrosis associated with tubular atrophy and drop out. Scattered lymphocytes were often present in association with areas with interstitial fibrosis. The viable glomeruli showed retraction of capillary tufts with segmental thickening and wrinkling of capillary loops (Figure 1B). The interlobular arteries revealed intimal fibrous thickening and the arterioles showed thickening of their walls with segmental hyalinosis (Figure 2B). Except for the vascular disease-associated changes, there was no morphologic evidence of a specific glomerular disorder, such as proliferative glomerulonephritis, immune complex mediated glomerulonephritis or diabetic glomerulopathy. There was no evidence of tubular necrosis or interstitial nephritis. Ultrastructurally, segmental wrinkling and thickening of capillary basement membranes were common in glomeruli. There were no significant endothelial structural alterations. No immune complexes or paraprotein deposits were identified in any of the renal compartments in any of these cases.


Expression of eNOS in kidneys from hypertensive patients.

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

Small arteries. A) A small artery in control kidney. B) A small artery in the kidney from patient with chronic hypertension. The artery showed thickening and hyalinosis of vascular wall. C) A small artery in the kidney from patient with malignant hypertension. The artery revealed significant thickening of vascular wall, myxoid degeneration of intima and obliteration of lumen. The endothelial cells showed edema with enlarged nuclei and pale cytoplasm.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3108783&req=5

f2-ijnrd-3-011: Small arteries. A) A small artery in control kidney. B) A small artery in the kidney from patient with chronic hypertension. The artery showed thickening and hyalinosis of vascular wall. C) A small artery in the kidney from patient with malignant hypertension. The artery revealed significant thickening of vascular wall, myxoid degeneration of intima and obliteration of lumen. The endothelial cells showed edema with enlarged nuclei and pale cytoplasm.
Mentions: Control kidneys were normal. There was no significant interstitial fibrosis, tubular atrophy or thickening of vascular intima. The glomeruli showed open loops. The capillary walls were thin and smooth (Figure 1A). There was no fibrinoid thickening of the intima of arteriole and interlobular arteries (Figure 2A). The kidneys from patients in the chronic primary hypertensive group showed patchily distributed interstitial fibrosis associated with tubular atrophy and drop out. Scattered lymphocytes were often present in association with areas with interstitial fibrosis. The viable glomeruli showed retraction of capillary tufts with segmental thickening and wrinkling of capillary loops (Figure 1B). The interlobular arteries revealed intimal fibrous thickening and the arterioles showed thickening of their walls with segmental hyalinosis (Figure 2B). Except for the vascular disease-associated changes, there was no morphologic evidence of a specific glomerular disorder, such as proliferative glomerulonephritis, immune complex mediated glomerulonephritis or diabetic glomerulopathy. There was no evidence of tubular necrosis or interstitial nephritis. Ultrastructurally, segmental wrinkling and thickening of capillary basement membranes were common in glomeruli. There were no significant endothelial structural alterations. No immune complexes or paraprotein deposits were identified in any of the renal compartments in any of these cases.

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