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      Chronic Renal Failure Leads to Reduced Flow-Dependent Dilation in Isolated Rat Skeletal Muscle Arterioles due to Lack of NO Mediation

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          Background: Chronic renal failure (CRF) is frequently accompanied by systemic vascular alterations which further increase the morbidity and mortality of these patients. However, the nature and the underlying mechanisms of vascular dysfunction are not completely understood. We hypothesized that – in addition to other factors – CRF alters local vasomotor mechanisms that are intrinsic to the vascular wall. Methods: Changes in the diameter of isolated, pressurized (at 80 mm Hg) gracilis skeletal muscle arterioles (diameter approximately 150 µm) of female Wistar rats were investigated by videomicroscopy. Arteriolar responses to an increase in flow and vasoactive agents in partially nephrectomized (NX) and sham-operated (control) rats were compared. Results: In NX rats, serum creatinine and urine protein excretion were increased. Compared to controls, increases in intraluminal flow (from 0 to 40 µl/min) resulted in significantly reduced dilation in arterioles of NX rats (maximum: 32 ± 4 vs. 15 ± 4 µm, p < 0.05). Inhibition of nitric oxide (NO) synthesis with L-NAME reduced the dilation of control arterioles but did not affect responses of NX arterioles. Also, dilations in response to histamine were significantly reduced in arterioles from NX rats as compared to control rats. L-NAME significantly decreased histamine-induced dilations of control arterioles, but it did not affect responses of NX arterioles. Dilations in response to the NO donor sodium nitroprusside were also significantly decreased in NX arterioles as compared to responses of control vessels, whereas responses to adenosine and norepinephrine were not significantly different in the two groups. Conclusions: We conclude that in rat skeletal muscle arterioles, CRF induced by renal mass reduction alters the mechanosensitive and agonist-induced responses of peripheral arterioles, in part by interfering with NO-signaling mechanisms. These alterations could contribute to increased peripheral vascular resistance and further aggravate the cardiovascular complications in CRF.

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          Most cited references 5

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          Chronic renal failure--a vasculopathic state.

           R K Luke (1998)
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            Enhanced Nitric Oxide Inactivation and Protein Nitration by Reactive Oxygen Species in Renal Insufficiency

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              Hypertension in chronic renal failure and ESRD: prevalence, pathophysiology, and outcomes.

              Hypertension and cardiovascular disease were detected to be major problems in end-stage renal disease patients soon after the application of chronic dialysis to treat uremia. Nearly 40 years later, and despite awesome technological and pharmacological advances, cardiovascular diseases remain the number one cause of death in all categories of renal patients, ie, chronic renal insufficiency, end-stage renal disease on dialysis and the renal transplant recipient. This is quite likely related to the massive clinical burden of cardiovascular risk factors: hypertension, cardiac fibrosis and hypertrophy, abnormal lipid profiles, smoking, dietary factors, and enhanced sympathetic activity. For example, left ventricular hypertrophy and abnormal echocardiograms are present in up to 75% to 80% of incident dialysis patients related to the interactions of these cardiovascular risks. It is important to understand how hypertension and the other cardiovascular disease risk factors interact in these patients. Based on the latest national data from the USRDS, the prevalence of underlying cardiac disease is increasing during the period of chronic renal failure. A proper understanding of the pathophysiology and prevalence of hypertension and its consequences in renal patients may lead to more rational therapies and clinical trials. At this time, the nephrologists are dealing with an epidemic of cardiovascular diseases in their patients. Copyright 2001 by W.B. Saunders Company.

                Author and article information

                Kidney Blood Press Res
                Kidney and Blood Pressure Research
                S. Karger AG
                24 April 2003
                : 26
                : 1
                : 19-26
                aDepartment of Pathophysiology, Semmelweis University, Budapest, Hungary, and bDepartment of Physiology, New York Medical College, Valhalla, N.Y., USA
                69762 Kidney Blood Press Res 2003;26:19–26
                © 2003 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 1, References: 30, Pages: 8
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/69762
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