Effect of oral contraceptives on the renin angiotensin system and renal function

2001 ◽  
Vol 280 (3) ◽  
pp. R807-R813 ◽  
Author(s):  
Amrit K. Kang ◽  
John A. Duncan ◽  
Daniel C. Cattran ◽  
John S. Floras ◽  
Vesta Lai ◽  
...  
Keyword(s):  
Lower Body Negative Pressure ◽  
Renal Plasma Flow ◽  
Premenopausal Women ◽  
Renin Angiotensin System ◽  
Renin Secretion ◽  
Control Group ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Active Renin

We examined the effect of oral contraceptive (OC) usage on the renin angiotensin system (RAS) in two related experiments. In the first experiment, subjects were 34 healthy, normotensive, premenopausal women, 15 OC users and 19 OC nonusers, mean age 25 ± 1 yr, ingesting a controlled sodium diet. We assessed arterial pressure, glomerular filtration rate, effective renal plasma flow, renal vascular resistance (RVR), and filtration fraction (FF) using inulin and p-aminohippurate clearance techniques, both at baseline and in response to the ANG II receptor blocker losartan. In the second experiment, in similar subjects, 10 OC users and 10 nonusers, we examined circulating RAS components [angiotensinogen, ANG II, aldosterone, plasma renin activity (PRA), and active renin] in response to incremental lower body negative pressure (LBNP), to determine whether renin secretion is suppressed by OC usage. OC users exhibited elevations in systolic blood pressure, RVR, and FF compared with nonusers, which were partially corrected by losartan. In the LBNP phase of the study, baseline measures of PRA, angiotensinogen, ANG II, and aldosterone were all increased in the OC group compared with the control group. Active renin levels did not differ between groups. Incremental LBNP resulted in increased circulating levels of RAS components in both groups. We conclude that the RAS is activated in women using OCs. There was no evidence that decreases in renin secretion result in normalization of the RAS as a whole.

Splanchnic blood flow and hepatic glucose production in exercising humans: role of renin-angiotensin system

2001 ◽  
Vol 281 (6) ◽  
pp. R1854-R1861 ◽  
Author(s):  
Raynald Bergeron ◽  
Michael Kjær ◽  
Lene Simonsen ◽  
Jens Bülow ◽  
Dorthe Skovgaard ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renin Angiotensin System ◽  
Glucose Production ◽  
Splanchnic Blood Flow ◽  
Control Group ◽  
Moderate Exercise ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

The study examined the implication of the renin-angiotensin system (RAS) in regulation of splanchnic blood flow and glucose production in exercising humans. Subjects cycled for 40 min at 50% maximal O2 consumption (V˙o 2 max) followed by 30 min at 70% V˙o 2 maxeither with [angiotensin-converting enzyme (ACE) blockade] or without (control) administration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was estimated by indocyanine green, and splanchnic substrate exchange was determined by the arteriohepatic venous difference. Exercise led to an ∼20-fold increase ( P < 0.001) in ANG II levels in the control group (5.4 ± 1.0 to 102.0 ± 25.1 pg/ml), whereas this response was blunted during ACE blockade (8.1 ± 1.2 to 13.2 ± 2.4 pg/ml) and in response to an orthostatic challenge performed postexercise. Apart from lactate and cortisol, which were higher in the ACE-blockade group vs. the control group, hormones, metabolites, V˙o 2, and RER followed the same pattern of changes in ACE-blockade and control groups during exercise. Splanchnic blood flow (at rest: 1.67 ± 0.12, ACE blockade; 1.59 ± 0.18 l/min, control) decreased during moderate exercise (0.78 ± 0.07, ACE blockade; 0.74 ± 0.14 l/min, control), whereas splanchnic glucose production (at rest: 0.50 ± 0.06, ACE blockade; 0.68 ± 0.10 mmol/min, control) increased during moderate exercise (1.97 ± 0.29, ACE blockade; 1.91 ± 0.41 mmol/min, control). Refuting a major role of the RAS for these responses, no differences in the pattern of change of splanchnic blood flow and splanchnic glucose production were observed during ACE blockade compared with controls. This study demonstrates that the normal increase in ANG II levels observed during prolonged exercise in humans does not play a major role in the regulation of splanchnic blood flow and glucose production.

scholarly journals Variation in the Renin Angiotensin System throughout the Normal Menstrual Cycle

2002 ◽  
Vol 13 (2) ◽  
pp. 446-452
Author(s):  
Mala Chidambaram ◽  
John A. Duncan ◽  
Vesta S. Lai ◽  
Daniel C. Cattran ◽  
John S. Floras ◽  
...  
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Lower Body Negative Pressure ◽  
Premenopausal Women ◽  
Renin Angiotensin System ◽  
Follicular Phase ◽  
Systemic Hemodynamic ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Normal Menstrual Cycle

ABSTRACT. It has been demonstrated elsewhere that circulating renin angiotensin system (RAS) components peak when plasma estrogen levels are highest, during the luteal phase of the normal menstrual cycle. This phenomenon has been attributed to “activation” of the RAS. The end-organ vasoconstrictive response to this phenomenon has not been well established. In two related experiments, the RAS was studied in healthy, premenopausal women during predefined phases of the normal menstrual cycle. In the first experiment, the circulating components of the RAS and the systemic hemodynamic response to incremental lower body negative pressure (LBNP) during the follicular and luteal phases of the menstrual cycle were examined. Response variables included mean arterial pressure (MAP), renin, plasma renin activity (PRA), angiotensin II (AngII), and aldosterone. Baseline levels of renin, PRA, and aldosterone were significantly higher in the luteal phase. In response to LBNP, there were significant increases in all variables in both phases; however, the humoral response to this stimulus was significantly augmented in the luteal phase compared with the follicular phase. Despite these elevations in circulating components of the RAS during the luteal phase, subjects were unable to maintain MAP in response to LBNP, exhibiting a dramatic depressor response that did not occur during the follicular phase. In the second experiment, renal and peripheral hemodynamic function at baseline, and in response to AngII blockade with losartan, were examined in women during these high and low estrogen phases of the menstrual cycle. The renal and peripheral hemodynamic responses were similar in the luteal phase and the follicular phase. These results demonstrate that, despite an increase in circulating RAS components during the luteal phase of the menstrual cycle, the system is blunted rather than “activated,” at least at a tissue level. Further studies are needed to clarify this mechanism.

scholarly journals Effect of captopril on the release of the components of the renin-angiotensin system into plasma and lymph.

1992 ◽  
Vol 2 (7) ◽  
pp. 1241-1250 ◽  
Author(s):  
C S Wilcox ◽  
V J Dzau
Keyword(s):  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Lymph ◽  
Active Renin ◽  
Renal Interstitium ◽  
Arterial Plasma ◽  
Renal Vascular ◽  
Venous Plasma

The effects of captopril on the intrarenal renin-angiotensin system were assessed from measurements in arterial plasma, renal venous plasma, and renal lymph from salt-depleted dogs. In the basal state, immunoreactive angiotensin II (Ang II) in renal venous plasma averaged only 60 +/- 12% (P less than 0.01) of arterial plasma, although the concentration of Ang II in renal lymph was 2.0 +/- 0.4-fold (P less than 0.05) greater. The Ang II concentration of renal lymph incubated ex vivo at 37 degrees C doubled in 10 to 15 min, which was the time taken to collect renal lymph samples. Compared with arterial plasma, renal lymph contained lower concentrations (P less than 0.01) of renin substrate and angiotensin-converting enzyme but higher concentrations of active (5.3 +/- 2.1-fold) and inactive (8.9 +/- 3.2-fold) renin. Although captopril increased the secretion of active renin into renal venous plasma by six-fold, the secretion of total renin was unchanged because of a reciprocal fall in the secretion of inactive renin. The percent reduction in renal vascular resistance with captopril correlated with the percent fall in Ang II in renal lymph (r = 0.70). In conclusion: (1) all components of the renin-angiotensin system are represented in the renal interstitium, as reflected in lymph; (2) Ang II concentrations in renal lymph in vivo approximate arterial levels; (3) increased secretion of active renin into plasma during intrarenal infusion of captopril into denervated kidneys is due predominantly to renin activation; and (4) renal vascular resistance may depend on the concentration of Ang II in the renal interstitium.

Role of the renin-angiotensin system in mediating the effects of posture on renal function

1996 ◽  
Vol 271 (1) ◽  
pp. R282-R288 ◽  
Author(s):  
G. A. Reinhart ◽  
T. E. Lohmeier
Keyword(s):  
Renal Function ◽  
Sodium Excretion ◽  
Renal Plasma Flow ◽  
Renin Angiotensin System ◽  
Renal Hemodynamics ◽  
Conscious Dogs ◽  
Plasma Norepinephrine ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

This study was designed to quantitate the influence of the neurohumoral activation associated with orthostatic stress on renal hemodynamics and sodium excretion and, furthermore, to determine the importance of the renin-angiotensin system in mediating these changes in renal function. Seven conscious dogs were studied while lying in the recumbent position and, subsequently, after standing in a supporting sling. Experiments were conducted under control conditions and after plasma angiotensin II (ANG II) concentration was fixed at control levels by chronic infusion of captopril (14 micrograms.kg-1.min-1) and ANG II (0.5 +/- 0.02 ng.kg-1.min-1). During control experiments, 45 min of standing increased plasma renin activity twofold, whereas mean arterial pressure, heart rate, and plasma norepinephrine concentration remained unchanged. During standing, glomerular filtration rate (GFR) and renal plasma flow (RPF) fell to 88 +/- 2 and 77 +/- 3% of recumbent values, respectively, whereas filtration fraction (FF) increased 16 +/- 1%. Additionally, urinary (UNaV) and fractional sodium excretion (FENa) decreased to 27 +/- 6 and 30 +/- 7% of recumbent values, respectively. When plasma ANG II concentration was fixed at control levels during standing, there were no significant changes in GFR, whereas increments in FF and reductions in RPF, UNaV, and FENa were attenuated by 63, 40, 30, and 33%, respectively. These data suggest that, in conscious dogs, standing in a supporting sling causes reflex activation of the sympathetic nervous and renin-angiotensin systems, eliciting reductions in GFR, RPF, and UNaV. Furthermore, ANG II contributes significantly to the effects of passive standing on renal hemodynamics and UNaV.

Abstract P003: Hyperactive Brain Renin Angiotensin System Induces Polydipsia Through mTORC1 Pathway

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Kenjiro Muta ◽  
Donald A Morgan ◽  
Justin L Grobe ◽  
Curt D Sigmund ◽  
Kamal Rahmouni
Keyword(s):  
Renin Angiotensin System ◽  
Vehicle Group ◽  
Control Group ◽  
Ang Ii ◽  
Critical Determinant ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Mtorc1 Signaling ◽  
Wide Range ◽  
Mtorc1 Pathway

Mechanistic target of rapamycin complex 1 (mTORC1) is a molecular hub for signaling pathways mediating a wide range of cellular events involved in the regulation of various physiological and pathophysiological processes. We previously demonstrated that Angiotensin II (Ang II) activates mTORC1 and its downstream effector ribosomal protein S6 kinase in neurons in vitro . Here, we investigated the role of brain mTORC1 in hypertension and polydipsia induced by Ang II. In wild-type mice, acute stimulation of angiotensin type 1 receptor signaling by intracerebroventricular (ICV) injection of Ang II (1 μg, 30 min) activated mTORC1 signaling in the subfornical organ (SFO), a critical brain region in cardiovascular control and fluid balance, as indicated by the significant increase in the number of phosphorylated S6-positive cells (32±2 vs 13±3 in vehicle group). Similar upregulation of the mTORC1 pathway in the SFO was also found in the mice treated subcutaneously with Ang II (1000 ng/kg/min) using an osmotic minipump for 1 week (27±3 vs 11±2 in vehicle group). To verify functional roles of the Ang II activation of mTORC1 in the SFO, we utilized hypertensive and polydipsic transgenic mice (sRA) that have a hyperactive brain renin-angiotensin system, resulting in SFO-overproduction of Ang II. Interestingly, sRA mice exhibited substantially elevated phospho-S6 immunoreactivity only in the SFO (64±6 vs 36±8 in controls) but not in other cardiovascular regulatory regions including the paraventricular nucleus. ICV delivery of mTORC1 blocker, rapamycin (10 ng/day for 7 days) significantly (p<0.05) reduced daily water intake (-4.5±0.7 mL) compared to vehicle-treated sRA mice (-0.7±0.6 mL). In contrast, systolic blood pressure remained unchanged with rapamycin treatment (123±1 vs 125±4 mmHg in pre-treatment) and was consistently higher than the control group (110±4 mmHg). These results suggest that mTORC1 activity in the SFO is a critical determinant of the polydipsia evoked by Ang II.

Abstract 020: A Mitochondrial Renin-Angiotensin System: Internalization of Angiotensinogen

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Bryan A Wilson ◽  
Nancy T Pirro ◽  
TanYa M Gwathmey ◽  
James C Rose ◽  
Mark C Chappell
Keyword(s):  
Renin Angiotensin System ◽  
Anion Channel ◽  
Protein Band ◽  
Receptor Subtypes ◽  
Ang Ii ◽  
Voltage Dependent Anion Channel ◽  
Cell Organelles ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Active Renin

There is compelling evidence for actions of an intracellular renin-angiotensin system (RAS) in various cell organelles including the endoplasmic reticulum, nucleus and the mitochondria (Mito). Indeed, angiotensin (Ang) AT1 and AT2 receptor subtypes were functionally linked to Mito respiration and nitric oxide production, respectively in a previous study. Since elucidation of mitochondrial pathways for expression of RAS protein components as well as Ang II or Ang-(1-7) is equivocal at this time, we undertook a biochemical analysis of the Mito RAS from adult male sheep kidney. Cortical Mito were isolated by differential centrifugation and a discontinuous Percoll gradient. Purified Mito were co-enriched in the voltage-dependent anion channel, an outer Mito membrane marker as well as ATP synthase, an inner membrane marker. Angiotensinogen (Aogen; 55 kDa) was detected in Mito extracts by an Aogen antibody to an internal sequence of the protein, but not with an antibody directed against the Ang I N-terminus. Two different renin antibodies identified a major 35 kDa protein band in the isolated Mito. Using the Ang I-directed Aogen antibody, active renin was confirmed by hydrolysis of Aogen that was abolished by aliskiren; however, trypsin exposure did not increase renin activity in the Mito. A pro-renin receptor (PRR) antibody failed to identify proteins in three Mito preparations, but revealed a prominent band in renal cortical membranes that corresponds to the size of PRR. Angiotensin peptides were quantified by three direct RIAs; the Mito content of Ang II and Ang-(1-7) were higher as compared to Ang I [23 ± 8 and 58 ± 17 vs. 2 ± 1 fmol/mg protein; p<0.01, n=3]. Additionally, both neprilysin and thimet oligopeptidase activities that processed Ang I to Ang-(1-7) were evident. Finally, cortical Mito internalized radiolabeled Aogen at a rate of 33 ± 9 fmol/min/mg protein (n=3) at 37°C. The subsequent analysis of the labeled Mito by SDS-gel fractionation revealed a predominant radioactive band of 55 kDa for Aogen. Collectively, our data suggest that the internalization of Aogen and subsequent processing by active renin may yield des-[Ang I]-Aogen and the active peptides Ang II and Ang-(1-7) that may potentially contribute to mitochondrial function within the kidney.

Low LBNP tolerance in men is associated with attenuated activation of the renin-angiotensin system

2000 ◽  
Vol 279 (3) ◽  
pp. R822-R829 ◽  
Author(s):  
John E. Greenleaf ◽  
Trine Welløw Petersen ◽  
Anders Gabrielsen ◽  
Bettina Pump ◽  
Peter Bie ◽  
...  
Keyword(s):  
Lower Body Negative Pressure ◽  
Venous Pressure ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
The Body ◽  
Ang Ii ◽  
Lower Body ◽  
Central Venous ◽  
Angiotensin System ◽  
Renin Angiotensin

Plasma vasoactive hormone concentrations [epinephrine (pEpi), norepinephrine (pNE), ANG II (pANG II), vasopressin (pVP), endothelin-1 (pET-1)] and plasma renin activity (pRA) were measured periodically and compared during lower body negative pressure (LBNP) to test the hypothesis that responsiveness of the renin-angiotensin system, the latter being one of the most powerful vasoconstrictors in the body, is of major importance for LBNP tolerance. Healthy men on a controlled diet (2,822 cal/day, 2 mmol · kg−1· day−1 Na+) were exposed to 30 min of LBNP from −15 to −50 mmHg. LBNP was uneventful for seven men [25 ± 2 yr, high-tolerance (HiTol) group], but eight men (26 ± 3 yr) reached presyncope after 11 ± 1 min [ P < 0.001, low-tolerance (LoTol) group]. Mean arterial pressure (MAP) did not change measurably, but central venous pressure and left atrial diameter decreased similarly in both groups (5–6 mmHg, by ≈30%, P < 0.05). Control (0 mmHg LBNP) hormone concentrations were similar between groups, however, pRAdiffered between them (LoTol 0.6 ± 0.1, HiTol 1.2 ± 0.1 ng ANG I · ml−1 · h−1, P < 0.05). LBNP increased ( P < 0.05) pRA and pANG II, respectively, more in the HiTol group (9.9 ± 2.2 ng ANG I · ml−1· h−1 and 58 ± 12 pg/ml) than in LoTol subjects (4.3 ± 0.9 ng ANG I · ml−1 · h−1 and 28 ± 6 pg/ml). In contrast, the increase in pVP was higher ( P < 0.05) in the LoTol than in the HiTol group. The increases ( P < 0.05) for pNE were nonsignificant between groups, and pET-1 remained unchanged. Thus there may be a causal relationship between attenuated activation of pRA and pANG II and presyncope, with pVP being a possible cofactor. Measurement of resting pRA may be of predictive value for those with lower hypotensive tolerance.

scholarly journals Testosterone-dependent hypertension and upregulation of intrarenal angiotensinogen in Dahl salt-sensitive rats

2009 ◽  
Vol 296 (4) ◽  
pp. F771-F779 ◽  
Author(s):  
Licy L. Yanes ◽  
Julio C. Sartori-Valinotti ◽  
Radu Iliescu ◽  
Damian G. Romero ◽  
Lorraine C. Racusen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Injury ◽  
Premenopausal Women ◽  
Renin Angiotensin System ◽  
Progressive Increase ◽  
Glomerular Sclerosis ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Low Salt

Blood pressure (BP) is more salt sensitive in men than in premenopausal women. In Dahl salt-sensitive rats (DS), high-salt (HS) diet increases BP more in males than females. In contrast to the systemic renin-angiotensin system, which is suppressed in response to HS in male DS, intrarenal angiotensinogen expression is increased, and intrarenal levels of ANG II are not suppressed. In this study, the hypothesis was tested that there is a sexual dimorphism in HS-induced upregulation of intrarenal angiotensinogen mediated by testosterone that also causes increases in BP and renal injury. On a low-salt (LS) diet, male DS had higher levels of intrarenal angiotensinogen mRNA than females. HS diet for 4 wk increased renal cortical angiotensinogen mRNA and protein only in male DS, which was prevented by castration. Ovariectomy of female DS had no effect on intrarenal angiotensinogen expression on either diet. Radiotelemetric BP was similar between males and castrated rats on LS diet. HS diet for 4 wk caused a progressive increase in BP, protein and albumin excretion, and glomerular sclerosis in male DS rats, which were attenuated by castration. Testosterone replacement in castrated DS rats increased BP, renal injury, and upregulation of renal angiotensinogen associated with HS diet. Testosterone contributes to the development of hypertension and renal injury in male DS rats on HS diet possibly through upregulation of the intrarenal renin-angiotensin system.

scholarly journals A novel role for miR-133a in centrally mediated activation of the renin-angiotensin system in congestive heart failure

2017 ◽  
Vol 312 (5) ◽  
pp. H968-H979 ◽  
Author(s):  
Neeru M. Sharma ◽  
Shyam S. Nandi ◽  
Hong Zheng ◽  
Paras K. Mishra ◽  
Kaushik P. Patel
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Paraventricular Nucleus ◽  
Renin Angiotensin System ◽  
Luciferase Reporter ◽  
Mrna Levels ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin

An activated renin-angiotensin system (RAS) within the central nervous system has been implicated in sympathoexcitation during various disease conditions including congestive heart failure (CHF). In particular, activation of the RAS in the paraventricular nucleus (PVN) of the hypothalamus has been recognized to augment sympathoexcitation in CHF. We observed a 2.6-fold increase in angiotensinogen (AGT) in the PVN of CHF. To elucidate the molecular mechanism for increased expression of AGT, we performed in silico analysis of the 3′-untranslated region (3′-UTR) of AGT and found a potential binding site for microRNA (miR)-133a. We hypothesized that decreased miR-133a might contribute to increased AGT in the PVN of CHF rats. Overexpression of miR-133a in NG108 cells resulted in 1.4- and 1.5-fold decreases in AGT and angiotensin type II (ANG II) type 1 receptor (AT1R) mRNA levels, respectively. A luciferase reporter assay performed on NG108 cells confirmed miR-133a binding to the 3′-UTR of AGT. Consistent with these in vitro data, we observed a 1.9-fold decrease in miR-133a expression with a concomitant increase in AGT and AT1R expression within the PVN of CHF rats. Furthermore, restoring the levels of miR-133a within the PVN of CHF rats with viral transduction resulted in a significant reduction of AGT (1.4-fold) and AT1R (1.5-fold) levels with a concomitant decrease in basal renal sympathetic nerve activity (RSNA). Restoration of miR-133a also abrogated the enhanced RSNA responses to microinjected ANG II within the PVN of CHF rats. These results reveal a novel and potentially unique role for miR-133a in the regulation of ANG II within the PVN of CHF rats, which may potentially contribute to the commonly observed sympathoexcitation in CHF. NEW & NOTEWORTHY Angiotensinogen (AGT) expression is upregulated in the paraventricular nucleus of the hypothalamus through posttranscriptional mechanism interceded by microRNA-133a in heart failure. Understanding the mechanism of increased expression of AGT in pathological conditions leading to increased sympathoexcitation may provide the basis for the possible development of new therapeutic agents with enhanced specificity.

scholarly journals The Biochemical Effects of Angiotensin-(1-7) on the Oxidative Stress Metabolism and Their Specific Parameters from the Temporal Lobe

2020 ◽  
Vol 71 (6) ◽  
pp. 307-311
Author(s):  
Sorin Ungurianu ◽  
Constantin Trus ◽  
Roxana-Rosmary Enciu
Keyword(s):  
Oxidative Stress ◽  
Temporal Lobe ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Angiotensin Peptides ◽  
Vascular Area ◽  
Ang Iv ◽  
The One

It is already known from a variety of previous reports that an independent brain renin�angiotensin system (RAS) exists, completely separated from the one in the periphery. This independent brain RAS has all the precursors and the enzymatic structures necessary for the generation of the angiotensin peptides. Thus, in the last few years various groups started focusing on the more central effects of less known angiotensins (e.g in comparison with Angiotensin (Ang) II), namely Ang III, Ang IV, Ang-(1�7) or Ang 5-8. One of these newly emerging angiotensins which has become an increased center of interest in many studies is Ang-(1-7), which is a heptapeptide previously described especially for its opposite effects to Ang II, in the peripheral vascular area, but also described for some opposite central functions vs. Ang II. These aspects are completed with the fact that it was recently suggested that the renin�angiotensin system could modulate the oxidative stress metabolism, and also it seems that the manifestations of Angiotensin-(1-7) on the basal oxidative stress status are contradictory, with a variety of reports describing controversial (e.g. both pro-oxidant and antioxidant actions) effects for this heptapeptide. Our results presented here are confirming a possible antioxidant effect of Ang-(1�7) administration on rat, as shown by the increased levels of antioxidant enzymes from the temporal lobe (superoxide dismutase and glutathione peroxidase) and decreased levels of malondialdehyde, as an important lipid peroxidation parameter.

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