Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0920646 (renal ischemia)
 2,515 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of ketanserin (Kt) has been analyzed during the development of two-kidney-two-clip (2k-2c) renovascular hypertension in the rat. Male Wistar rats were divided into four experimental groups: (1) clip Kt (ClKt) (n = 12)--A silver clip (0.25 mm width) was placed in each renal artery 3 days after beginning the administration of Kt (10 mg/kg/day) in the drinking water; (2) sham Kt (ShKt) (n = 13)--Similar to group 1, but the clips were placed in, and immediately removed from, the renal arteries; (3) untreated clip (UCl) (n = 10)--Similar to group 1, but the rats drank water; (4) untreated sham (USh) (n = 10)--Similar to group 2, but the rats drank water. Blood pressure (BP) was measured before surgery and was followed weekly for 7 weeks. At the end of this period, blood and cerebrospinal fluid (CSF) samples were obtained in all the animals. Plasma renin activity (PRA) and plasma and CSF angiotensinogen concentration (AoC) were evaluated. The results have shown that Kt partially inhibited the increase in BP induced by bilateral renal ischemia (BP: UCl rats 180.5 +/- 12.4 versus ClKt rats 149.8 +/- 5.1 mm Hg; p less than 0.01; USh rats 116.7 +/- 3.7; ShKt rats 114.4 +/- 5.0 mm Hg). PRA was similar in hypertensive and control rats whether or not they had received Kt. AoC in plasma was decreased in clipped treated and untreated rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic administration of ketanserin and the development of two-kidney-two-clip Goldblatt renovascular hypertension in the rat. 244 74

Water-electrolyte balance, plasma renin activity and urinary catecholamine excretion were studied for a period of 10 weeks after clipping the renal artery in the rat. Two groups of rats were examined; in Group I, a silver clip was applied on the left renal artery leaving the contralateral kidney untouched; in Group II, both renal arteries were clipped. Neither water-salt retention nor the increase inthe activity of the renin-angiotensin system or in the neural tone seem to be essential in the development of high arterial pressure after renal ischemia. All these factors would seem to be secondary mechanisms the contribution of which would depend on the experimental model or the hypertensive period under consideration.
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PMID:Water-salt balance, plasma renin activity and catecholamine excretion in renovascular hypertension in the rat. 616 29

The purpose of this study was to examine the pharmacokinetics of gentamicin renal uptake in dogs and assess the role of chronic renal ischemia. A stenosing silver clip was place on the left renal artery of four mongrel dogs. Six months later, each dog received an infusion of gentamicin and inulin. Blood and urine samples were collected serially. In each dog, the ischemic left kidney was smaller and had a lower RPF and CCR. The decrease in CCR was highly correlated with the decrease in RPF. Measured gentamicin kidney concentrations were found to be in good agreement with predicted values based on the amount reabsorbed and the kidney weight. Within each animal (control vs. ischemic kidney), there was a significant correlation between the filtered load of gentamicin and both the renal reabsorption and excretion of gentamicin. These relationships exhibited high R2 values, demonstrating that the induced ischemia did not alter the filtration or reabsorbtive mechanisms of gentamicin within the animal, but only decreased the filtered load. Between animals, gentamicin excretion was proportional to filtered load, but gentamicin reabsorption had the lowest r2 value, explaining only 49% of the observed variance. The unexplained variance encountered in gentamicin reabsorption between animals establishes that there are important determinants of renal tissue concentration that are independent of filtration or filtered load. This study suggests that a reduction in glomerular filtration is not an important risk factor for elevated gentamicin renal tissue concentrations, provided that serum concentrations are controlled within the therapeutic range.
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PMID:Renal handling of gentamicin by normal and ischemic canine kidneys. 709 7

Some reports have stated that central norepinephrine (NE) depletion inhibited the development of hypertension in the rat. On the other hand, this pharmacological treatment induces changes on the central renin-angiotensin system. The present study was designed to follow the development of 2 kidney-2 clip (2k-2c) renovascular hypertension in rats depleted of central NE and to analyze the central and peripheral renin-angiotensin system. Male Wistar rats (n = 40) were used. Half of the animals was injected, intracisternally, with 6-hydroxydopamine (6-OHDA), the remaining rats only received the vehicle. One week later a silver clip was placed on each renal artery on half of the 6-OHDA treated rats and on half of the vehicle treated animals. A sham operation was performed on the remaining rats. Blood pressure was measured weekly during 7 weeks. Then, blood and cerebrospinal fluid (CSF) samples were obtained. The brain was dissected in several areas. NE and angiotensinogen concentration (AoC) were determined in tissue samples. AoC was evaluated in plasma and CSF; plasma renin activity was also measured. Hypertension development was not prevented by central NE depletion, which was significant in all central areas (p < 0.001). Other significant results showed that renal ischemia and/or NE depletion induced a significant increase in angiotensinogen concentration in the hypothalamus (p < 0.01) and in CSF (p < 0.05). In summary: central NE depletion was not able to modify the development of 2 k - 2 c hypertension. Treatment and renal ischemia induced an increase of central AoC.
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PMID:Effect of central norepinephrine depletion on renovascular hypertension and on the renin system. 837 8

By means of a silver chain attached to a silver ring around the main renal artery, intermittent renal arterial occlusion, up to 30 minutes daily, was practiced for as long as 5 months in unilaterally nephrectomized dogs. This did not result in the development of persistently elevated blood pressure. Persistent moderate constriction of the renal artery of such animals by a silver clamp, after intermittent temporary occlusion had failed to affect the blood pressure, produced the usual rise of blood pressure, without accompanying significant impairment of renal excretory function. When the renal artery accidentally became persistently constricted to a great degree, or actually occluded, or if occlusion was deliberately produced by continuous pulling of the chain, hypertension and renal insufficiency (the malignant phase) quickly developed. The results do not lend support to the view that brief daily periods of renal ischemia from intrarenal vasospasm, or from any other cause, can produce persistent hypertension of renal origin.
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PMID:STUDIES ON EXPERIMENTAL HYPERTENSION : XIV. THE EFFECT OF INTERMITTENT RENAL ARTERIAL OCCLUSION ON THE BLOOD PRESSURE OF THE DOG. 1987 Oct 88

Renal artery stenosis (RAS) is one of the main reasons of renovascular hypertension and its pathogenesis remains unclear. In this study, we aimed to investigate histopathological characteristics in a rat model of RAS. Sprague-Dawley (SD) male rats were randomly divided into unilateral RAS group (Model group, n=30) and Sham group (n=30). The left renal artery was clamped with miniature silver clip for the rats in RAS group, while it was exposed but not clamped for the rats in Sham group. After the surgery, the rats were randomly divided into ten subgroups based on the time after surgery (n=3). Blood pressure, urinary albumin/creatinine ratio, and serum albumin and creatinine levels were measured. The kidneys were dissected for histological and electron microscopy analysis. The results showed that systolic blood pressure was significantly higher since 4 weeks after surgery compared to before surgery. There were no significant differences in urinary albumin/creatinine ratio as well as serum albumin and creatinine levels in Model and Sham groups. During the early acute renal ischemia the stenotic kidney exhibited acute tubular injury, podocyte injury and some crescent formation, and the main components of crescent are podocytes. Although renal tubules and vascular lesions gradually recover and crescent disappears, segmental lesions of podocyte appear in the late stage of RAS. These data reveal ultrastructural pathological changes during RAS, and suggest the role of podocyte lesions in chronic renal ischemia.
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PMID:Ultrastructural pathological features of unilateral renal artery stenosis in the rats. 2619 Nov 71

Renal ischemia-reperfusion injury (IRI) is a severe complication of major surgery and a risk factor for increased morbidity and mortality. Here, we investigated mechanisms that might contribute to IRI-induced progression to chronic kidney disease (CKD). Acute kidney injury (AKI) was induced by unilateral IRI for 35 min in CD1 and C57BL/6 (B6) mice. Unilateral IRI was used to overcome early mortality. Renal morphology, NGAL upregulation, and neutrophil infiltration as well as peritubular capillary density were studied by immunohistochemistry. The composition of leukocyte infiltrates in the kidney after IRI was investigated by flow cytometry. Systemic blood pressure was measured with a tail cuff, and renal perfusion was quantified by functional magnetic resonance imaging (fMRI). Mesangial matrix expansion was assessed by silver staining. Following IRI, CD1 and B6 mice developed similar morphological signs of AKI and increases in NGAL expression, but neutrophil infiltration was greater in CD1 than B6 mice. IRI induced an increase in systemic blood pressure of 20 mmHg in CD1, but not in B6 mice; and CD1 mice also had a greater loss of renal perfusion and kidney volume than B6 mice ( P < 0.05). CD1 mice developed substantial interstitial fibrosis and decreased peritubular capillary (PTC) density by day 14 while B6 mice showed only mild renal scarring and almost normal PTC. Our results show that after IRI, CD1 mice develop more inflammation, hypertension, and later mesangial matrix expansion than B6 mice do. Subsequently, CD1 animals suffer from CKD due to impaired renal perfusion and pronounced permanent loss of peritubular capillaries.
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PMID:Renal ischemia-reperfusion injury causes hypertension and renal perfusion impairment in the CD1 mice which promotes progressive renal fibrosis. 2935 37