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This study investigated the impact of intrarenal angiotensin 1–7 (Ang [1–7]) infusion on renal excretory function in a rat model of hypertension. Eleven‐week‐old spontaneously hypertensive rats (SHRs, n = 7) and Han Wistar controls (NCR, n = 7) were anaesthetised with sodium pentobarbital (60 mg/kg i.p.) and prepared for the measurement of mean arterial pressure (MAP) and left renal function during renal interstitial infusion of Ang (1–7) (50 ng/min). The kidneys were harvested, the renal cortex and medulla separated, prepared for measurement of Ang II and Ang (1–7) and Western blot determination of AT1 and Mas receptor protein expression. MAP, glomerular filtration rate (GFR), urine flow (UF) and absolute sodium excretion (UNaV) were 109 ± 16 mmHg, 4.4 ± 1.0 mL/min/kg, 102 ± 16 µL/min/kg and 16 ± 3 µmol/min/kg, respectively in the NCR and 172 ± 24 mmHg, 3.4 ± 0.7 mL/min/kg, 58 ± 30 μL/min/kg and 8.6 ± 4.8 μmol/min/kg respectively in the SHR. Ang (1–7) increased UF (31%), UNaV (50%) and fractional sodium excretion (FENa+) (22%) in the NCR group (all p < 0.05) but had no effect on GFR in either group. The magnitudes of the Ang (1–7)‐induced increases in UF and UNaV were significantly blunted in the SHR group (model × drug p < 0.05). The renal cortical AT1: Mas receptor expression ratio was significantly higher in the SHR group (p < 0.05) but renal Ang II and Ang (1–7) levels were not statistically different between groups. The Ang (1–7)‐induced increases in sodium and water excretion were impaired in the SHR group in the context of an unstimulated RAS. The decrease in responsiveness of the SHR kidney to Ang (1–7) appears to be associated with higher levels of AT1 receptor expression in the renal cortex. [ABSTRACT FROM AUTHOR]

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 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]

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]

1. Acute renal failure develops as a result of periods of renal ischaemia during cardiovascular surgery or hypovolaemic shock. The present study investigated the importance of endogenous prostaglandin production and nitric oxide (NO) in the renal haemodynamic and excretory responses to ischaemia–reperfusion both normally and in the hypertensive state by chronic administration of cyclo-oxygenase (COX) inhibitors. 2. Male Wistar and stroke-prone spontaneously hypertensive rats (SHRSP) were subjected to 30 min renal ischaemia and 2 h reperfusion following 7 day treatment with vehicle, aspirin, NO–aspirin or celecoxib. 3. Renal blood flow was higher in the SHRSP treatment groups. Renal ischaemia increased blood pressure in all Wistar groups except that given aspirin, had no effect in the SHRSP and did not change renal blood flow in any group. Glomerular filtration rate was reduced throughout the reperfusion period in both rat strains. The postischaemic diuresis in the Wistar was enhanced by COX-2 inhibition, but not by aspirin or NO–aspirin. Urine flow increased in SHRSP during the postischaemic period, which was blunted by aspirin and NO–aspirin, but not by celecoxib. There was a postischaemic increase in fractional sodium excretion, the magnitude of which was unaltered by any drug in the Wistar rats, but was blunted by aspirin, NO–aspirin and celecoxib in SHRSP. 4. These results suggest that products of COX activity contribute to the renal responses to ischaemia–reperfusion injury, but in different ways, in SHRSP, which may reflect variations in renal prostaglandin and NO production in the hypertensive state. [ABSTRACT FROM AUTHOR]

Summary 1. The present study explored the impact of endothelin (ET) and its interaction with renal sympathetic nerves in the control of volume homeostasis in obesity. 2. Groups of lean and obese Zucker rats with innervated and denervated kidneys were subjected to an acute isotonic saline volume expansion (VE), 10% bodyweight and renal haemodynamics and excretory function were evaluated following administration of SB209670 (a non-selective ET antagonist) or UK 350 926 (a selective ET[sub A] receptor antagonist). 3. Volume expansion in untreated obese rats resulted in a blunted cumulative urine sodium excretion (CuU[sub Na] V) after 40 min, VE compared with untreated lean rats being 36 and 51% in the denervated and innervated kidneys, respectively (both P < 0.001). 4. In lean rats, both SB209670 and UK 350 926 caused a depressed ability to excrete the saline load and CuU[sub Na] V after 40 min, VE compared with untreated being decreased by 51 and 60% in the denervated and innervated kidneys, respectively (both P < 0.001). 5. SB209670 and UK 350 926 given to obese rats reduced (both P < 0.001) CuU[sub Na] V after VE by 43% in denervated kidneys compared with untreated obese rats, whereas they were without effect on the magnitude of the excretory response in innervated kidneys. 6. These findings show that the blunted renal excretory responses to VE present in obese rats were not mediated by ET. Conversely, ET, acting through ET[sub A] receptors, plays a role as a diuretic and natriuretic factor in maintaining volume homeostasis by, at least in lean rats, renal nerve-independent mechanisms. [ABSTRACT FROM AUTHOR]

Examines the role of brain angiotensin (ANG) II in the somatosensory induced antinatriuresis in the anaesthetized rat. Ability of the brain to modulate autonomic reflexes; Attempts to block the generation of ANGII within the brain by giving captopril i.c.v.; Analysis on the effect of ANGII with captopril into the central nervous system.

Develops an approach whereby the high-dimensional signal of renal sympathetic nerve activity (RSNA) was reduced to a low-dimensional one by extracting the peak interval sequence in order to allow the use of non-linear dynamics analysis. Effect of brachial nerves stimulation on the blood pressure and heart rate of Wistar rats; Description of the renal sympathetic innervation process.