Glomerular dynamics in the hypothyroid rat and the role of the renin-angiotensin system

1987 ◽  
Vol 253 (1) ◽  
pp. F170-F179 ◽  
Author(s):  
D. M. Gillum ◽  
S. A. Falk ◽  
W. S. Hammond ◽  
J. D. Conger
Keyword(s):  
Renin Angiotensin System ◽  
Systemic Blood Pressure ◽  
Systemic Hemodynamic ◽  
Angiotensin System ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Glomerular Hemodynamics ◽  
Ultrafiltration Pressure ◽  
Proximal Tubular Reabsorption

Munich-Wistar rats underwent thyroidectomy (TX) with reimplantation of the parathyroid glands. Systemic hemodynamic and micropuncture studies were performed at 1 and 3 wk post-TX, and the results were compared with levothyroxine replaced controls (TXT4). Cardiac output (CO) in TX rats fell progressively and was 40% of that in TXT4 at 3 wk. Renal blood flow declined in parallel with CO. Systemic blood pressure did not fall in TX rats because of a 50% increase in systemic vascular resistance by 3 wk post-TX. Glomerular dynamics were not significantly different between TX and TXT4 rats at 1 wk; however, by 3 wk single-nephron glomerular filtration rate (SNGFR) had fallen to 16.5 +/- 1.1 vs. 34.1 +/- 3.4 nl/min in TXT4 controls (P less than 0.001). In 3-wk TX rats, glomerular plasma flow (QA) was 50.9 +/- 3.7 vs. 108.0 +/- 8.7 nl/min in TXT4 rats (P less than 0.001), net hydraulic ultrafiltration pressure (delta P) was 33 +/- 2 vs. 37 +/- 1 mmHg in TXT4 rats (P less than 0.01), and the ultrafiltration coefficient (Kf) was 0.025 +/- 0.003 vs. 0.084 +/- 0.008 nl X s-1 X mmHg-1 in TXT4 controls (P less than 0.001). Although the changes in systemic and glomerular hemodynamics were progressive over 3 wk, proximal tubular reabsorption fell maximally within 1 wk. Similar patterns of alterations in glomerular dynamics are known physiological consequences of angiotensin II (ANG II).(ABSTRACT TRUNCATED AT 250 WORDS)

Abstract 336: Angiotensinogen Gene Polymorphism Confers a Multiple Risk Factor for Atherosclerosis and Its Susceptibility Traits

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Nduna Dzimiri ◽  
Samar Elhawari ◽  
Mohammed Al-Najai ◽  
Paul Muiya ◽  
Daisy Gueco ◽  
...  
Keyword(s):  
Gene Polymorphism ◽  
Significant Risk ◽  
Renin Angiotensin System ◽  
Systemic Blood Pressure ◽  
Multiple Risk Factor ◽  
Systemic Blood ◽  
Angiotensin System ◽  
Cardiovascular Functions

Angiotensinogen (AGT) constitutes a pivotal component of the renin-angiotensin system which controls the systemic blood pressure and several other cardiovascular functions. In order to evaluate the role of the AGT gene polymorphism in atherosclerosis (CAD) and its risk factors, we first sequenced the gene in 200 individuals in search of informative SNPs. Of the >100 SNPs identified, we proceeded to evaluate the association of 8 variants in 3232 CAD cases versus 2292 angiographed controls by the Applied Biosystems real-time PCR system. Of the studied variants, the recessive mode of inheritance (TT) of rs3789679C>T [Odds ratio(95% Confidence Interval) = 1.23(1.05-1.45); p=0.012]; TT of rs699C>T [1.21(1.11-1.32); p<0.0001] as well as the dominant models (AG+GG) of rs5051A>G [1.22(1.10-1.37; p<0.0001) and AG+GG of rs2067853A>G [1.23(1.07-140);p=0.003] conferred risk for CAD. Interestingly, rs699 (p<0.0001), rs5051 (p=0.003) and rs2067853 (p=0.001) were equally implicated in hypertension, while the rs699 was further associated with hypercholesterolaemia (p=0.002) and hypertriglyceridaemia (p<0.0001), and the rs5051 was similarly associated with type 2 diabetes mellitus (T2DM) (p=0.011). One 8-mer haplotype from the 8 studied SNPs ACGGATAT (χ 2 =9.83; p=0.0017) and several of its variants, including the 7-mer ACGGATA (χ 2 =9.40; p=0.0022), 6-mer GGATAT (χ 2 =11.54; p=0.0007) and 5-mer GATAT (χ 2 =10.89; p=0.001) conferred significant risk for CAD. Furthermore, three 8-mer haploptypes GTGGGTGG (χ 2 =6.96; p=0.0083), ACGGGTAT (χ 2 =4.70; p=0.030) and GTAGGCGG (χ 2 =5.69; p=0.017) were associated with HTN. Similar trends were also observed for T2DM, obesity and hyperlipidaemia. These observations show that the AGT gene polymorphism confers a common risk for atherosclerosis and its major susceptibility traits.

Angiotensin-dependent renal mechanisms in two-kidney, one-clip renal vascular hypertension

1983 ◽  
Vol 245 (2) ◽  
pp. F131-F141 ◽  
Author(s):  
D. W. Ploth
Keyword(s):  
Blood Pressure ◽  
Renin Angiotensin System ◽  
Systemic Blood Pressure ◽  
Systemic Circulation ◽  
Systemic Hemodynamic ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Renal Vascular ◽  
Pharmacologic Agents

Our understanding of the physiology of the renin-angiotensin system has advanced remarkably in the last decade as a result of the development of several pharmacologic agents that effectively block components of this humoral cascade. The use of these antagonists has also advanced our understanding of the contribution of the renin-angiotensin system to the development and maintenance of two-kidney, one-clip renal vascular hypertension. These antagonists have contributed greatly to the characterization of the systemic hemodynamic changes that occur in this model and, particularly, to the delineation of the behavior of the nonclipped kidney, a previously normal kidney that is subjected acutely to an environment of elevated systemic blood pressure and the input of a variety of other extrinsic influences. This kidney not only allows the blood pressure to increase and persist at elevated levels but appears to actively participate in the development and propagation of the hypertension. Although a variety of mechanisms impinge on the function of the nonclipped kidney in this model, the goal of this review is to analyze the behavior of this kidney and how its functional state is perturbed, primarily by the influence of angiotensin, which is believed to be delivered to it by the systemic circulation.

Role of angiotensin II in modulating the hemodynamic effects of nitric oxide synthesis inhibition

1999 ◽  
Vol 277 (1) ◽  
pp. R104-R111 ◽  
Author(s):  
Isabel Hernández ◽  
Luis F. Carbonell ◽  
Tomas Quesada ◽  
Francisco J. Fenoy
Keyword(s):  
Nitric Oxide ◽  
Peripheral Resistance ◽  
Physiological Role ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Plasma Protein Concentration ◽  
Systemic Hemodynamic ◽  
Angiotensin System ◽  
Albumin Content

This study examined the role of ANG II in modulating the increase of hematocrit and vascular permeability that follows nitric oxide (NO) synthesis blockade, that are contributing to the decrease in cardiac index (CI) in conscious, chronically catheterized rats. Pretreatment with losartan attenuated the N ω-nitro-l-arginine methyl ester (l-NAME)-induced increase in total peripheral resistance by 26% and also blunted the fall in CI (28%) and stroke volume. l-NAME produced an increase in hematocrit (4.5%) and in 125I-labeled albumin content in the heart and small intestine in untreated rats, but the increase was prevented in rats pretreated with losartan. Furthermore, l-NAME induced a transient increase of plasma protein concentration and tissue intestinal blood flow, which was abolished in rats given losartan. The results of the present study indicate that the systemic hemodynamic responses, the fall in plasma volume, and the increase in albumin escape observed after inhibition of NO synthesis are in part the consequence of unmasking the actions of endogenous ANG II. These data suggest a physiological role for NO by restraint of the vascular actions of the renin-angiotensin system.

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.

Glomerular hemodynamics in aortocaval fistula rats: role of renin-angiotensin system

1993 ◽  
Vol 264 (4) ◽  
pp. R681-R686 ◽  
Author(s):  
T. Nishikimi ◽  
E. D. Frohlich
Keyword(s):  
Plasma Flow ◽  
Diastolic Pressure ◽  
Renal Plasma Flow ◽  
Renin Angiotensin System ◽  
Left Ventricular ◽  
Angiotensin System ◽  
Av Fistula ◽  
Renin Angiotensin ◽  
Single Nephron

To investigate intrarenal hemodynamics of aortocaval, arteriovenous (AV)-fistula rats and the effect of angiotensin-converting-enzyme (ACE) inhibition, micropuncture studies were obtained before and after administration of quinapril (100 micrograms.kg-1 x min-1), an ACE inhibitor. AV fistula produced by needle multipuncture was characterized by elevated left ventricular end-diastolic pressure (LVEDP), lower mean arterial pressure, and increased left and right ventricular weights. Effective renal plasma flow was lower in AV-fistula rats, and single-nephron glomerular filtration rate (SNGFR) and plasma flow (SNPF) were reduced. Single-nephron filtration faction (SNFF), stop-flow pressure, and glomerular pressure (PG) were increased. The lower SNGFR and SNPF and higher PG and SNFF were associated with higher afferent and efferent arteriolar resistances (RA and RE) and lower ultrafiltration coefficient (Kf). LVEDP correlated positively with with RA, RE, and SNFF (all P < 0.01) and negatively with SNGFR (P < 0.05) and SNPF (P < 0.01). After quinapril these variables returned toward normal. Thus this method for producing AV fistula was useful in creating mild and moderately severe cardiac failure (CHF). Intrarenal hemodynamics of AV were characterized by increased PG and SNFF and lower SNGFR and SNPF associated with increased RA and RE and lower Kf and SNPF correlated and with severity of CHF. Restoration of intrarenal hemodynamics to or toward normal with quinapril supports an important pathophysiological role of renin-angiotensin system in this CHF.

Role of genetic variability in the renin-angiotensin system in diabetic and nondiabetic renal disease

2001 ◽  
Vol 21 (6) ◽  
pp. 580-592 ◽  
Author(s):  
Arnold Boonstra ◽  
Dick de Zeeuw ◽  
Paul E. de Jong ◽  
Gerjan Navis
Keyword(s):  
Genetic Variability ◽  
Renal Disease ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

The Renin Angiotensin System and Bipolar Disorder: A Systematic Review

2020 ◽  
Vol 27 (6) ◽  
pp. 520-528 ◽  
Author(s):  
Izabela Guimarães Barbosa ◽  
Giulia Campos Ferreira ◽  
Diomildo Ferreira Andrade Júnior ◽  
Cássio Rocha Januário ◽  
André Rolim Belisário ◽  
...  
Keyword(s):  
Systematic Review ◽  
Bipolar Disorder ◽  
Cardiovascular Diseases ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin Receptors ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Search Terms

Bipolar Disorder (BD) is a chronic a multifactorial psychiatric illness that affects mood, cognition, and functioning. BD is associated with several psychiatric conditions as well clinical comorbidities, particularly cardiovascular diseases. The neurobiology of BD is complex and multifactorial and several systems have been implicated. Considering that the Renin Angiotensin System (RAS) plays an important role in cardiovascular diseases and that recently evidence has suggested its role in psychiatric disorders, the aim of the present study is to summarize and to discuss recent findings related to the modulation of RAS components in BD. A systematic search of the literature using the electronic databases MEDLINE and LILACS was conducted through March 2019. The search terms were: “Bipolar Disorder”; “Renin Angiotensin System”; “Angiotensin 2”; “Angiotensin receptors”; “Angiotensin 1-7”; “ACE”; “ACE2”; “Mas Receptor”. We included original studies assessing RAS in BD patients. Two hundred twenty-two citations were initially retrieved. Eleven studies were included in our systematic review. In the majority of studies (6 of 8), the ACE insertion/deletion (I/D) polymorphism did not differ between BD patients and controls. BD patients presented higher plasma renin activity in comparison with controls. The studies evaluating the RAS molecules in BD are very scarce and heterogeneous. The literature suggests a potential role of RAS in BD. Further studies are necessary to investigate this relationship.

scholarly journals Hyperactivated RAGE in Comorbidities as a Risk Factor for Severe COVID-19—The Role of RAGE-RAS Crosstalk

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 876
Author(s):  
Sara Chiappalupi ◽  
Laura Salvadori ◽  
Rosario Donato ◽  
Francesca Riuzzi ◽  
Guglielmo Sorci
Keyword(s):  
Gene Polymorphisms ◽  
Renin Angiotensin System ◽  
Molecular Target ◽  
Advanced Glycation ◽  
Angiotensin System ◽  
Major Player ◽  
Glycation End Products ◽  
End Products ◽  
And Oxidative Stress

The receptor for advanced glycation-end products (RAGE) is a multiligand receptor with a role in inflammatory and pulmonary pathologies. Hyperactivation of RAGE by its ligands has been reported to sustain inflammation and oxidative stress in common comorbidities of severe COVID-19. RAGE is essential to the deleterious effects of the renin–angiotensin system (RAS), which participates in infection and multiorgan injury in COVID-19 patients. Thus, RAGE might be a major player in severe COVID-19, and appears to be a useful therapeutic molecular target in infections by SARS-CoV-2. The role of RAGE gene polymorphisms in predisposing patients to severe COVID-19 is discussed. 

scholarly journals TCA Cycle and Fatty Acids Oxidation Reflect Early Cardiorenal Damage in Normoalbuminuric Subjects with Controlled Hypertension

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1100
Author(s):  
Aranzazu Santiago-Hernandez ◽  
Marta Martin-Lorenzo ◽  
Ariadna Martin-Blazquez ◽  
Gema Ruiz-Hurtado ◽  
Maria G Barderas ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Tricarboxylic Acid Cycle ◽  
Renin Angiotensin System ◽  
Roc Curves ◽  
Tca Cycle ◽  
Urinary Metabolites ◽  
Organ Damage ◽  
Fatty Acid Binding ◽  
Angiotensin System

Moderately increased albuminuria, defined by an albumin to creatinine ratio (ACR) > 30 mg/g, is an indicator of subclinical organ damage associated with a higher risk of cardiovascular and renal disease. Normoalbuminuric subjects are considered at no cardiorenal risk in clinical practice, and molecular changes underlying early development are unclear. To decipher subjacent mechanisms, we stratified the normoalbuminuria condition. A total of 37 hypertensive patients under chronic renin–angiotensin system (RAS) suppression with ACR values in the normoalbuminuria range were included and classified as control (C) (ACR < 10 mg/g) and high-normal (HN) (ACR = 10–30 mg/g). Target metabolomic analysis was carried out by liquid chromatography and mass spectrometry to investigate the role of the cardiorenal risk urinary metabolites previously identified. Besides this, urinary free fatty acids (FFAs), fatty acid binding protein 1 (FABP1) and nephrin were analyzed by colorimetric and ELISA assays. A Mann–Whitney test was applied, ROC curves were calculated and Spearman correlation analysis was carried out. Nine metabolites showed significantly altered abundance in HN versus C, and urinary FFAs and FABP1 increased in HN group, pointing to dysregulation in the tricarboxylic acid cycle (TCA) cycle and fatty acids β-oxidation. We showed here how cardiorenal metabolites associate with albuminuria, already in the normoalbuminuric range, evidencing early renal damage at a tubular level and suggesting increased β-oxidation to potentially counteract fatty acids overload in the HN range.

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