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Renin–angiotensin system in visceral fat plays a crucial role in the pathogenesis of metabolic syndrome in fructose-fed rats. However, the effects of renin inhibition on visceral adiposity in metabolic syndrome are not fully investigated. We investigated the effects of renin inhibition on visceral adiposity in fructose-fed rats. Male Wistar–Kyoto rats were divided into 4 groups for 8-week experiments: Group Con (standard chow diet), Group Fru (high-fructose diet; 60% fructose), Group FruA (high-fructose diet and concurrent aliskiren treatment; 100 mg/kg body weight [BW] per day), and Group FruB (high-fructose diet and subsequent, i.e. 4 weeks after initiating high-fructose feeding, aliskiren treatment; 100 mg/kg BW per day). The high-fructose diet induced metabolic syndrome, increased visceral fat weights and adipocyte sizes, and augmented angiotensin II (Ang II), NADPH oxidase (NOX) isoforms expressions, oxidative stress, and dysregulated production of adipocytokines from visceral adipose tissues. Concurrent and subsequent aliskiren administration ameliorated metabolic syndrome, dysregulated adipocytokines, and visceral adiposity in high fructose-fed hypertensive rats, and was associated with reducing Ang II levels, NOX isoforms expressions and oxidative stress in visceral fat tissues. Therefore, this study demonstrates renin inhibition could improve metabolic syndrome, and reduce Ang II levels and oxidative stress in visceral fat tissue in fructose-fed rats, and suggests that visceral adipose Ang II plays a crucial role in the pathogenesis of metabolic syndrome in fructose-fed rats. [ABSTRACT FROM AUTHOR]

Natriuretic response and glomerular hemodynamics depend on various intrarenal regulation systems; however, most of them possess some degree of dependence on the renin-angiotensin system. Tissue distribution and hemodynamic effects of this system are of vital importance for understanding of the natriuretic and glomerular filtration regulation in the context of different diseases characterized by dysregulation of sodium balance or glomerular filtration rate, such as nephrotic syndrome, acute and chronic renal failure and hypertension. [ABSTRACT FROM AUTHOR]

The renin-angiotensin system (RAS) is a hormone system that has been classically known as a blood pressure regulator but is becoming well recognized as a proinflammatory mediator. In many diverse tissues, RAS pathway elements are also produced intrinsically, making it possible for tissues to respond more dynamically to systemic or local cues. While RAS is important for controlling normal inflammatory responses, hyperactivation of the pathway can cause neural dysfunction by inducing accelerated degradation of some neuronal proteins such as synaptophysin and by activating pathological glial responses. Chronic inflammation and oxidative stress are risk factors for high incidence vision-threatening diseases such as diabetic retinopathy (DR), age-related macular degeneration (AMD), and glaucoma. In fact, increasing evidence suggests that RAS inhibition may actually prevent progression of various ocular diseases including uveitis, DR, AMD, and glaucoma. Therefore, RAS inhibition may be a promising therapeutic approach to fine-tune inflammatory responses and to prevent or treat certain ocular and neurodegenerative diseases. [ABSTRACT FROM AUTHOR]

The renin-angiotensin-aldosterone system controls blood pressure and salt-volume homeostasis. Renin, which is the first enzymatic step of the cascade, is critically regulated at the transcriptional level. In the present study, we investigated the role of liver X receptor alpha (LXR(alpha)) and LXR(beta) in the regulation of renin. In vitro, both LXRs could bind to a noncanonical responsive element in the renin promoter and regulated renin transcription. While LXR(alpha) functioned as a cAMP-activated factor, LXR(beta) was inversely affected by cAMP. In vivo, LXRs colocalized in juxtaglomerular cells, in which LXR(alpha) was specifically enriched, and interacted with the renin promoter. In mouse models, renin-angiotensin activation was associated with increased binding of LXR(alpha) to the responsive element. Moreover, acute administration of LXR agonists was followed by upregulation of renin transcription. In LXR(alpha) mice, the elevation of renin triggered by adrenergic stimulation was abolished. Untreated LXR(beta) mice exhibited reduced kidney renin mRNA levels compared with controls. LXR(alpha)LXR(beta) mice showed a combined phenotype of lower basal renin and blunted adrenergic response. In conclusion, we show herein that LXR(alpha) and LXR(beta) regulate renin expression in vivo by directly interacting with the renin promoter and that the cAMP/LXR(alpha) signaling pathway is required for the adrenergic control of the renin-angiotensin system. [ABSTRACT FROM AUTHOR]

We found that when a site-specific binding protein interacts with the "handle" region of the prorenin prosegment, the prorenin molecule undergoes a conformational change to its enzymatically active state. This nonproteolytic activation is completely blocked by a decoy peptide with the handle region structure, which competitively binds to such a binding protein. Given increased plasma prorenin in diabetes, we examined the hypothesis that the nonproteolytic activation of prorenin plays a significant role in diabetic organ damage. Streptozotocin-induced diabetic rats were treated with subcutaneous administration of handle region peptide. Metabolic and renal histological changes and the renin-Ang system components in the plasma and kidneys were determined at 8, 16, and 24 weeks following streptozotocin treatment. Kidneys of diabetic rats contained increased Ang I and II without any changes in renin, Ang-converting enzyme, or angiotensinogen synthesis. Treatment with the handle region peptide decreased the renal content of Ang I and II, however, and completely inhibited the development of diabetic nephropathy without affecting hyperglycemia. We propose that the nonproteolytic activation of prorenin may be a significant mechanism of diabetic nephropathy. The mechanism and substances causing nonproteolytic activation of prorenin may serve as important therapeutic targets for the prevention of diabetic organ damage. [ABSTRACT FROM AUTHOR]

The renin–angiotensin system (RAS) modulates a diverse set of physiological processes including development, blood pressure, renal function and inflammation. The principal effector molecule of this system, angiotensin II, mediates most of these actions. The classically recognized functions of the RAS are triggered via the type 1 (AT1) class of angiotensin receptors. Pharmacological blockade of the AT1 receptor lowers blood pressure and slows the progression of cardiovascular and renal diseases. Gene-targeting technology provides an experimental approach for precisely dissecting the physiological functions of the RAS. Here, we review how gene-targeting experiments have elucidated AT1 receptor functions. [ABSTRACT FROM AUTHOR]

Recent data from studies in rodents with targeted gene disruption and pharmacological antagonists have shown that the renin–angiotensin–aldosterone system (RAAS) and cyclooxygenase type-2 (COX-2) are necessary for late stages of kidney development. The present review summarizes data on the developmental changes of RAAS and COX-2 and the pathways by which they are activated; their possible interplay and the mechanisms by which they affect kidney development. Intrarenal and circulating renin and angiotensin II (ANG II) are stimulated at birth in most mammals. In rats, renin and ANG II stay significantly elevated in the suckling period while aldosterone stabilizes at an adult level. COX-2 is stimulated in thick ascending limb of Henle's loop in the suckling period at a time when urine concentrating ability is not developed. Data suggest that this induction is mediated by combined low plasma glucocorticoid concentration and by a low NaCl intake. Studies with selective inhibitors of COX-2 and COX-2 null mice show that COX-2 activity stimulates renin secretion from JG-cells during postnatal kidney development and that lack of COX-2 activity leads to pathological change in cortical architecture and eventually to renal failure. In the postnatal period, ANG II initiates and maintains pelvic and ureteric contractions necessary for urine flow. Lack of ANG II in the neonatal period is thought to cause injury by a chronic increase of renal pelvic pressure. Aldosterone is crucial for survival and growth in the neonatal period through its effects on sodium reabsorption and the intrarenal sensitivity to aldosterone is increased in the postnatal period. Final maturation of the kidney occurs through an intimate interplay between a low dietary sodium intake and a non-responsive HPA-axis which stimulates cortical COX-2 activity. COX-2 supports increased activity of the RAAS and may contribute to a low concentrating ability. [ABSTRACT FROM AUTHOR]

Hypertension is a polygenic and multi-factorial disorder that is extremely prevalent in western societies, and thus has received a great deal of attention by the research community. The renin–angiotensin system has a strong impact on the control of blood pressure both in the short- and long-term, making it one of the most extensively studied physiological systems. Nevertheless, despite decades of research, the specific mechanisms implicated in its action on blood pressure and electrolyte balance, as well as its integration with other cardiovascular pathways remains incomplete. The production of transgenic models either over-expressing or knocking-out specific components of the renin–angiotensin system has given us a better understanding of its role in the pathogenesis of hypertension. Moreover, our attention has recently been refocused on local tissue renin–angiotensin systems and their physiological effect on blood pressure and end-organ damage. Herein, we will review studies using genetic manipulation of animals to determine the role of the endocrine and tissue renin–angiotensin system in hypertension. We will also discuss some untraditional approaches to target the renin–angiotensin system in the kidney. [ABSTRACT FROM AUTHOR]

The adipose renin-angiotensin system (RAS) has been assigned to participate in the control of adipose tissue development and in the pathogenesis of obesity-related hypertension. In adipose cells, the biological responses to β-adrenergic stimulation are mediated by an increase in intracellular cAMP. Because cAMP is known to promote adipogenesis and because an association exists between body fat mass, hypertension, and increased sympathetic stimulation, we examined the influence of cAMP on angiotensinogen (ATG) expression and secretion in rat adipose tissue. Exposure of primary cultured differentiated preadipocytes to the cAMP analog 8-bromoadenosine 3',5'-cyclic monophosphate (8BrcAMP) or cAMP-stimulating agents (forskolin and IBMX) results in a significant increase in ATG mRNA levels. In adipose tissue fragments, 8-BrcAMP also increases ATG mRNA levels and protein secretion, but not in the presence of the protein kinase A inhibitor H89. The addition of isoproterenol, known to stimulate the synthesis of intracellular cAMP via β-adrenoreceptors, had the same stimulatory effect on ATG expression and secretion. These results indicate that cAMP in vitro upregulates ATG expression and secretion in rat adipose tissue via the protein kinase A-dependent pathway. Further studies are required to determine whether this regulatory pathway is activated in human obesity, where increased sympathetic tone is frequently observed, and to elucidate the importance of adipose ATG to the elevated blood pressure observed in this pathological state. [ABSTRACT FROM AUTHOR]

The aim of this study was to estimate and analyse circadian variations of the renin–angiotensin–aldosterone system (RAA) activity in blood of goats and the influence of late pregnancy on the circadian variations of RAA system. The study was carried out on a group of 17 non-pregnant and 9 pregnant goats. The animals were kept in uniform environmental conditions, (9 h light/15 h darkness). Blood samples were collected seven times over a period of 24 h, every 4 h. Plasma renin activity (PRA), plasma aldosterone (PA), sodium, potassium and chloride concentrations were determined. PRA and PA of both groups changed during 24 h, with the highest values in the dark phase and with higher RAA system activity (especially during the night) in the pregnant goats. In the non-pregnant goats, no circadian changes in PRA and PA were observed. The circadian changes in PRA and PA found in pregnant goats had acrophases at 06:27 h and 01:13 h, respectively. Plasma electrolyte concentrations in both groups of goats also changed during 24 h. These results suggest that circadian changes of potassium concentration in plasma of goats during late pregnancy may be one of the main factors affecting the RAA system. [Copyright &y& Elsevier]

Background: In rats maintained on a high salt diet (H/S) to suppress basal renal angiotensinogen levels, angiotensin II (Ang II) infusion for 13 days increased renal angiotensinogen mRNA and protein, thus providing a mechanism for further augmentation of intrarenal Ang II levels. The present study tested the hypothesis that enhanced intrarenal angiotensinogen formation during Ang II infusion is reflected by secretion into the tubular fluid leading to increased urinary excretion of angiotensinogen (UAGT).Methods: The effects of chronic Ang II infusion were examined on kidney and plasma Ang II levels and UAGT in male Sprague-Dawley rats maintained on an 8% salt diet for three weeks (N=10). Following one week on the H/S diet, Ang II (40 ng/min) was administered for two weeks via an osmotic minipump to one group (H/S + Ang II, N=5), while the remaining rats were sham-operated (H/S + Sham, N=5). Additionally, a control group was prepared with normal salt diet and sham-operation (N/S + Sham, N=5).Results: H/S alone did not alter systolic blood pressure (BP) (103 +/- 2 vs. 104 +/- 2 mm Hg), while Ang II infusion to H/S rats significantly increased systolic BP from 103 +/- 2 to 154 +/- 2 after two weeks. Intrarenal Ang II content in H/S + Ang II was significantly greater than H/S + Sham (435 +/- 153 vs. 65 +/- 14 fmol/g). Ang II infusion significantly increased UAGT (4.0 +/- 0.5 vs. 1.0 +/- 0.2 nmol Ang I/day by radioimmunoassay of generated Ang I; 57 +/- 15 vs. 14 +/- 2 densitometric units by Western blotting analysis) compared to Sham. UAGT by radioimmunoassay was highly correlated with kidney Ang II content (r=0.79); but not with plasma Ang II concentration (r=0.20).Conclusions: These data demonstrate that chronic Ang II infusion increases urinary excretion rate of angiotensinogen, and suggest that UAGT provides a specific index of intrarenal angiotensinogen production in Ang II-dependent hypertension. [ABSTRACT FROM AUTHOR]

Objective: Many patients with diabetic nephropathy (DN) have levels of albuminuria > 1 g/day and blood pressure >135/85 mmHg, despite antihypertensive combination therapy, including recommended doses of ACE inhibitors, e.g., lisinopril/enalapril at 20 mg daily. We tested the concept that such patients might benefit from dual blockade of the renin-angiotensin system (RAS).Research Design and Methods: We performed a randomized double-blind crossover study of 2 months treatment with candesartan cilexetil 8 mg once daily and placebo in addition to previous antihypertensive treatment. We included 18 type 2 diabetic patients with DN fulfilling the above-mentioned criteria. All received recommended doses of ACE inhibitor and, in addition, 15 patients received diuretics, 11 received a calcium channel antagonist, and 3 received a beta-blocker. At the end of each treatment period, we measured the glomerular filtration rate (GFR), 24-h blood pressure, albuminuria, and IgGuria.Results: The addition of candesartan to usual antihypertensive therapy induced a mean (95% CI) reduction in albuminuria of 25% (2-58), P = 0.036 (geometric mean [95% CI] from 1,764 mg/24 h [1,225-2,540] to 1,334 mg/24 h [890-1,998]). It also produced a mean reduction of 35% (9-53) in the fractional clearance of albumin (P = 0.016), a reduction of 32% (1-54) in fractional clearance of IgG (P = 0.046), a reduction in 24-h systolic blood pressure of 10 mmHg (2-18) (P = 0.019) (mean +/- +/- SE) from 148 +/- 3 to 138 +/- 5 mmHg, and a mean reduction in GFR of 5 ml. min(-1). 1.73 m(-2) (0.1-9) (P = 0.045).Conclusions: Dual blockade of the RAS reduces albuminuria and blood pressure in type 2 diabetic patients with DN responding insufficiently to previous antihypertensive therapy, including ACE inhibitors in recommended doses. [ABSTRACT FROM AUTHOR]

Examines the implication of the renin-angiotensin system in regulating splanchnic blood flow and glucose production in exercising humans. Elevation of hepatic glucose production during exercise; Administration of enalapril injections to the subjects; Inhibition of angiotensin II by angiotensin-converting enzyme blockade.

Presents a study which examined the implication of the renin-angiotensin system in regulation of splanchnic blood flow and glucose production in exercising humans. Methods; Results; Discussion.

Investigates the role of renin-angiotensin system during alterations of sodium intake in conscious mice. Quantification of the circulating components of the renin-angiotensin-aldosterone axis; Importance of the physiological suppression of circulating angiotensin II in maintaining constancy of arterial pressure during alterations in sodium intake.

Presents a study which determined how the different components of the renin-angiotensin-aldosterone axis respond to alterations in sodium intake in conscious mice. Methods; Results; Discussion.

Over the past 5 years, genetic manipulation has revolutionized the way we examine physiological processes by providing a targeted specificity that was not possible previously. The application of transgenesis and gene targeting has been applied to numerous physiological pathways; and both will remain important tools as we reach the completion of the human genome project and begin to assess the function of newly identified genes. The renin–angiotensin system (RAS) has been the target of numerous transgenic and gene targeting studies designed to help uncover its role in cardiovascular regulation and organ development. Each gene of the system has now been both over-expressed and knocked out. It will be discussed as to how new advances in tissue-specific gene targeting by both over-expression and gene ablation can be used as powerful tools to dissect the role of the RAS in individual tissues. [ABSTRACT FROM AUTHOR]

Aims Endothelin-1 (ET-1) is a potent vasoconstrictor produced by the vascular endothelium. The interactions of ET with the mediators of the sympathetic nervous system and the renin-angiotensin-system in humans are unclear. Methods We studied the effects of the ETA-selective antagonist BQ-123 and the ETB-selective antagonist BQ-788 (both 10-10-10-8 m) on ET-1 (10-16-10-10 m), angiotensin II (AT, 10-16-10-10 m) and noradrenaline (NA, 10-16-10-10 m) induced vasoconstriction in the human skin microcirculation in vivo in 25 healthy male volunteers using laser Doppler flowmetry and double injection technique. Results BQ-123 caused a dose-dependent vasodilatation (maximum effect: + 949 ± 84 AUC-PU, P < 0.001), whereas BQ-788 induced mild vasoconstriction (maximum effect: -388 ± 96 AUC-PU, P < 0.01). In the presence of BQ-123, but not BQ-788, ET-1, AT and NA caused markedly less vasoconstriction at any tested agonist dose; the effect was most pronounced on ET-1 (maximum effect at 10-14 m: + 814 ± 93 AUC-PU vs ET alone, P < 0.001), followed by noradrenaline (maximim effect at 10-16 m: + 580 ± 107 AUC-PU vs NA alone, P < 0.01) and angiotensin II (maximim effect at 10-14 m: + 493 ± 111 AUC-PU vs AT alone, P < 0.001). Conclusions ETA-selective antagonism inhibits vasoconstriction to AT and NA in vivo in healthy subjects. This beneficial effect may be useful for the treatment of patients with cardiovascular disease including hypertension especially in combination therapy with sympatholytic agents and inhibitors of the renin-angiotensin system. [ABSTRACT FROM AUTHOR]

Studies the interaction between genetic variability of the renin-angiotension system and metabolic risk factors in premature myocardial infarction. Analysis of gene polymorphisms of angiotensin-I converting enzyme gene, angiotensinogen gene, and angiotensin-II type-1 receptor gene.

Presents information on a study which examined the effects of blockade of the renin-angiotensin system on the renal metabolism of arachidonic acid in rats. Methods used; Results; Discussion.

Presents a study which determined the effect of renin-angiotensin system inhibition on noradrenergic nerve terminal function in pacing-induced heart failure. Methods; Results; Discussion.

Presents a study which determined the temporal sequence for activation of the renin-angiotensin and sympathetic nervous system in response to cardiac pressure overload. Factors which offset the benefits of cardiac hypertrophy; Methodology; Results and discussion.

Evaluates the role of the renin-angiotensin system in drinking of seawater-adapted eels. Role of angiotensin II in drinking of seawater fish; Changes in drinking rate, plasma angiotensin II concentration, and arterial blood pressure after infusion of SQ-14225; Comparison of plasma renin activity and angiotensin II levels in freshwater and seawater eels.

Presents information on a study which evaluated the role of endogenous renin-angiotensin system in copius drinking of seawater eels. Methodology; Effects of SQ-14225 and an anti-ANG II serum on drinking, plasma ANG II hormone, and blood pressure; Role of ANG II hormone in drinking of seawater fish.

Focuses on a study which discussed the low lower body negative pressure tolerance in men associated with attenuation of the renin-angiotensin system. Information on the mechanisms for reduction of cerebral blood pressure; Methodology; Results of the study.

Presents information on a study which investigated the existence of an intrarenal renin-angiotensin system in rainbow trout. Materials and methods; Results and discussion.

Studies the role of adrenal renin-angiotensin system (RAS) in the control of aldosterone secretion in sodium-restricted rats. Pharmacological manipulation of RAS; Effects on basal aldosterone outputs; Indicators of the role of RAS in the regulation of aldosterone secretion.

Presents information on a study which discussed the renin-angiotensin system (RAS) physiology in heart failure and the techniques used to measure the RAS components. Components of the RAS and the synthesis of the angiotensin (ANG) II, the effector hormone of the RAS; Role of the ANG II in the pathogenesis of heart failure; Physiology and measurement of Renin; Clinical applications of the RAS measurement.

SUMMARY1. To explore the role of nitric oxide (NO) in the regulation of the renin–angiotensin system (RAS) in Dahl salt-sensitive (DS) rats, the effects of NG-nitro-L-arginine methyl ester (L-NAME) on plasma renin activity (PRA), and concentrations of angiotensin (Ang)I and AngII in the plasma, aorta and kidney were investigated in DS and Dahl salt-resistant (DR) rats. 2. NG-Nitro-L-arginine methyl ester (12–18 mg/kg per day) administration for 1 week increased mean arterial pressure (MAP) in DS and DR rats fed a 0.3% NaCl diet and in DR rats fed an 8% NaCl diet compared with corresponding vehicle (water)-treated groups. However, L-NAME administration did not change MAP in DS rats fed an 8% NaCl diet. 3. NG-Nitro-L-arginine methyl ester administration increased PRA in DS rats fed an 8% NaCl diet, but not in DR rats fed an 8% NaCl diet. NG-Nitro-L-arginine methyl ester administration increased AngI and AngII concentrations in plasma, aorta and kidney only in DS rats fed an 8% NaCl diet. The ratio of AngI to AngII did not change following L-NAME administration in any rats. 4. These results suggest that NO has an inhibitory role on renin release in DS rats fed a high-salt diet. [ABSTRACT FROM AUTHOR]

1. The role of the renin–angiotensin system (RAS) in cardiac hypertrophy and nephropathy was examined in Tsukuba hypertensive mice (THM) carrying both human renin and angiotensinogen genes. 2. Tsukuba hypertensive mice were treated with 20 mg/kg per day lisinopril, 30 mg/kg per day hydralazine or nothing. Administration of drugs was performed for 6 months from 12 weeks of age; water intake and urine volume were measured and urine albumin excretion, heart to bodyweight ratio and the glomerulosclerosis index were examined. 3. Systolic blood pressure was significantly lowered by treatment with lisinopril and hydralazine. Urine volume, water intake and urinary albumin excretion were significantly decreased by lisinopril. When hydralazine was administered to THM, these parameters were transiently decreased, but eventually reached almost the same levels as those in the untreated group. The heart to bodyweight ratio was significantly decreased by lisinopril, but not by hydralazine. The glomerulosclerosis index was significantly lowered by lisinopril, but the index in the hydralazine group was not significantly different from that in the untreated group. 4. These results suggest that the RAS plays an important role in the progression of cardiac hypertrophy in THM. In addition, the RAS may also play an important role in the progression of nephropathy; however, this may also be partially regulated by elevated blood pressure in the short term. [ABSTRACT FROM AUTHOR]

Discusses how the author teaches the subject of the renin-angiotensin system in the areas of physiology, pathophysiology and pharmacology. Significance of the system; Discussion on the biosynthesis of angiotensin II; Role of angiotensin in body fluid and blood pressure regulation.

Hypertrophy is an adaptive response of the heart to hemodynamic overload such as hypertension. However, it is generally accepted that cardiac hypertrophy is one of the most critical risk factors of heart disease. Therefore, for the treatment of hypertension it is important to understand the mechanism of cardiac hypertrophy and to establish effective pharmaceutical interventions. Mechanical stretch induced by hypertension is an initial factor leading to cardiac hypertrophy. In an in vivo study using spontaneously hypertensive rats, an angiotensin II type 1 receptor antagonist, TCV116, decreased left ventricular weight, left ventricular wall thickness, transverse myocyte diameter, relative amount of V3 myosin heavy chain, and interstitial fibrosis, whereas treatment with hydrolazine did not. In an in vitro study using cultured cardiomyocytes of neonatal rats, mechanical stretch activated second messengers, such as extracellular signal-regulated protein kinase (ERK), followed by increased protein synthesis. Additionally, in the stretch-conditioned medium, the levels of angiotensin II and endothelin-1 concentrations were increased. Moreover, the Na+/H+ exchanger activated by mechanical stretch modulated the hypertrophic responses of cardiomyocytes. To further elucidate whether angiotensin II is indispensable for mechanical stress-induced cardiac hypertrophy, mechanical stretch-induced ERK activation was examined in angiotensin II type 1a receptor knock-out mice. Although the addition of angiotensin II had no effects on the ERK activity in cardiomyocytes of angiotensin II type 1a receptor knockout mice, mechanical stretch induced a larger increase in the ERK activity in cardiac myocytes from these mice compared with cardiac myocytes of wild-type mice. These results suggest that mechanical stretch could induce hypertrophic responses in cardiac myocytes even in the absence of angiotensin II. The pathways leading to ERK activation differed between cell types. In cardiac fibroblasts, angiotensin II activated ERK via the G(beta)gamma subunit of Gi, Src, Shc, Grb2, and Ras, whereas Gq and protein kinase C were critical in cardiomyocytes. [ABSTRACT FROM AUTHOR]

Examines the potential role for the renin-angiotensin system in the growth of human pulmonary artery (PA) smooth muscle. Localization of angiotensin (ANG) II-receptor subtypes by autoradiography in sections of human PA and in cultured PA smooth muscle cells; Expression of ANG II type 1 receptor by human PA smooth muscle cells in vivo and in vitro.

Measures renin and angiotensinogen in plasma and myocardium 10 days after myocardial infarction. Increase in plasma and myocardial renin after infarction; Maintenance of myocardial angiotensinogen after infarction despite decreased plasma angiotensinogen and increased levels of myocardial renin; Renin-angiotensin system; Renin glycoforms.

Assesses the changes in the renin-angiotensin (RAS) messenger ribonucleic acid (MRNA) in the brain and the kidney of rats after the administration of deoxycorticosterone acetate (DOCA) and/or sodium chloride. Use of a competitive polymerase chain reaction (PCR) method to assess the changes; Infusion of benzamil, a blocker of amiloride-sensitive sodium channels.

Assesses whether chronic treatment with the AT1-receptor blocker losertan given centrally normalizes the sympathetic hyperactivity and impairment of baroreflex function in Wistar rats with congestive heart failure (CHF) post-myocardial infarction (MI). Activation of the brain renin-angiotensin system; Peripheral effects of intracerebroventricular losartan.

Details a study which tested the hypothesis that the renin-angiotensin system (RAS) in the developing animal plays and important role in the long-term regulation of renal function and arterial pressure. How the study was conducted; Effects of perinatal angiotensin (AT) receptor blockade on growth; Effects of perinatal AT receptor blockade on renal structure; Description of the perinatal RAS and long-term physiological regulation.

Examines whether the renin-angiotensin system contributes to hyperthyroidism-induced cardiac hypertrophy without involving the sympathetic nervous system. Hemodynamic changes produced by thyroxine treatment and sympathetic denervation; Effect of nephrectomy; Effects of Losartan and Nicardipine.

Demonstrates the in vivo pressor effects mediated by renin-angiotensin system type 1B (AT1B) receptors and that when AT1A receptors are absent, the AT1B receptors contribute to the regulation of resting blood pressure. Critical role of renin-angiotensin system (RAS) as regulator of blood pressure and sodium hemostasis.

Investigates the renin-angiotensin-aldosterone system (RAS) in experimental mineralocorticoid-salt-induced cardiac fibrosis. Aldosterone effects; Potassium canrenoate; Reversal of aldosterone-induced increase in cardiac collage with canrenoate.

Investigates the regulation of glomerular and preglomerular vascular angiotensin II (ANG II) receptors by changes in the renin-angiotensin system (RAS) activity in rats. Determination of ANG II receptor characteristics by radioligand binding assays; Downregulation of vascular receptor density by sodium restriction.

Evaluates the effects of renin-angiotensin system blockade by enalapril and losartan in a salt-dependent model of cyclosporin-associated chronic tubulointerstitial fibrosis (TIF). Suggestion that cyclosporin-related chronic interstitial injury is mediated by angiotensin II.

Determines the extent to which the retention of sodium (Na) and water and the increase in systematic arterial pressure during servo-controlled reduced renal perfusion pressure (rRPP) are dependent on the renin-angiotensin-aldosterone system. Reduced renal perfusion pressure; Cumulative sodium balance.

Determines whether intravertebral angiotensin II infusion decreases renin release by increasing renal perfusion pressure. Other possible effects on renal function; Servocontrol; Renal baroreceptor; Macula densa mechanisms.

Investigates the overflows of angiotensin-decapeptide (ANG I) and angiotensin-octapeptide (ANG II) from blood-perfused canine gracilis muscle in situ. Effects of sympathetic nerve stimulation, propranolol and isoprenaline; Arterial and venous plasma concentrations of ANG I and ANG II; Plasma renin activity.

Investigates the effect of the interruption of the renin-angiotensin system with enalapril on the collecting duct changes observed in potassium (K) depletion. Metabolic balance study in normal and low-K diets; Interruption of the renin-angiotensin system with angiotensin converting enzyme inhibitors.

Characterizes the functional, immunohistochemical and molecular correlations of renal renin-angiotensin system (RAS) in diabetes. Study of nondiabetic and hyperglycemic diabetic (DM) rats; Effect of chronic therapy with losartan; Intrarenal hemodynamic responsiveness to RAS inhibition; Concentration of angiotensin-converting enzyme.

Investigates the hypothesis that the increase in plasma angiotensinogen after nephrectomy is mediated by endogenous renin and angiotensin (ANG) II. Division of rats into control, nephrectomy or nephrectomy plus adrenalectomy groups; Increase in plasma angiotensinogen levels; Effect of pretreatment with atenolol.

Studies the effects of adenosine and angiotensin on macula densa-stimulated renin secretion in the presence of NaCl. Effect of A1 receptor antagonist; Influence of pentostatin; Implications.

Examines the hypothesis that renal bradykinin production during sodium depletion is mediated by the renin-angiotensin system. Use of the in vivo renal microdialysis technique in determining renal interstitial fluid; Changes in renal excretory and hemodynamic function; Sodium and fluid balance.