scholarly journals Role of Angiotensin II in the Neural Control of Renal Function

Hypertension ◽  
2003 ◽  
Vol 41 (3) ◽  
pp. 583-591 ◽  
Author(s):  
Marie E. Le Fevre ◽  
Sarah-Jane Guild ◽  
Rohit Ramchandra ◽  
Carolyn J. Barrett ◽  
Simon C. Malpas
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Neural Control

scholarly journals Role of angiotensin II in the altered renal function of congestive heart failure.

1984 ◽  
Vol 55 (5) ◽  
pp. 669-675 ◽  
Author(s):  
I Ichikawa ◽  
J M Pfeffer ◽  
M A Pfeffer ◽  
T H Hostetter ◽  
B M Brenner
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Renal Function ◽  
Angiotensin Ii

Abstract 7: Angiotensin II Type 2 Receptor Deficiency Increases Renal ACE/ACE2 Ratio-Ang II-AT1R Expression In Male but not in Female Mice

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Quaisar Ali ◽  
Yonnie Wu ◽  
Tadashi Inagami ◽  
Tahir Hussain
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Angiotensin Ii ◽  
Renin Activity ◽  
Ang Ii ◽  
Male And Female ◽  
Female Mice ◽  
Gender Specific

Angiotensin II acting via Angiotensin II type 2 receptors (AT2Rs) is believed to be protective against blood pressure increase and affects renal function under pathophysiological condition. Recently we have observed that stimulation of AT2Rs in male obese Zucker rats has shifted the two opposing arms of renin angiotensin system (RAS) i.e. ACE-Ang II-AT1 vs ACE2/Ang-(1-7)-Mas. Evidence suggests that estrogen regulates RAS, including AT2R in female mice. We hypothesized that AT2R has a gender specific regulation of RAS. In the present study, we investigated the role of AT2Rs in regulating RAS components in male and female mice. Kidney cortex from AT2R knockout (AT2RKO) male and female mice and wild type (WT) with similar background (C57BL/6) of 20 weeks of age were used in the study. The cortical ACE expression (ng ACE/μg tissue) was significantly increased in AT2RKO mice (3±0.02) compared to WT males (1.9±0.02). LC/MS analysis of cortical tissue revealed that Ang II was also significantly increased in AT2RKO mice (WT: 31±3, AT2RKO: 47±3 fmoles/mg tissue). Deletion of AT2R significantly increased AT1R (204%, 204 of 100) expression and had no effect on renin activity compared to WT males. The cortical expression of ACE2 activity (WT: 113±8, AT2RKO: 40±11, RFU/min), Ang-(1-7) levels (WT: 7.3±1.4, AT2RKO: 3±0.8 fmoles/mg tissue) and Mas receptor (AT2RKO: 54±15, % of WT) was significantly decreased in AT2RKO males compared to WT. The cortical expression of the AT2R and MasR was 2-fold greater in WT females compared to WT male. The renin activity (WT: 32±2, AT2RKO: 21±0.3, RFU/min) and MasR expression (WT: 187.5±55, AT2KO: 47±9) was significantly decreased in AT2RKO females compared to the female WT. Interestingly, Ang-(1-7) level (WT: 5.7±0.7, AT2RKO 2.6±0.7 fmoles/mg tissue) was decreased but no changes in ACE or ACE2 activity was observed in AT2KO females compared to their WT, suggesting a role of non-ACE2 pathway. This study suggests that AT2R regulates ACE/ACE2 ratio-Ang II-AT1R expression negatively only in males, whereas in females, it regulates Ang-(1-7) potentially via non-ACE2 pathway. Such changes indicate a gender specific mechanisms potentially associated with AT2R-mediated regulation of renal function and blood pressure control.

Physiology in perspective: The Wisdom of the Body. Neural control of the kidney

2005 ◽  
Vol 289 (3) ◽  
pp. R633-R641 ◽  
Author(s):  
Gerald F. DiBona
Keyword(s):  
Nervous System ◽  
Renal Function ◽  
Autonomic Nervous System ◽  
Neural Control ◽  
Sympathetic Nerves ◽  
The Body ◽  
Regulatory Agencies ◽  
Internal Environment ◽  
Renal Sympathetic

Cannon equated the fluid matrix of the body with Bernard’s concept of the internal environment and emphasized the importance of “the safe-guarding of an effective fluid matrix.” He further emphasized the important role of the autonomic nervous system in the establishment and maintenance of homeostasis in the internal environment. This year’s Cannon Lecture discusses the important role of the renal sympathetic nerves to regulate various aspects of overall renal function and to serve as one of the major “self-regulatory agencies which operate to preserve the constancy of the fluid matrix.”

scholarly journals The role of angiotensin II and TGF-beta on the progression of chronic allograft nephropathy

2001 ◽  
Vol 2 (1_suppl) ◽  
pp. S188-S190
Author(s):  
Matthew R Weir ◽  
Chiming Wei
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Transforming Growth Factor ◽  
Experimental Studies ◽  
Chronic Allograft Nephropathy ◽  
Angiotensin Ii Receptor ◽  
Direct Stimulation ◽  
Converting Enzyme Inhibitors ◽  
Transplant Patients

Chronic allograft nephropathy is the most prevalent cause of graft dysfunction and failure. Its pathogenesis and treatment remains poorly defined. The calcineurin inhibitors, cyclosporine and tacrolimus, may play a role in the progressive loss of renal function in patients with chronic allograft nephropathy. This effect may be either related to the direct stimulation of profibrogenic cytokines such as transforming growth factor (TGF-β) or indirect mechanisms, through increases in blood pressure or alterations in either carbohydrate or lipid metabolism. Experimental studies have demonstrated that angiotensin-converting enzyme inhibitors (ACE-I) and angiotensin II receptor blockers (ARBs) can attenuate cyclosporine-mediated increases in TGF-β production in renal tissue. Clinical studies have demonstrated that either cyclosporine or tacrolimus dose reduction may help reduce the rate of loss of renal function in patients with chronic allograft nephropathy. Moreover, other studies have demonstrated that a chronic reduction in the dose of cyclosporine in transplant patients can reduce serum TGF-β levels. Treatment with an ARB can normalise the plasma levels of TGF-β in renal transplant patients receiving cyclosporine. All these observations suggest that there may be a role of cyclosporine, and possibly tacrolimus, in worsening chronic allograft nephropathy through their effects on the renin-angiotensin-aldosterone system (RAAS) and TGF-β production.

scholarly journals Role of nNOS in Regulation of Renal Function in Angiotensin II–Induced Hypertension

Hypertension ◽  
2001 ◽  
Vol 38 (2) ◽  
pp. 280-285 ◽  
Author(s):  
Luděk Červenka ◽  
Herbert J. Kramer ◽  
Jan Malý ◽  
Jiří Heller
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Induced Hypertension

Abstract 135: Obesity Accelerates the Deterioration of Renal Function in Developmental Programming of Hypertension. Role of Angiotensin Ii and Oxidative Stress

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Antonio Tapia ◽  
Juan M Moreno ◽  
Maria T Llinas ◽  
F. Javier Salazar
Keyword(s):  
Oxidative Stress ◽  
Renal Function ◽  
Angiotensin Ii ◽  
Perinatal Period ◽  
Developmental Programming ◽  
Ang Ii ◽  
Obese Rats ◽  
Renal Vascular ◽  
And Oxidative Stress

Numerous studies have shown gender-dependent differences in the deterioration of renal function in models of developmental programming of hypertension (DPH). It is also known that obesity is associated to changes in renal function and that both angiotensin II (Ang II) and oxidative stress are involved in the renal alterations that occur in obesity and in animals with DPH. The main objectives were to examine whether the increment of arterial pressure (AP) and the deterioration of renal function are accelerated as a consequence of obesity in SD rats with DPH; whether these changes are gender-dependent; and to evaluate the role of Ang II and oxidative stress in these AP and renal function changes. A high fat diet (60%) was given during the first 4 months of age and DPH was induced by an AT receptor antagonist during nephrogenic period (ARAnp). Systolic AP (mmHg) was greater (P<0.05) in ARAnp-obese rats (167 ± 3 in ♂; 146 ± 4 in ♀) than in ARAnp (155 ± 3 in ♂; 137 ± 3 in ♀); obese (147 ± 2 in ♂; 137 ± 2 in ♀) or control (127 ± 1 in ♂; 119 ± 2 in ♀) rats. Three days administration of candesartan (7 mg/kg/day) led to a decrease in AP that was greater (P<0.05) in ARAnp-obese rats (55 ± 3 in ♂; 45 ± 4 in ♀) than in ARAnp (40 ± 3 in ♂; 37 ± 4 in ♀); obese (38 ± 4 in ♂; 27 ± 4 in ♀) or control (12 ± 2 in ♂; 14 ± 3 in ♀) rats. The acute Ang II infusion (30 ng/kg/min) induced an increase in renal vascular resistance (mmHg/ml/min/gr kw) that was also greater in ARAnp-obese rats (217 ± 45% in ♂; 145 ± 38% in ♀) than in ARAnp (103 ± 9% in ♂; 97 ± 8% in ♀); obese (106 ± 14% in ♂; 106 ± 17 in ♀) or control (51 ± 7% in ♂; 51 ± 10% in ♀) rats. The response to candesartan or Ang II infusion in ARAnp-obese rats was gender-dependent and may be explained by an enhanced oxidative stress. The expression of P67phox in the renal cortex was greater (P<0.05) in ARAnp-obese rats (3,00 ± 0,05 in ♂; 2,60 ± 0,04 in ♀) than in ARAnp (1,16 ± 0,04 in ♂; 1,66 ± 0,03 in ♀); obese (0,94 ± 0,06 in ♂; 1,02 ± 0,02 in ♀) or control (1,00 ± 0,02 in ♂; 1,02 ± 0,023 in ♀) rats. The results of this study suggest that obesity at an early age enhances the hypertension and accelerates the deterioration of renal function that occurs when cardiovascular disease is programmed during the perinatal period. It is also shown that Ang II and oxidative stress seems to play an important role in these AP and renal function changes.

Renal function during reflexly activated catecholamine flow through an adrenorenal rete

1981 ◽  
Vol 240 (1) ◽  
pp. F30-F37
Author(s):  
R. E. Katholi ◽  
S. P. Bishop ◽  
S. Oparil ◽  
T. N. James
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Renal Plasma Flow ◽  
Sympathetic Nerves ◽  
Urinary Sodium Excretion ◽  
Intrarenal Blood Flow ◽  
Reflex Activation ◽  
Flow Through ◽  
Renal Sympathetic

Reflex vasoconstriction that occurs in the kidney of the dog can be the result of either of two mechanisms. The first is by activation of the renal sympathetic nerves and the second by reflex activation of catecholamine flow through an adrenorenal rete. Both reflex mechanisms can be activated by transient hypotension caused by experimentally induced atrial fibrillation in the sodium-replete pentobarbital-anesthetized dog. This study was undertaken to measure and compare the magnitude of changes in renal function that occur when these reflex mechanisms are activated and to evaluate the possible role of intrarenal angiotensin II in these two reflex effects. Reflex activation of catecholamine flow through an adrenorenal rete in intact or denervated kidneys produced a 26 +/- 3% decrease in renal plasma flow, a 23 +/- 4% decrease in glomerular filtration rate, a 58 +/- 7% decrease in urinary sodium excretion, and a 4 +/- 1% increase in filtration fraction, but no change in the fractional distribution of intrarenal blood flow. Changes of a similar direction and magnitude were seen in the same animals during reflex activation of the renal sympathetic nerves in the kidneys with intact or ligated adrenorenal rete. The same studies were performed after the intrarenal action of angiotensin II was blocked with [Sar1,Ala8]angiotensin II and similar responses were seen. Both of these reflexes appear to be important mechanisms by which the kidney can maintain vascular volume, and neither depends on intrarenal angiotensin II activity.

In the Lyon hypertensive rat, renal function alterations are angiotensin II dependent

1996 ◽  
Vol 271 (2) ◽  
pp. R346-R351 ◽  
Author(s):  
K. L. Liu ◽  
J. Sassard ◽  
D. Benzoni
Keyword(s):  
Renal Function ◽  
Angiotensin Ii ◽  
Blood Pressure Level ◽  
Renin Angiotensin System ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Angiotensin System ◽  
Pressure Natriuresis

To assess the role of the renin-angiotensin system (RAS) in the renal alterations of the lyon hypertensive (LH) rat, the renal function of LH rats and of their normotensive (LN) controls was studied at different pressure levels after an early and chronic blockade of the RAS by perindopril (3 mg.kg-1.day-1 orally from 3 to 15 wk of age) and after an acute infusion of angiotensin II (ANG II, 10 or 50 ng.kg-1.min-1). Over the range of renal perfusion pressures studied (115-165 mmHg), control LH differed from LN rats by an increased preglomerular vasoconstriction and a blunted pressure-natriuresis curve. Perindopril fully prevented the development of hypertension in LH rats, suppressed their preglomerular vasoconstriction, and markedly improved their pressure-natriuresis. In perindopril-treated LH, ANG II produced a greater reduction in renal blood flow, glomerular filtration rate, and urinary sodium excretion that was not significantly modified by blockade of thromboxane A2-prostaglandin H2 receptors. These results indicate that the blood pressure level and the renal function of LH rats are closely dependent on an active RAS.

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