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.

Thermal responses to central angiotensin II, SQ 20881, and dopamine infusions in sheep

1985 ◽  
Vol 248 (3) ◽  
pp. R371-R377 ◽  
Author(s):  
B. S. Huang ◽  
M. J. Kluger ◽  
R. L. Malvin
Keyword(s):  
Angiotensin Ii ◽  
Body Temperature ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Significant Rise ◽  
Ang Ii ◽  
Deep Body Temperature ◽  
Angiotensin System ◽  
Conscious Sheep

The thermoregulatory role of brain angiotensin II (ANG II) was tested by intracerebroventricular (IVT) infusion of ANG II or the converting enzyme inhibitor SQ 20881 (SQ) in 15 conscious sheep. Deep body temperature decreased 0.30 +/- 0.07 degree C (SE) during the 3-h period of IVT ANG II (25 ng/min) infusion (P less than 0.05) and increased 0.50 +/- 0.13 degree C during IVT SQ (1 microgram/min) infusion (P less than 0.01). To determine whether the rise in body temperature after IVT SQ infusion might be the result of a central renin-angiotensin system (RAS), SQ was infused IVT in five conscious sheep 20 h after bilateral nephrectomy. This resulted in a significant rise in body temperature of 0.28 +/- 0.05 degree C (P less than 0.05). When vasopressin antidiuretic hormone (ADH) was infused intravenously at the same time of IVT SQ infusion, the rise in temperature was depressed, but ADH did not lower the temperature below basal. IVT dopamine (20 micrograms/min) increased body temperature by 0.40 +/- 0.04 degree C (P less than 0.01), which was qualitatively similar to the result with IVT SQ. These data support the hypothesis that endogenous brain ANG II may play a role in thermoregulation. Furthermore, plasma ADH level, regulated in part by brain ANG II, is probably not the mediator of that thermoregulation. The similar effects of IVT dopamine and SQ on body temperature strengthen the hypothesis that dopamine may be involved in the central action of brain ANG II.

Natriuretic response to renal interstitial hydrostatic pressure during angiotensin II blockade

1994 ◽  
Vol 266 (1) ◽  
pp. F117-F119 ◽  
Author(s):  
J. A. Haas ◽  
J. C. Lockhart ◽  
T. S. Larson ◽  
T. Henrikson ◽  
F. G. Knox
Keyword(s):  
Angiotensin Ii ◽  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Urinary Sodium Excretion ◽  
Treated Group ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Angiotensin System ◽  
Before And After

Increases in renal interstitial hydrostatic pressure (RIHP) increase urinary sodium excretion (UNaV). Experimentally increasing RIHP by direct renal interstitial volume expansion (DRIVE) has been shown to decrease proximal tubule sodium reabsorption. The purpose of the present study was to investigate whether the renin-angiotensin system modulates the natriuretic response to DRIVE. Unilateral nephrectomy and implantation of two polyethylene matrices were performed 3 wk before the acute experiment. Fractional sodium excretion (FENa), RIHP, and glomerular filtration rate (GFR) were measured before and after DRIVE in control rats (n = 9) and in rats receiving the angiotensin II (ANG II) receptor antagonist, losartan potassium (10 mg/kg i.v.; n = 10). DRIVE was achieved by infusing 100 microliters of 2.5% albumin solution directly into the renal interstitium. GFR remained unchanged by DRIVE in both groups. In control animals, DRIVE significantly increased both RIHP (delta 3.8 +/- 0.5 mmHg) and FENa (delta 0.92 +/- 0.19%). In the losartan-treated group, RIHP (delta 2.8 +/- 0.4 mmHg) and FENa (delta 1.93 +/- 0.41%) also significantly increased. The natriuretic response to DRIVE was significantly enhanced during ANG II receptor blockade compared with control animals (delta UNaV/delta RIHP = 2.01 +/- 0.67 vs. 0.44 +/- 0.17 mu eq.min-1 x mmHg-1, respectively; P < 0.05). These results suggest that the blockade of angiotensin enhances the natriuretic response to increased RIHP during DRIVE.

Atrial natriuretic peptide and pressure natriuresis: interactions with the renin-angiotensin system

1989 ◽  
Vol 257 (5) ◽  
pp. R1169-R1174 ◽  
Author(s):  
H. L. Mizelle ◽  
J. E. Hall ◽  
D. A. Hildebrandt
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Sodium Excretion ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Pressure Natriuresis ◽  
Atrial Natriuretic

The aim of this study was to quantitate the effects of increases in atrial natriuretic peptide (ANP), within the pathophysiological range, on the acute pressure natriuresis mechanism and the role of the renin-angiotensin system (RAS) in modulating these effects. Renal hemodynamics and electrolyte excretion were measured in anesthetized dogs while renal perfusion pressure (RPP) was controlled at three levels (120-122, 100, and 75 mmHg) with and without intrarenal infusion of ANP at 5 ng.kg-1.min-1. Sodium excretion was significantly higher during ANP infusion at RPP of 122 +/- 3 mmHg, averaging 55.8 +/- 13.7 during control and 113.3 +/- 23.3 mueq/min during ANP infusion. AT RPP of 101 +/- 1 mmHg, sodium excretion was 51.8 +/- 17.4 during control and 93.0 +/- 17.6 mueq/min during ANP infusion, but at RPP of 75 +/- 0 mmHg there was no difference in sodium excretion between control and ANP infusion. In a second set of dogs, angiotensin II (ANG II) formation was blocked with captopril (20 micrograms.kg-1.min-1), circulating (5 ng.kg-1.min-1), and the above protocol was repeated. When the RAS was fixed, the renal responses to ANP infusion were abolished, even at the higher pressure levels. These data indicate that ANP increases the slope of pressure natriuresis; at higher levels of RPP, ANP potentiates pressure natriuresis but not at lower pressures. In addition, part of this effect may be due to suppression of the RAS, because the ANP-induced shift in the pressure natriuresis relationship was abolished when circulating ANG II was maintained constant.

Role of angiotensin II in brown adipose thermogenesis during cold acclimation

1993 ◽  
Vol 265 (6) ◽  
pp. E860-E865 ◽  
Author(s):  
L. A. Cassis
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Synaptic Cleft ◽  
Neuronal Uptake ◽  
Ang Ii ◽  
Angiotensin System ◽  
Brown Adipose ◽  
Wet Weight ◽  
And Control

The role of angiotensin II (ANG II) in increased sympathetic neuroeffector mechanisms observed in cold-induced thermogenesis of brown adipose tissue (BAT) was examined. Cold exposure (4 degrees C) for 7 days resulted in an increase in interscapular fat (ISF) ANG II content expressed per gram wet weight or per lobe of ISF, without concomitant changes in plasma components of the renin-angiotensin system. Additionally, in ISF slices preloaded with [3H]norepinephrine (NE), ANG II (10 nM) resulted in an increase (3-fold) in evoked 3H overflow from ISF slices from cold-exposed rats compared with ambient temperature controls. However, although basal 3H outflow was increased (2-fold) in ISF slices from cold-exposed rats, evoked 3H overflow was not different between ISF slices from cold-exposed and control rats. Specific neuronal uptake of [3H]NE in ISF slices from cold-exposed rats was decreased by 64%. Administration of the non-peptide AT1-receptor antagonist losartan to cold-exposed rats resulted in complete inhibition of ANG II-mediated presynaptic facilitation of evoked 3H overflow from ISF slices. However, losartan administration had no effect on cold-induced increases in ANG II content, protein content, and decreases in neuronal [3H]NE uptake in ISF. Results from these studies suggest that cold-induced thermogenesis of BAT results in alterations in presynaptic ANG II facilitation of NE release and defects in removal of NE from the synaptic cleft (neuronal uptake), both of which would enhance sympathetic nervous system-mediated thermogenesis. Furthermore, these results demonstrate a role for ANG II in enhanced sympathetic activity of cold-induced thermogenesis in BAT.

scholarly journals Renoprotective impact of angiotensin 1-7: Is it certain?

2018 ◽  
Vol 8 (1) ◽  
pp. 1-1
Author(s):  
Mehdi Nematbakhsh
Keyword(s):  
Angiotensin Ii ◽  
Physiological Condition ◽  
Renin Angiotensin System ◽  
Short Review ◽  
Protective Role ◽  
Ang Ii ◽  
Angiotensin System ◽  
Normal Physiological Condition ◽  
Current Article

The two important arms of renin angiotensin system (RAS) are angiotensin II (Ang II) and angiotensin1-7 (Ang1-7). Both of these peptides are present in the kidney, while the renal hemodynamic responses to these peptides act differently in kidney circulation. For this short-review, we used a variety of sources including PubMed, Google Scholar, and Scopus. Although in normal physiological condition, Ang1-7 has been known as an inactive agent in the renal system, however in past years many experimental and clinical reports indicated the protective role of Ang1-7 in renal hemodynamics and functions under different circumstances. In the current article, the possible renoprotective role of Ang1-7 was briefly reviewed.

Measurement of the Renin-Angiotensin System in Heart Failure

2000 ◽  
Vol 1 (3) ◽  
pp. 210-226 ◽  
Author(s):  
Shann Dixon Kim
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Advantages And Disadvantages ◽  
Angiotensin I Converting Enzyme

Angiotensin II (ANG II), the effector hormone of the renin-angiotensin system (RAS), has been implicated in the pathophysiology and progression of heart failure. Therefore, the measurement of ANGII has become important to characterize the role of this neurohormone in heart failure. However, because ANG II has been difficult to measure, other components of the RAS have been measured to characterize ANG II production. The RAS components (e.g., renin, angiotensin I–converting enzyme [ACE], angiotensin II) have been measured with a variety of techniques. In this review, RAS physiology and the techniques used to measure the RAS components are discussed. In addition, the advantages and disadvantages of the RAS measurement methods are described.

Involvement of renin-angiotensin system in the reduced pressure natriuresis response of hyperthyroid rats

1995 ◽  
Vol 268 (5) ◽  
pp. E897-E901 ◽  
Author(s):  
J. Garcia-Estan ◽  
N. M. Atucha ◽  
T. Quesada ◽  
F. Vargas
Keyword(s):  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor ◽  
Reduced Pressure ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Pressure Natriuresis

Previous studies have indicated that the pressure diuresis and natriuresis (PDN) response is greatly impaired in thyroxine-treated hypertensive rats. In the present study, we have examined the role of the renin angiotensin system (RAS) as a mediator of these alterations by characterizing the relationships between renal perfusion pressure and urine flow and sodium excretion in hyperthyroid rats acutely treated with a converting-enzyme inhibitor (captopril, 2 mg/kg) or an AT1 angiotensin II receptor blocker (losartan, 10 mg/kg). In the control animals, captopril did not change mean arterial pressure (MAP) or renal blood flow (RBF) but significantly decreased MAP and increased RBF and glomerular filtration rate in the hyperthyroid rats. Captopril did not change the PDN response of the control animals but improved significantly that of the hyperthyroid rats, although it was not completely normalized. Losartan also significantly improved renal hemodynamics and excretion in hyperthyroid rats. These results indicate that an increased intrarenal activity of the RAS is partly responsible for the blunted renal PDN mechanism of the hyperthyroid rats.

Possible modulatory role of angiotensin II on atrial peptide-induced natriuresis

1987 ◽  
Vol 253 (5) ◽  
pp. F880-F883
Author(s):  
F. J. Salazar ◽  
J. P. Granger ◽  
M. J. Fiksen-Olsen ◽  
M. D. Bentley ◽  
J. C. Romero
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Fractional Excretion ◽  
Ang Ii ◽  
Angiotensin System ◽  
Fractional Excretion Of Sodium ◽  
Proximal Tubular ◽  
Anesthetized Dogs ◽  
Natriuretic Effect

Studies showing that atrial natriuretic peptides (ANP) induce a suppression of the renin-angiotensin system suggest that there might be a modulatory influence of angiotensin II (ANG II) on the natriuretic effect of the ANP system. To evaluate this possibility we assessed, in anesthetized dogs, the net increments in fractional excretion of sodium (FENa) and lithium (FELi) produced by ANP and by the inhibition of ANG II formation with captopril. These agents were infused at separate time periods into the renal artery at a maximal level that has been shown not to alter glomerular filtration rate (GFR). ANP caused an increment in FENa of 4.0 +/- 0.2, whereas captopril caused a much smaller increase of 0.2 +/- 0.04, indicating that most of the natriuretic effect of ANP is unlikely to be solely accounted for by inhibition of ANG II. The administration of both ANP and captopril produced increases in the FELi used as a marker for proximal tubular reabsorption. An infusion of ANG II superimposed on the infusion of captopril reduced the FENa from 1.5 +/- 0.3 to 0.8 +/- 0.1. Under these conditions the administration of ANP produced an increment of 2.7 +/- 0.4 in the FENa. This increase in FENa is 32.5% less than the net increase obtained when ANP was given in the absence of ANG II, whereas under these conditions FELi remained statistically unchanged. These results suggest that the modulatory activity of ANG II on the natriuretic affect of ANP could be negligible under normal conditions.

Renin-angiotensin system and aldosterone secretion during aortic constriction in the rat

1977 ◽  
Vol 232 (5) ◽  
pp. F434-F437 ◽  
Author(s):  
R. H. Freeman ◽  
J. O. Davis ◽  
W. S. Spielman
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Bilateral Nephrectomy ◽  
Aortic Constriction ◽  
Aldosterone Secretion ◽  
Experimental Conditions ◽  
Angiotensin System ◽  
Renin Angiotensin

Suprarenal aortic constriction sufficient to reduce renal perfusion pressure by approximately 50% increased aldosterone secretion in anesthetized rats pretreated with dexamethasone. Bilateral nephrectomy under the same experimental conditions blocked the aldosterone response. Additionally, [1-sarcosine, 8-alanine]angiotensin II blocked the response in aldosterone secretion to aortic constriction in dexamethasone-treated rats. Finally, in rats hypophysectomized to exclude the influence of ACTH, the aldosterone response to aortic constriction was blocked by [1-sarcosine, 8-alanine]angiotensin II. The results indicate that angiotensin II increased aldosterone secretion during aortic constriction in the rat. These observations, along with those reported previously in sodium-depleted rats, point to an important overall role for the renin-angiotensin system in the control of aldosterone secretion in the rat.

scholarly journals Intracrine angiotensin II functions originate from noncanonical pathways in the human heart

2016 ◽  
Vol 311 (2) ◽  
pp. H404-H414 ◽  
Author(s):  
Carlos M. Ferrario ◽  
Sarfaraz Ahmad ◽  
Jasmina Varagic ◽  
Che Ping Cheng ◽  
Leanne Groban ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Functional Significance ◽  
Vascular Remodeling ◽  
Human Heart ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Extended Form ◽  
Angiotensin I ◽  
Angiotensin System ◽  
Ras Genes

Although it is well-known that excess renin angiotensin system (RAS) activity contributes to the pathophysiology of cardiac and vascular disease, tissue-based expression of RAS genes has given rise to the possibility that intracellularly produced angiotensin II (Ang II) may be a critical contributor to disease processes. An extended form of angiotensin I (Ang I), the dodecapeptide angiotensin-(1–12) [Ang-(1–12)], that generates Ang II directly from chymase, particularly in the human heart, reinforces the possibility that an alternative noncanonical renin independent pathway for Ang II formation may be important in explaining the mechanisms by which the hormone contributes to adverse cardiac and vascular remodeling. This review summarizes the work that has been done in evaluating the functional significance of Ang-(1–12) and how this substrate generated from angiotensinogen by a yet to be identified enzyme enhances knowledge about Ang II pathological actions.

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