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

<p>Abstract</p> <p>Background</p> <p>The effects of renal denervation on cardiovascular reflexes and markers of nephropathy in diabetic-hypertensive rats have not yet been explored.</p> <p>Methods</p> <p>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).</p> <p>Results</p> <p>Higher glycemia (p < 0.05) and lower mean AP were observed in diabetics <it>vs. </it>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 <it>vs</it>. SHR.</p> <p>Conclusions</p> <p>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.</p

Bradykinin or Acetylcholine as Vasodilators to Test Endothelial Venous Function in Healthy Subjects

INTRODUCTION: The evaluation of endothelial function has been performed in the arterial bed, but recently evaluation within the venous system has also been explored. Endothelial function studies employ different drugs that act as endothelium-dependent vasodilatory response inductors. OBJECTIVES: The aim of this study is to compare the endothelium-dependent venous vasodilator response mediated by either acetylcholine or bradykinin in healthy volunteers. METHODS AND RESULTS: Changes in vein diameter after phenylephrine-induced venoconstriction were measured to compare venodilation induced by acetylcholine or bradykinin (linear variable differential transformer dorsal hand vein technique). We studied 23 healthy volunteers; 31% were male, and the subject had a mean age of 33 ± 8 years and a mean body mass index of 23 ± 2 kg/m2. The maximum endothelium-dependent venodilation was similar for both drugs (p = 0.13), as well as the mean responses for each dose of both drugs (r = 0.96). The maximum responses to acetylcholine and bradykinin also had good agreement. CONCLUSION: There were no differences between acetylcholine and bradykinin as venodilators in this endothelial venous function investigation

Maximal exercise test is a useful method for physical capacity and oxygen consumption determination in streptozotocin-diabetic rats

BACKGROUND: The aim of the present study was to investigate the relationship between speed during maximum exercise test (ET) and oxygen consumption (VO(2)) in control and STZ-diabetic rats, in order to provide a useful method to determine exercise capacity and prescription in researches involving STZ-diabetic rats. METHODS: Male Wistar rats were divided into two groups: control (CG, n = 10) and diabetic (DG, n = 8). The animals were submitted to ET on treadmill with simultaneous gas analysis through open respirometry system. ET and VO(2 )were assessed 60 days after diabetes induction (STZ, 50 mg/Kg). RESULTS: VO(2 )maximum was reduced in STZ-diabetic rats (72.5 ± 1 mL/Kg/min(-1)) compared to CG rats (81.1 ± 1 mL/Kg/min(-1)). There were positive correlations between ET speed and VO(2 )(r = 0.87 for CG and r = 0.8 for DG), as well as between ET speed and VO(2 )reserve (r = 0.77 for CG and r = 0.7 for DG). Positive correlations were also obtained between measured VO(2 )and VO(2 )predicted values (r = 0.81 for CG and r = 0.75 for DG) by linear regression equations to CG (VO(2 )= 1.54 * ET speed + 52.34) and DG (VO(2 )= 1.16 * ET speed + 51.99). Moreover, we observed that 60% of ET speed corresponded to 72 and 75% of VO(2 )reserve for CG and DG, respectively. The maximum ET speed was also correlated with VO(2 )maximum for both groups (CG: r = 0.7 and DG: r = 0.7). CONCLUSION: These results suggest that: a) VO(2 )and VO(2 )reserve can be estimated using linear regression equations obtained from correlations with ET speed for each studied group; b) exercise training can be prescribed based on ET in control and diabetic-STZ rats; c) physical capacity can be determined by ET. Therefore, ET, which involves a relatively simple methodology and low cost, can be used as an indicator of cardio-respiratory capacity in future studies that investigate the physiological effect of acute or chronic exercise in control and STZ-diabetic male rats

Cardiovascular Changes in Animal Models of Metabolic Syndrome

Metabolic syndrome has been defined as a group of risk factors that directly contribute to the development of cardiovascular disease and/or type 2 diabetes. Insulin resistance seems to have a fundamental role in the genesis of this syndrome. Over the past years to the present day, basic and translational research has used small animal models to explore the pathophysiology of metabolic syndrome and to develop novel therapies that might slow the progression of this prevalent condition. In this paper we discuss the animal models used for the study of metabolic syndrome, with particular focus on cardiovascular changes, since they are the main cause of death associated with the condition in humans

Maximal exercise test is a useful method for physical capacity and oxygen consumption determination in streptozotocin-diabetic rats

Abstract Background The aim of the present study was to investigate the relationship between speed during maximum exercise test (ET) and oxygen consumption (VO2) in control and STZ-diabetic rats, in order to provide a useful method to determine exercise capacity and prescription in researches involving STZ-diabetic rats. Methods Male Wistar rats were divided into two groups: control (CG, n = 10) and diabetic (DG, n = 8). The animals were submitted to ET on treadmill with simultaneous gas analysis through open respirometry system. ET and VO2 were assessed 60 days after diabetes induction (STZ, 50 mg/Kg). Results VO2 maximum was reduced in STZ-diabetic rats (72.5 ± 1 mL/Kg/min-1) compared to CG rats (81.1 ± 1 mL/Kg/min-1). There were positive correlations between ET speed and VO2 (r = 0.87 for CG and r = 0.8 for DG), as well as between ET speed and VO2 reserve (r = 0.77 for CG and r = 0.7 for DG). Positive correlations were also obtained between measured VO2 and VO2 predicted values (r = 0.81 for CG and r = 0.75 for DG) by linear regression equations to CG (VO2 = 1.54 * ET speed + 52.34) and DG (VO2 = 1.16 * ET speed + 51.99). Moreover, we observed that 60% of ET speed corresponded to 72 and 75% of VO2 reserve for CG and DG, respectively. The maximum ET speed was also correlated with VO2 maximum for both groups (CG: r = 0.7 and DG: r = 0.7). Conclusion These results suggest that: a) VO2 and VO2 reserve can be estimated using linear regression equations obtained from correlations with ET speed for each studied group; b) exercise training can be prescribed based on ET in control and diabetic-STZ rats; c) physical capacity can be determined by ET. Therefore, ET, which involves a relatively simple methodology and low cost, can be used as an indicator of cardio-respiratory capacity in future studies that investigate the physiological effect of acute or chronic exercise in control and STZ-diabetic male rats.</p