Expression of eNOS in kidneys from hypertensive patients

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.

Thymoquinone Upregulates Catalase Gene Expression and Preserves the Structure of the Renal Cortex of Propylthiouracil-Induced Hypothyroid Rats

“…In addition, another set of paraffin sections at same thickness was immunohistochemically stained using the streptavidin-biotin-peroxidase technique described by Gu and Herrera [21]. Anti-alpha-smooth muscle actin (ASMA) antibody (Dako Company, Cairo, Egypt; at a dilution of 1/1000), antiendothelial nitric oxide synthetase (eNOS) antibody (Dako Company, Cairo, Egypt; at a dilution of 1/100), and anti-CD68 antibodies were utilized in this study.…”

Mechanisms underlying blood pressure reduction by dietary inorganic nitrate

“…eNOS is expressed primarily in the endothelium of the afferent arteriole and neuronal NOS (nNOS) in the macula densa cells. Both experimental and clinical studies show that reduction in eNOS‐ or nNOS‐derived NO can increase preglomerular resistance, lower glomerular filtration rate (GFR), increase tubular sodium reabsorption (especially in the thick ascending limb and collecting duct), thereby contributing to the development or worsening of hypertension and associated renal injuries . Therefore, novel treatment modalities that reduce oxidative stress and/or increase NO production may have important implications in preventing and treating hypertension and cardiovascular disease.…”

The ameliorating effect of sodium selenite on the histological changes and expression of caspase-3 in the testis of monosodium glutamate-treated rats: Light and electron microscopic study

“…Avidin-biotin-peroxidase technique[ 34 ] was used for the detection of activated caspase-3 as an apoptotic marker. Brown cytoplasmic or nuclear staining is considered positive reaction.…”