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      Renal denervation in an animal model of diabetes and hypertension: Impact on the autonomic nervous system and nephropathy

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          Abstract

          Background

          The effects of renal denervation on cardiovascular reflexes and markers of nephropathy in diabetic-hypertensive rats have not yet been explored.

          Methods

          Aim: To evaluate the effects of renal denervation on nephropathy development mechanisms (blood pressure, cardiovascular autonomic changes, renal GLUT2) in diabetic-hypertensive rats. Forty-one male spontaneously hypertensive rats (SHR) ~250 g were injected with STZ or not; 30 days later, surgical renal denervation (RD) or sham procedure was performed; 15 days later, glycemia and albuminuria (ELISA) were evaluated. Catheters were implanted into the femoral artery to evaluate arterial pressure (AP) and heart rate variability (spectral analysis) one day later in conscious animals. Animals were killed, kidneys removed, and cortical renal GLUT2 quantified (Western blotting).

          Results

          Higher glycemia (p < 0.05) and lower mean AP were observed in diabetics vs. nondiabetics (p < 0.05). Heart rate was higher in renal-denervated hypertensive and lower in diabetic-hypertensive rats (384.8 ± 37, 431.3 ± 36, 316.2 ± 5, 363.8 ± 12 bpm in SHR, RD-SHR, STZ-SHR and RD-STZ-SHR, respectively). Heart rate variability was higher in renal-denervated diabetic-hypertensive rats (55.75 ± 25.21, 73.40 ± 53.30, 148.4 ± 93 in RD-SHR, STZ-SHR- and RD-STZ-SHR, respectively, p < 0.05), as well as the LF component of AP variability (1.62 ± 0.9, 2.12 ± 0.9, 7.38 ± 6.5 in RD-SHR, STZ-SHR and RD-STZ-SHR, respectively, p < 0.05). GLUT2 renal content was higher in all groups vs. SHR.

          Conclusions

          Renal denervation in diabetic-hypertensive rats improved previously reduced heart rate variability. The GLUT2 equally overexpressed by diabetes and renal denervation may represent a maximal derangement effect of each condition.

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          Most cited references37

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          Housekeeping proteins: a preliminary study illustrating some limitations as useful references in protein expression studies.

          Roisean E. Ferguson, Helen P. Carroll, Adrian Harris … (2005)
          A primary objective of many protein expression studies is to define expression patterns that can distinguish between normal and diseased states, enabling a better understanding of molecular events associated with disease development and progression and ultimately potentially finding novel markers or therapeutic targets. Exploration and confirmation of many proteins is often done using Western blotting with normalization against "housekeeping proteins", such as glyceraldehyde-3-phosphate dehydrogenase (GAPDH), beta-actin, or beta-tubulin, to correct for protein loading and factors, such as transfer efficiency. Increasingly, in studies examining gene transcript levels, it has been shown that some of the commonly used housekeeping genes may be unsuitable due to the influence of various physiological and pathological factors on their expression. This has not been examined to any great extent for proteins, however. This study examines the degree of variability of three commonly used "housekeeping" proteins (GAPDH, beta-actin, and beta-tubulin) together with class I beta-tubulin, with comparisons being made between a number of different established renal cancer cell lines, matched pairs of renal tumor and normal kidney lysates as well as nine different human tissues and highlights some of the problems encountered.
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            Identification of blood pressure control mechanisms by power spectral analysis.

            Harald Stauss (2007)
            1. Blood pressure and organ perfusion are controlled by a variety of cardiovascular control systems, such as the baroreceptor reflex and the renin-angiotensin system (RAS), and by local vascular mechanisms, such as shear stress-induced release of nitric oxide (NO) from the endothelium and the myogenic vascular response. Deviations in arterial blood pressure from its set point activate these mechanisms in an attempt to restore blood pressure and/or secure organ perfusion. However, the response times at which different cardiovascular mechanisms operate differ considerably (e.g. blood pressure control by the RAS is slower than blood pressure control via the baroreceptor reflex). 2. Owing to these different response times, some cardiovascular control systems affect blood pressure more rapidly and others more slowly. Thus, identifying the frequency components of blood pressure variability (BPV) by power spectral analysis can potentially provide important information on individual blood pressure control mechanisms. 3. Evidence is presented that the RAS, catecholamines, endothelial-derived NO and myogenic vascular function affect BPV at very low frequencies (0.02-0.2 Hz) and that low-frequency (LF) BPV (0.2-0.6 Hz) is affected by sympathetic modulation of vascular tone and endothelial-derived NO in rats. In humans, LF BPV (0.075-0.15 Hz) is affected by sympathetic modulation of vascular tone and myogenic vascular function. The impact of the RAS and endothelial-derived NO on BPV in humans requires further investigation. 4. In conclusion, power spectral analysis is a powerful diagnostic tool that allows identification of pathophysiological mechanisms contributing to cardiovascular diseases, such as hypertension, heart failure and stroke, because it can separate slow from fast cardiovascular control mechanisms. The limitation that some cardiovascular control mechanisms affect the same frequency components of BPV requires the combination of blood pressure spectral analysis with other techniques.
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              Changes in sodium or glucose filtration rate modulate expression of glucose transporters in renal proximal tubular cells of rat.

              M. Okamoto, Helliner Vestri, U Blas-Machado … (2001)
              Renal glucose reabsorption is mediated by luminal sodium-glucose cotransporters (SGLTs) and basolateral facilitative glucose transporters (GLUTs). The modulators of these transporters are not known, and their substrates glucose and Na+ are potential candidates. In this study we examined the role of glucose and Na+ filtration rate on gene expression of glucose transporters in renal proximal tubule. SGLT1, SGLT2, GLUT1 and GLUT2 mRNAs were assessed by Northern blotting; and GLUT1 and GLUT2 proteins were assessed by Western blotting. Renal cortex and medulla samples from control rats (C), diabetic rats (D) with glycosuria, and insulin-resistant 15-month old rats (I) without glycosuria; and from normal (NS), low (LS), and high (HS) Na+-diet fed rats were studied. Compared to C and I rats, D rats increased (P < 0.05) gene expression of SGLT2 by approximately 36%, SGLT1 by approximately 20%, and GLUT2 by approximately 100%, and reduced (P < 0.05) gene expression of GLUT1 by more than 50%. Compared to NS rats, HS rats increased (P < 0.05) SGLT2, GLUT2, and GLUT1 expression by approximately 100%, with no change in SGLT1 mRNA expression, and LS rats increased (P < 0.05) GLUT1 gene expression by approximately 150%, with no changes in other transporters. In summary, the results showed that changes in glucose or Na+ filtrated rate modulate the glucose transporters gene expression in epithelial cells of the renal proximal tubule.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Cardiovasc Diabetol
                Title: Cardiovascular Diabetology
                Publisher: BioMed Central
                ISSN (Electronic): 1475-2840
                Publication date Collection: 2011
                Publication date (Electronic): 17 April 2011
                Volume: 10
                Page: 33
                Affiliations
                [1 ]Instituto de Cardiologia do Rio Grande do Sul/Fundação Universitária de Cardiologia (IC/FUC), Porto Alegre, Brazil
                [2 ]Universidade Federal do Rio Grande do Sul, Endocrine Division HCPA, Porto Alegre, Brazil
                [3 ]Institute of Biomedical Scientes, University of São Paulo, São Paulo, Brazil
                [4 ]Instituto do Coração (INCOR), São Paulo, Brazil
                Article
                Publisher ID: 1475-2840-10-33
                DOI: 10.1186/1475-2840-10-33
                PMC ID: 3110548
                PubMed ID: 21496329
                SO-VID: 91b03467-23d9-4fea-a3fb-8a7c5f6a1527
                Copyright © Copyright ©2011 Dias et al; licensee BioMed Central Ltd.
                License:

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 6 February 2011
                Date accepted : 17 April 2011
                Categories
                Subject: Original Investigation

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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