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.

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.

Angiotensin II downregulates ACE2-mediated enhancement of MMP-2 activity in human cardiofibroblasts

2013 ◽  
Vol 91 (6) ◽  
pp. 435-442 ◽  
Author(s):  
Tang-Ching Kuan ◽  
Mu-Yuan Chen ◽  
Yan-Chiou Liao ◽  
Li Ko ◽  
Yi-Han Hong ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Signaling Pathway ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Lentiviral Infection ◽  
And Control

Angiotensin converting enzyme II (ACE2) is a component of the renin-angiotensin system (RAS) that negatively regulates angiotensin II (Ang II). Ang II, in turn, affects the expression of matrix metalloproteinases (MMPs) to induce heart remodeling. The specific mechanisms by which ACE2 regulates MMP-2, however, remain unclear. The aim of this study was to investigate the regulatory relationships between Ang II, ACE2, and MMP-2. ACE2 expression was upregulated and downregulated in human cardiofibroblasts (HCFs) by lentiviral infection. Effects on MMP-2 activity, shed ACE2 activity, extracellular signal-regulated kinase (ERK) signaling pathway, and ADAM metallopeptidase domain 17 (ADAM17) expression were assessed. ACE2 increased MMP-2 activity, and Ang II inhibited this effect through the Ang II type-1 receptor (AT1R) and ERK1/2 signaling pathway. Ang II also reduced the effect of ACE2 on ERK1/2 levels, the activity of shed ACE2, and adam17 expression in HCFs. Additionally, these Ang II-mediated reductions could be attenuated by AT1R antagonist valsartan. In conclusion, these data help to clarify how ACE2 and Ang II interact to regulate MMP-2 and control tissue remodeling in heart disease.

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.

A novel mechanism for angiotensin II formation in streptozotocin-diabetic rat glomeruli

2005 ◽  
Vol 288 (6) ◽  
pp. F1183-F1190 ◽  
Author(s):  
Rekha Singh ◽  
Ashok K. Singh ◽  
David J. Leehey
Keyword(s):  
Angiotensin Ii ◽  
Renin Angiotensin System ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Ang Ii ◽  
Sprague Dawley ◽  
New Information ◽  
Sprague Dawley Rats ◽  
And Control

Recent evidence suggests that the intrarenal renin-angiotensin system (RAS) may play an important role in the development of glomerular changes associated with diabetic nephropathy. In this study, the glomerular RAS was examined in male Sprague-Dawley rats made diabetic with streptozotocin (STZ), and the findings compared with those obtained in control nondiabetic rats. In diabetic rat glomerular extracts, angiotensinogen and angiotensin II (ANG II) levels were increased significantly by 2.2- and 1.9-fold, respectively, compared with nondiabetic controls. No significant differences in ANG I and angiotensin-converting enzyme (ACE) levels were observed between these groups. The HPLC analysis of the glomerular extracts demonstrated that exogenous ANG I was converted into various ANG peptides including ANG II, ANG(1–9), and ANG(1–7). A significant increase in formation of ANG II from exogenous ANG I was observed in STZ rats compared with control rats. Preincubation of glomerular extracts with captopril resulted in a 20–30% decrease in ANG II conversion from exogenous ANG I in diabetic and control rats. The possible role of ANG(1–9) in formation of ANG II was examined by HPLC. Exogenous ANG(1–9) in glomerular extracts was converted into ANG II, this conversion being significantly higher in STZ rats than in control rats. These findings provide new information that ANG(1–9) is produced in rat glomerular extracts, can be converted to ANG II, and that this conversion is also stimulated in diabetic rat glomeruli. Thus this study demonstrates that in diabetic rats, glomerular ANG II levels are increased due to an increase in angiotensinogen and an increase in the formation of ANG II.

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.

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.

scholarly journals Angiotensin-II as a Trigger Factor in the Development of Retinopathy of Prematurity

2020 ◽  
Vol 17 (4) ◽  
pp. 746-751
Author(s):  
L. A. Katargina ◽  
N. B. Chesnokova ◽  
O. V. Beznos ◽  
N. A. Osipova ◽  
A. Yu. Panova
Keyword(s):  
Angiotensin Ii ◽  
Retinopathy Of Prematurity ◽  
Renin Angiotensin System ◽  
Trigger Factor ◽  
Practical Significance ◽  
Angiotensin System ◽  
Significant Difference ◽  
And Control ◽  
Experimental Group

The multifactorial nature of the retinopathy of prematurity (ROP) pathogenesis, makes the thorough study of the mechanism of pathological retinal neovascularization actual. However recently the attention of scientists has been attracted by the participation of renin-angiotensin system (RAS) in the development of retinal vasoproliferative diseases. Purpose: to study the role of AT-II in the pathogenesis of experimental ROP (EROP) in the original model of the disease. Material and methods. To reproduce EROP Wistar rats (n = 15) were exposed to the oxygen concentration varying from 60 to 15% every 12 hours for 14 days from the first day after birth followed by room air for 7 days. Throughout the experiment, the room maintained a constant temperature (+26 °C) and light regime (12 hours a day, 12 hours a night) modes. Control rats (n = 12) were born and kept under normal oxygen content (21 %). Batches of EROP (n = 5) and control (n = 4) rats were sacrificed on 7, 14 and 21 days. All rats underwent binocular enucleation, after which every eyeball was opened on the limb, the cornea and lens were removed with the remains of a persistent vascular bag and a hyaloid artery. Retinas were isolated, homogenized and stored at -20 °C. Angiotensin-II (AT-II) in homogenates was measured using the IFA kit. Results. On the 7th day of the experiment, the level of AT-II in the retina of the experimental group rats was 0.19 ± 0.02 pg/mg protein that was significantly higher than in controls (0.12 ± 0.01 pg/mg protein). On the 14th and 21st days concentrations of AT-II in EROP and control groups had no significant difference. Conclusion. On the 7th day of the experiment, i.e. at the period corresponding to the existence of avascular retinal zones in both groups concentration of AT-II in the retinas of rats with EROP was significantly higher than in controls. This fact indicate the role of this proangiogenic factor in the induction of pathological neovascularization in ROP. Possible prognostic function of this parameter during the period before ROP manifestation has undoubted practical significance.

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.

Central effects of angiotensin II and dopamine in sodium-depleted sheep

1985 ◽  
Vol 248 (5) ◽  
pp. R541-R548
Author(s):  
B. S. Huang ◽  
R. L. Malvin ◽  
R. J. Grekin
Keyword(s):  
Angiotensin Ii ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Ang Ii ◽  
Angiotensin System ◽  
Aldosterone Level ◽  
Central Effects ◽  
Dopaminergic Pathway

The effects of intracerebroventricular (IVT) infusion of angiotensin II (ANG II), the converting enzyme inhibitor SQ 20881, and dopamine were studied in 15 conscious Na-depleted sheep. IVT ANG II (25 ng/min) significantly increased plasma aldosterone (163 +/- 24%) and vasopressin (ADH) (533 +/- 100%). Plasma renin activity (PRA) was decreased to 64 +/- 10% of basal. IVT SQ (1 microgram/min) decreased aldosterone to 70 +/- 10% and ADH to 55 +/- 9% of basal. PRA increased to 124 +/- 10%. There were no significant changes in plasma Na, K, or cortisol levels nor in mean arterial or intracranial pressure after either infusion. Increasing the dose of SQ to 10 micrograms/min resulted in an increased magnitude of change in the same variables. IVT SQ (1 microgram/min) significantly decreased aldosterone level in five nephrectomized sheep. The responses to IVT dopamine (20 micrograms/min) were qualitatively similar to those elicited by IVT SQ. These data support the existence of an endogenous brain renin-angiotensin system (RAS) independent of the renal RAS. ANG II acts centrally to regulate plasma ADH, aldosterone, and PRA levels. The similarity of the responses to SQ and dopamine suggests that a dopaminergic pathway may be involved in these responses.

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