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This study examined the effect of leptin and orexin‐A on autonomic baroreflex control in conscious Wistar rats exposed to high‐fat (45% fat) or normal (3.4%) diet for 4 weeks. Renal sympathetic nerve activity (RSNA), mean arterial pressure (MAP) and heart rate (HR) were monitored during the generation of baroreflex gain curves and acute volume expansion (VEP). Intracerebroventricular (ICV) leptin (1 μg/min) increased RSNA in the normal diet group (0.31 ± 0.04 vs 0.23 ± 0.03 mV/s) and MAP in the high‐fat diet group (115 ± 5 vs 105 ± 5 mm Hg, P <.05). Orexin‐A (50 ng/min) increased RSNA, HR and MAP in the high‐fat diet group (0.26 ± 0.03 vs 0.22 ± 0.02 mV/s, 454 ± 8 vs 417 ± 12 beats/min, 117 ± 1 vs 108 ± 1 mm Hg) and the normal diet group (0.18 ± 0.05 vs 0.17 ± 0.05 mV/s, 465 ± 10 vs 426 ± 6 beats/min, 116 ± 2 vs 104 ± 3 mm Hg). Baroreflex sensitivity for RSNA was increased during ICV leptin by 50% in the normal diet group, compared to 14% in the high‐fat diet group (P <.05). Similarly, orexin‐A increased baroreflex sensitivity by 56% and 50% in the high‐fat and normal diet groups, respectively (all P <.05). During ICV saline, VEP decreased RSNA by 31 ± 5% (P <.05) after 10 minutes and the magnitude of this response was blunted during ICV infusion of leptin (17 ± 2%, P <.05) but not orexin‐A in the normal diet group. RSNA response to VEP was not changed during ICV leptin or orexin‐A in the high‐fat diet group. These findings indicate possible central roles for leptin and orexin‐A in modulating the baroreflexes under normal or increased fat intake in conscious rats and potential therapeutic approaches for obesity associated hypertension. [ABSTRACT FROM AUTHOR]

The purpose of the present study was to investigate the interaction between H2S and NO (nitric oxide) in the kidney and to evaluate its impact on the functional contribution of α1A and α1B-adrenoreceptors subtypes mediating the renal vasoconstriction in the kidney of rats with left ventricular hypertrophy (LVH). In rats the LVH induction was by isoprenaline administration and caffeine in the drinking water together with intraperitoneal administration of H2S. The responsiveness of α1A and α1B to exogenous noradrenaline, phenylephrine and methoxaminein the absence and presence of 5-methylurapidil (5-MeU) and chloroethylclonidine (CEC) was studied. Cystathione gamma lyase (CSE), cystathione β synthase (CBS), 3-mercaptopyruvate sulphar transferase (3-MST) and endothelial nitric oxide synthase (eNOS) were quantified. There was significant up regulation of CSE and eNOS in the LVH-H2S compared to the LVH group (P<0.05). Baseline renal cortical blood perfusion (RCBP) was increased (P<0.05) in the LVH-H2S compared to the LVH group. The responsiveness of α1A-adrenergic receptors to adrenergic agonists was increased (P<0.05) after administration of low dose 5-Methylurapidil in the LVH-H2S group while α1B-adrenergic receptors responsiveness to adrenergic agonists were increased (P<0.05) by both low and high dose chloroethylclonidine in the LVH-H2S group. Treatment of LVH with H2S resulted in up-regulation of CSE/H2S, CBS, and 3-MST and eNOS/NO/cGMP pathways in the kidney. These up regulation of CSE/H2S, CBS, and 3-MST and eNOS/NO/cGMP pathways enhanced the responsiveness of α1A and α1B-adrenoreceptors subtypes to adrenergic agonists in LVH-H2S. These findings indicate an important role for H2S in modulating deranged signalling in the renal vasculature resulting from LVH development. [ABSTRACT FROM AUTHOR]

Hydrogen sulphide (H2S) is an emerging molecule in many cardiovascular complications but its role in left ventricular hypertrophy (LVH) is unknown. The present study explored the effect of exogenous H2S administration in the regression of LVH by modulating oxidative stress, arterial stiffness and expression of cystathione γ lyase (CSE) in the myocardium. Animals were divided into four groups: Control, LVH, Control-H2S and LVH-H2S. LVH was induced by administering isoprenaline (5mg/kg, every 72 hours, S/C) and caffeine in drinking water (62mg/L) for 2 weeks. Intraperitoneal NaHS, 56μM/kg/day for 5 weeks, was given as an H2S donor. Myocardial expression of Cystathione γ lyase (CSE) mRNA was quantified using real time polymerase chain reaction (qPCR).There was a 3 fold reduction in the expression of myocardial CSE mRNA in LVH but it was up regulated by 7 and 4 fold in the Control-H2S and LVH-H2S myocardium, respectively. Systolic blood pressure, mean arterial pressure, pulse wave velocity were reduced (all P<0.05) in LVH-H2S when compared to the LVH group. Heart, LV weight, myocardial thickness were reduced while LV internal diameter was increased (all P<0.05) in the LVH-H2S when compared to the LVH group. Exogenous administration of H2S in LVH increased superoxide dismutase, glutathione and total antioxidant capacity but significantly reduced (all P<0.05) plasma malanodialdehyde in the LVH-H2S compared to the LVH group. The renal cortical blood perfusion increased by 40% in LVH-H2S as compared to the LVH group. Exogenous administration of H2S suppressed the progression of LVH which was associated with an up regulation of myocardial CSE mRNA/ H2S and a reduction in pulse wave velocity with a blunting of systemic hemodynamic. This CSE/H2S pathway exhibits an antihypertrophic role by antagonizing the hypertrophic actions of angiotensin II(Ang II) and noradrenaline (NA) but attenuates oxidative stress and improves pulse wave velocity which helps to suppress LVH. Exogenous administration of H2S augmented the reduced renal cortical blood perfusion in the LVH state. [ABSTRACT FROM AUTHOR]

Oxidative stress and suppressed H2S production lead to increased renal vascular resistance, disturbed glomerular hemodynamics, and abnormal renal sodium and water handling, contribute to the pathogenesis and maintenance of essential hypertension in man and the spontaneously hypertensive rat. This study investigated the impact of H2S and tempol alone and in combination on blood pressure and renal hemodynamics and excretory functions in the SHR. Groups of WKY rats or SHR ( n = 6) were treated for 4 weeks either as controls or received NaHS (SHR + NaHS), tempol (SHR + Tempol), or NaHS plus tempol (SHR + NaHS + Tempol). Metabolic studies were performed on days 0, 14, and 28, thereafter animals were anaesthetized to measure renal hemodynamics and plasma oxidative and antioxidant markers. SHR control rats had higher mean arterial blood pressure (140.0 ± 2 vs. 100.0 ± 3 mmHg), lower plasma and urinary H2S, creatinine clearance, urine flow rate and urinary sodium excretion, and oxidative stress compared to WKY (all p < 0.05). Treatment either with NaHS or with tempol alone decreased blood pressure and oxidative stress and improved renal hemodynamic and excretory function compared to untreated SHR. Combined NaHS and tempol therapy in SHRs caused larger decreases in blood pressure (∼20-22% vs. ∼11-15% and ∼10-14%), increases in creatinine clearance, urinary sodium excretion and fractional sodium excretion and up-regulated the antioxidant status compared to each agent alone (all p < 0.05). These findings demonstrated that H2S and tempol together resulted in greater reductions in blood pressure and normalization of kidney function compared with either compound alone. [ABSTRACT FROM AUTHOR]

This study investigated the effects of tempol, a superoxide dismutase (SOD) mimetic and L-NAME, a nitric oxide (NO) synthase inhibitor on the renal function and hemodynamics in cyclosporine A (CsA) induced renal insufficiency rats. Male Sprague-Dawley rats were treated with either vehicle (C), tempol (T, 1 mmol/L in drinking fluid), L-NAME (L, 1 mmol/L in drinking fluid), CsA (Cs, 25 mg/kg/day via gavage), CsA plus tempol (TCs), CsA plus L-NAME (LCs) or CsA plus a combination of tempol and L-NAME (TLCs) for 21 consecutive days. At the end of treatment regimen, the renal responses to noradrenaline (NA), phenylephrine (PE), methoxamine and angiotensin II (Ang II) were determined. Cs and LCs rats had lower creatinine clearance (0.7 ± 0.1 and 0.6 ± 0.5 vs. 1.3 ± 0.2 mL/min/kg) and fractional excretion of sodium (0.12 ± 0.02 and 0.17 ± 0.01 vs. 0.67 ± 0.04%) but higher systolic blood pressure (145 ± 2 and 178 ± 4 vs. 116 ± 2) compared to the control (all p < 0.05), respectively. Tempol treatment in TCs or TLCs prevented the increase in blood pressure and improved creatinine clearance and sodium excretion compared to untreated Cs. The renal vasoconstriction in Cs or LCs to NA, PE and Ang II were lower than control by ∼35-48% (all p < 0.05). In TCs or TLCs, there was enhanced renal vasoconstriction to all agonist by ∼39-114% compared to Cs. SOD is important to counterbalance the hypertensive effect of a defective NO system and to allow the normal vasoconstrictor response of the renal vasculature to adrenergic agonists and Ang II in a model of CsA-induced renal insufficiency. [ABSTRACT FROM AUTHOR]

The present study compared the cardiovascular and renal actions of γ2-melanocyte-stimulating hormone (γ2 MSH) with those of the synthetic analogue [Nle3, d-Phe6]-γ2 MSH ( NDP-γ2 MSH) and explored the effects of high dietary salt intake on the renal actions of NDP-γ2 MSH., Both peptides were infused systemically (3-1000 nmol/kg) and intrarenally (500 fmol/min) into innervated and renally denervated rats fed either a normal (0.4% NaCl) or high-salt (4% NaCl; HS) diet. Mean arterial pressure ( MAP), glomerular filtration rate ( GFR), urinary sodium excretion ( UNaV), urinary output ( UV) and fractional sodium excretion were determined, as was expression of the melanocortin MC3 receptor in inner medullary collecting duct ( IMCD) epithelial cells., Both renal and systemic infusion of γ2 MSH increased MAP by 23 ± 2% and 54 ± 4%, respectively, but equivalent doses of NDP-γ2 MSH had no significant pressor effects. Both peptides had similar natriuretic and diuretic effects in rats fed a normal salt diet. However, NDP-γ2 MSH increased UNaV and UV by two- to threefold in rats fed the normal salt diet and by six- to sevenfold in rats fed the HS diet. Furthermore, NDP-γ2 MSH induced a 3.5-fold increase in GFR only in rats fed the HS diet. These renal effects of NDP-γ2 MSH were not abolished by prior renal denervation. Rats fed the HS diet also exhibited a 4.5-fold increase in MC3 receptor expression in IMCD epithelial cells., Intrarenal infusion of NDP-γ2 MSH induced the natriuretic but not the cardiovascular effects exhibited by γ2 MSH. The renal activities may be attributed to a direct binding of NDP-γ2 MSH to MC3 receptors expressed in IMCD cells, leading to a potent natriuretic effect that is independent of renal innervation. [ABSTRACT FROM AUTHOR]

Background. This study examined the effect of renal sympathetic innervation on adrenergically and angiotensin II (Ang II)- induced renal vasoconstriction in Wistar-Kyoto (WKY) rats. Methods. Forty-eight WKY rats were treated with either losartan (10 mg/kg/day p.o.) or carvedilol (5 mg/kg/day p.o.) or a combination of them (10 mg/kg/day + 5 mg/kg/day p.o.) for 7 days. On day 8, the rats were anaesthetized, and renal vasoconstrictor experiments were carried out. A group of rats was subjected to acute unilateral renal denervation during the acute study. Changes in the renal vasoconstrictor responses were determined in terms of reductions in renal blood flow caused by Ang II, noradrenaline (NA), and methoxamine (ME). Results. In normal animals, losartan decreased (P < 0.05) the renal vasoconstrictor response to Ang II but not to NA or ME. Carvedilol treatment, however, blunted (P < 0.05) the renal vasoconstrictor responses to Ang II and adrenergic agonists. Combination of losartan and carvedilol blunted (P < 0.05) the renal vasoconstrictor response to Ang II but augmented the responses to NA and ME (all P < 0.05). Interestingly, when denervated rats were treated with the same combination, there was a reduction (P < 0.05) in the renal vasoconstrictor responses to Ang II and adrenergic agonists. Conclusions. Data suggest that the renal sympathetic nerve contributes to adrenergic agonist-mediated renal vasoconstrictions in normal rats. The data further indicate an interactive relationship between renin-angiotensin and sympathetic nervous systems in modulating adrenergically and Ang II-induced renal vasoconstriction in WKY rats. [ABSTRACT FROM AUTHOR]

Pathophysiological states, including cardiovascular and renal diseases, are characterized by oxidative stress but what is less clear is whether physiological challenges incur a degree of altered oxidative metabolism. To this end, this study examined whether exposure to a high dietary sodium intake could cause an oxidative stress at the kidney. Animals, placed on either 0.3% or 3% sodium diets for 2 wk, were given a lethal dose of anesthetic, and kidneys were removed to analyze both NAD(P)H oxidase (NOX) and superoxide dismutase (SOD) expression and activities in the cortex and medulla. Placing animals on the high-sodium diet raised sodium and water excretion and caused an ∼14-fold increase in urinary excretion of 8-isoprostane, a marker of oxidative stress, which was attenuated by chronic treatment with apocynin to prevent NAD(P)H oxidase activity. The protein expression of the NAD(P)H oxidase subunits NOX2 and p47phox and overall NAD(P)H oxidase activity were approximately doubled in the cortex of the rats on the high-sodium diet compared with those on the normal sodium intake while both SOD activity and expression were unchanged. By contrast, neither NOX nor SOD protein expression or activity were altered in the medulla when the rats were placed on the high-sodium intake. These data suggest that an elevation in dietary sodium intake can lead to increased generation of reactive oxygen species and a state of oxidative stress in the cortex but not to such a degree that it extends to the medulla. [ABSTRACT FROM AUTHOR]

Cardiovascular complications are consistently observed in diabetic patients across all age groups. The objective of the present study was to investigate the effect of aqueous extract of the fruit pulp of Hylocereus undatus (DFE) on aortic stiffness and oxidative stress in streptozotocin (STZ)-induced diabetes in rats. Twenty-four male, Sprague-Dawley rats were randomized into four groups: I (control), II (diabetic), III (DFE, 250 mg/kg) and IV (DFE 500 mg/kg). Diabetes was induced in groups II, III and IV by intraperitoneal (i.p.) injection of STZ (40 mg/kg). After confirmation of diabetes, group III and IV received DFE for 5 weeks. Pulse wave velocity (PWV) was used as a marker of aortic stiffness and was determined at the end of 5 weeks. DFE significantly decreased (P , 0.05) the fasting blood glucose levels in diabetic rats, but not to normal levels. Systolic blood pressure, pulse pressure and PWV were significantly increased (P < 0.05) in diabetic rats at the end of 5 weeks in comparison with control group. DFE treatment significantly decreased (P < 0.05) these elevations. Oxidative damage was observed in group II after 5 weeks. Plasma malondialdehyde levels significantly decreased (P < 0.05), while superoxide dismutase and total antioxidant capacity significantly increased (P < 0.05) with DFE treatment in comparison with group II. These data demonstrate that DFE treatment was effective in controlling oxidative damage and decreasing the aortic stiffness measured by PWV in STZ-induced diabetes in rats. [ABSTRACT FROM AUTHOR]

1. Calcium channel blockade attenuates adrenergically induced renal vasoconstriction and the present study examined whether the magnitude of the supression was enhanced or blunted in rat models of renal failure or diabetes-induced glomerular hyperfiltration. 2. Male Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) were used that had either renal failure induced by cisplatin administration or early diabetic nephropathy (EDN) consequent to an injection of streptozotocin (STZ). After 7 days of cisplatin or 4 weeks of STZ, rats were anaesthetized and renal haemodynamic studies were performed. 3. Cisplatin-treated WKY rats and SHR exhibited reduced creatinine clearance (CCr) and increased fractional excretion of sodium (FENa) and kidney index (all P < 0.05), along with tubular damage in the kidney, compared with non-treated rats. In the EDN model, there was marked albuminuria and increased FENa, kidney index and CCr (all P < 0.05) compared with non-diabetic nephropathy (NDN) rats. Amlodipine significantly ( P < 0.05) and dose-dependently attenuated the magnitude of the neurally and adrenergically induced renal vasoconstriction in all experimental groups compared with their respective control groups (13–6 vs 9–5% in renal failure vs non-renal failure WKY rats; 26–15 vs 17–8% in renal failure vs non-renal failure SHR; 19–9 vs 14–5% in EDN vs NDN). 4. The data obtained demonstrate that not only does amlodipine blunt adrenergically induced renal vasoconstriction in normal rats, but that it also does so, and to a greater extent, in rats with either renal failure or hyperfiltration. [ABSTRACT FROM AUTHOR]

This study aimed to quantify the effect of cardiac hypertrophy induced with isoprenaline and caffeine on reflex regulation of renal sympathetic nerve activity by the arterial and cardiopulmonary baroreceptors. Male Wistar rats, untreated or given water containing caffeine and subcutaneous (s.c.) isoprenaline every 72 h for 2 weeks or thyroxines.c. for 7 days, were anaesthetized and prepared for measurement of renal sympathetic nerve activity or cardiac indices. Both isoprenaline–caffeine and thyroxine treatment blunted weight gain but increased heart weight and heart weight to body weight ratio by 40 and 14% (both P < 0.01), respectively. In the isoprenaline–caffeine group, the maximal rate of change of left ventricular pressure and the contractility index were higher by 17 and 14% (both P < 0.01), respectively, compared with untreated rats. In the isoprenaline–caffeine-treated rats, baroreflex gain curve sensitivity was depressed by approximately 30% ( P < 0/05), while the mid-point blood pressure was lower, by 15% ( P < 0/05), and the range of the curve was 60% ( P < 0.05) greater than in the untreated rats. An acute intravenous infusion of a saline load decreased renal sympathetic nerve activity by 42% ( P < 0.05) in the untreated rats but had no effect in the isoprenaline–caffeine- or the thyroxine-treated groups. The isoprenaline–caffeine treatment induced cardiac hypertrophy with raised cardiac performance and an associated depression in the reflex regulation of renal sympathetic nerve activity by both high- and low-pressure baroreceptors. The thyroxine-induced cardiac hypertrophy also blunted the low-pressure baroreceptor-mediated renal sympatho-inhibition. These findings demonstrate that in cardiac hypertrophy without impaired cardiac function, there is a blunted baroreceptor control of renal sympathetic outflow. [ABSTRACT FROM AUTHOR]

ANGII infused ICV in rats on a normal Na+ (NNa+) diet leads to a pressor response and a fall in renal sympathetic nerve activity (RSNA) while rats fed a high Na+ (HNa+) diet also express a later rise in RSNA. This study investigated the impact of peripheral V1 receptor blockade (V1B) on these responses. Male Wistar rats fed a NNa+ (0.3% Na+) or HNa+ (3.0%, Na+) diet for 6 weeks were anaesthetized, cannulae inserted into the femoral artery/vein and right ICV and RSNA recorded from the left kidney. Blood pressure (BP) and RSNA were measured after ICV ANGII (50-100ng in 2µL; NNa+ n=7-10) and during V1 blockade (V1B, Manning compound, 10µg/0.2mL IV; n=6). Data (mean±SE) were compared by ANOVA. P<0.05 indicated significance. Basal BP (mmHg) was similar between groups (ANGII: NNa+ 89±4, HNa+ 95±4; ANGII + V1B: NNa+ 89±4 , HNa+84±4). The 30 min area under the curve (AUC) BP response (ΔmmHg*min) was less during V1B in NNa+ (ANGII: 232±47 vs ANGII+ V1B: 60±29, P<0.05) and HNa+ (ANGII: 237±66 vs ANGII+ V1B: 73±i3, P<0.05). RSNA fell immediately after ICV ANGII in NNa+ (ANGII: 94±3%, ANGII+ V1B: 94±2, P<0.05) and HNa+ (ANGII: 84±6%, ANGII + V1: 91±3%, P<0.05 vs baseline) with no effect of V1B. The rise in RSNA in the HNa+rats 30 min after ICV ANGII was not present during V1B (ANGII:112±2%, ANGII + V1B: 96±6%, P<0.05). The results suggest that V1 receptor activation contributes to the BP and long term rise in RSNA to ICV ANGII. [ABSTRACT FROM AUTHOR]

This study determined the impact of AT1 receptor antisense ODN given icv on the baroreflex control of RSNA in conscious rats. Male Wistar and SHR (n=5-6) were chronically instrumented with cannulae in the femoral artery and jugular vein, electrodes sealed onto the left renal nerve and a cannula implanted into the right lateral cerebroventricle. Three days later, blood pressure (BP) was manipulated by iv phenylephrine and nitroprusside (both at 10µg) to generate baroreflex curves for RSNA (Huang et al 2006, J Physiol 574: 597-604) before and 1 day after the icy administration of 25µg AT1 receptor antisense ODN or 25µg sense ODN dissolved in 20µl lipofectin (1 µg/µl). Means ±SEM were subjected to Student's t test and significance taken at P<0.05. In Wistar rats, BP was 115±5mmHg and was unchanged after the ATI receptor antisense ODN, but there was a significant (P<0.05) increase in the sensitivity of the baroreflex curve of 86.0%. BP in the SHR, at 172±5mmHg, was decreased after the antisense ODN to 148±6mmHg (P<0.05), while the sensitivity of the baroreflex curve increased by 55.1% (P<0.05). Administration of the sense ODN had no effect on BP or the baroreflex curves in either Wistar or SHR. The data showed that whereas the ATI receptor antisense ODN decreased BP only in the SHR, it increased the sensitivity of the baroreflex control of RSNA in both conscious Wistar and SHR. [ABSTRACT FROM AUTHOR]

Purpose: To examine the hypothesis that in hypertensive diabetic rats hydrogen sulphide (H2S) reduces blood pressure through diuretic action in addition to its vasodilating effect. Methods: Spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats were used. SHR were divided into three groups: SHR (II), SHR diabetic (III), and SHR diabetic NaHS-Treated (IV) with a group of WKY (I) rats serving as normotensive nondiabetic control. Diabetes was produced in two SHR groups using intraperitoneal streptozotocin (STZ). One diabetic group received NaHS, a donor of H2S (56 μM/kg i.p.) daily for five weeks. Blood pressure was measured in conscious and anesthetized states in surgically prepared animals. Plasma and urinary H2S levels and electrolytes were measured weekly throughout the 35-day period. Results: SHR and diabetic SHR had higher blood pressure and lower plasma and urinary H2S levels compared to WKY controls (p < 0.05). Moreover, the SHR diabetic group had higher plasma sodium, higher absolute and fractional sodium excretions (p < 0.05) but with similar blood pressure compared to SHR controls. NaHS treatment reduced blood pressure and restored H2S and plasma sodium (p < 0.05) levels. Moreover, SHR diabetic-NaHS treated group had higher urine output and absolute urinary sodium excretion compared to the untreated SHR diabetic group (p < 0.05). Conclusion: These results suggest a possible diuretic effect of exogenous H2S in spontaneously hypertensive diabetic rats. [ABSTRACT FROM AUTHOR]

Abstract: This study set out to investigate the impact of chronic cumulative blockade of angiotensin II and adrenoceptors in WKY and SHR and to explore how the renovascular responses to adrenergic and angiotensin II receptor agonists may be interdependent. Rats were treated with either losartan, carvedilol or losartan+carvedilol for 7 days and on day eight, animals were pentobarbitone anaesthetized and prepared for renal haemodynamic study. Dose–response relationships were determined in terms of reduction/elevation in the magnitude of renal blood flow in response to intrarenal arterial injection of dopamine, phenylephrine and isoprenaline. Renal vascular responses were blunted in WKY and SHR treated with either losartan or carvedilol as compared to their untreated counterparts (P <0.05). In the combined treated rats, the vascular responses to isoprenaline and phenylephrine were restored to levels observed in the untreated rats, but the renal vasoconstrictor responses to dopamine decreased (P <0.05) in both WKY and SHR. There was a reduction of (P <0.05) in the magnitude of the isoprenaline induced renal vasodilation in all SHR as compared to WKY groups. The data obtained showed that the renal vascular action of dopamine, phenylephrine and isoprenaline depended on an intact renin–angiotensin system (RAS) in WKY and SHR. Treatment with losartan or carvedilol blunted the renal vasoconstrictor/vasodilator responses to sympathomimetics which was attenuated with the combined treatment. These observations using chronic blockade of adrenergic and angiotensin receptors demonstrated that there was a long standing interdependency between the RAS and sympathetic nervous system (SNS) in determining the responsiveness of the renal vasculature of normal and hypertensive rats. [Copyright &y& Elsevier]

Abstract: In this study we employed both detrended fluctuation analysis (DFA) and multiscale entropy (MSE) measurements to compare the long-range temporal correlation (LRTC) of multifibre renal sympathetic nerve activity (RSNA) between conscious and anesthetized Wistar rats. It was found that both methods showed the obvious LRTC properties in conscious state. Moreover, the scaling exponent of the RSNA in conscious rats was significantly higher than that in anesthetized rats. The results of MSE analysis showed that the entropy values, derived from the conscious group, increased on small time scales and then stabilized to a relatively constant value whereas the entropy measure, derived from anesthetized animals, almost monotonically decreased. This suggests that the fractal properties of underlying dynamics of the system have been reduced by anesthesia. The results demonstrate that apparently random fluctuations in multifibre RSNA are dictated by a complex deterministic process that imparts “long-term” memory to the dynamic system. However, this memory is significantly weakened by anesthesia. [Copyright &y& Elsevier]