scholarly journals Effects of Mild Mitral Valve Insufficiency, Sodium Intake, and Place of Blood Sampling on the Renin-Angiotensin System in Dogs

1996 ◽  
Vol 37 (1) ◽  
pp. 109-118
Author(s):  
H. D. Pedersen
Keyword(s):  
Mitral Valve ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Mitral Valve Insufficiency ◽  
Blood Sampling ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Valve Insufficiency

scholarly journals Activation of the Alternate Renin-Angiotensin System Correlates with the Clinical Status in Human Cirrhosis and Corrects Post Liver Transplantation

2019 ◽  
Vol 8 (4) ◽  
pp. 419 ◽  
Author(s):  
Stephen Casey ◽  
Robert Schierwagen ◽  
Kai Mak ◽  
Sabine Klein ◽  
Frank Uschner ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Liver Disease ◽  
Animal Studies ◽  
Clinical Status ◽  
Renin Angiotensin System ◽  
Blood Sampling ◽  
Ang Ii ◽  
Post Transplantation ◽  
Angiotensin System ◽  
Renin Angiotensin

Introduction: Recent animal studies have shown that the alternate renin-angiotensin system (RAS) consisting of angiotensin-converting enzyme 2 (ACE2), angiotensin-(1–7) (Ang-(1–7)) and the Mas receptor is upregulated in cirrhosis and contributes to splanchnic vasodilatation and portal hypertension. To determine the potential relevance of these findings to human liver disease, we evaluated its expression and relationship to the patients’ clinical status in subjects with cirrhosis. Methods: Blood sampling from peripheral and central vascular beds was performed intra-operatively for cirrhotic patients at the time of liver transplantation (LT) or trans-jugular intra-hepatic portosystemic shunt (TIPS) procedures to measure angiotensin II (Ang II) and Ang-(1–7) peptide levels and ACE and ACE2 enzyme activity. Relevant clinical and hemodynamic data were recorded pre-operatively for all subjects and peripheral blood sampling was repeated 3 months or later post-operatively. Results: Ang-(1–-7) and ACE2 activity were up-regulated more than twofold in cirrhotic subjects both at the time of LT and TIPS and levels returned to comparable levels as control subjects post-transplantation. Ang-(1–7) levels correlated positively with the degree of liver disease severity, as measured by the model for an end-stage liver disease (MELD) and also with clinical parameters of pathological vasodilatation including cardiac output (CO). There were strong correlations found between the ACE2:ACE and the Ang-(1–7):Ang II ratio highlighting the inter-dependence of the alternate and classical arms of the RAS and thus their potential impact on vascular tone. Conclusions: In human cirrhosis, the alternate RAS is markedly upregulated and the activation of this system is associated strongly with features of the hyperdynamic circulation in advanced human cirrhosis.

Neurohumoral Response to Hospitalization in Hypertensive Patients

1981 ◽  
Vol 61 (s7) ◽  
pp. 385s-387s ◽  
Author(s):  
P. W. De Leeuw ◽  
G. A. W. Van Soest ◽  
R. Punt ◽  
R. P. L. M. Hoogma ◽  
A. J. P. M. Smout ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Group 2 ◽  
Reduced Activity ◽  
Hypotensive Response ◽  
Group 1 ◽  
Noradrenaline Levels

1. To investigate whether reduced activity of pressor systems could explain the spontaneous drop in pressure upon hospitalization, 51 subjects with uncomplicated essential hypertension were admitted to hospital. Sodium intake was fixed at 55 mmol/day. 2. Blood samples for noradrenaline, adrenaline, active renin, angiotensin II and aldosterone were drawn on each morning of the first 3 days of hospitalization; blood pressure was measured at 2 h intervals and values were averaged for each day. 3. Subjects were divided in two groups depending on whether they became normotensive (group 1; n = 12) or remained hypertensive (group 2; n = 39). This distinction was thought to reflect mild and more severe hypertensive groups respectively. 4. Although both groups showed a comparable fall in blood pressure during hospitalization, noradrenaline levels fell more consistently in group 1, whereas adrenaline levels fell only in group 2. The components of the renin—angiotensin—aldosterone system rose, but more conspicuously in group 1. 5. It is concluded that withdrawal of sympathetic activity can only partly explain the hypotensive response to hospitalization. The renin—angiotensin system behaves only passively and appears to be counterproductive to alterations in blood pressure.

Role of the Renin-Angiotensin System in the Regulation of Late Steps in Aldosterone Biosynthesis by Sodium Intake of Potassium-Deficient Rats*

Endocrinology ◽  
1984 ◽  
Vol 115 (1) ◽  
pp. 350-356 ◽  
Author(s):  
JÜRG MÜLLER, ◽  
LILIAN HOFSTETTER ◽  
PATRICIA SCHWENDENER-CANLAS ◽  
DORETTE B. BRUNNER ◽  
EVA-GRETHE LUND
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Angiotensin System ◽  
Renin Angiotensin

Plasma Renin Activity, Plasma Angiotensin II and Extracellular Fluid Volume in Patients after Renal Transplantation

1976 ◽  
Vol 51 (s3) ◽  
pp. 227s-230s ◽  
Author(s):  
J. S. Horvath ◽  
C. Baxter ◽  
F. Furby ◽  
V. Hood ◽  
J. Johnson ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Plasma Angiotensin

1. Patients with cadaveric renal transplants and plasma creatinine less than 177 μmol/l who had their own kidneys removed were studied. 2. The renin—angiotensin system appeared to behave in a normal fashion in response to alterations in sodium intake and posture. 3. The renin—angiotensin system had no major role in the establishment or maintenance of hypertension. 4. Mean arterial pressure was directly related to expansion of the extracellular fluid volume.

scholarly journals Regression of cardiac hypertrophy in the SHR by combined renin-angiotensin system blockade and dietary sodium restriction

2001 ◽  
Vol 2 (1_suppl) ◽  
pp. S148-S153
Author(s):  
Emad Abro ◽  
Cory D Griffiths ◽  
Trefor O Morgan ◽  
Lea MD Delbridge
Keyword(s):  
Cardiac Hypertrophy ◽  
Spontaneously Hypertensive Rat ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Dietary Sodium ◽  
Angiotensin Ii Receptor Blocker ◽  
Renin Angiotensin Aldosterone System ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Regression Of Cardiac Hypertrophy

Altered operation of the renin-angiotensin-aldosterone system (RAAS) and dietary sodium intake have been identified as independent risk factors for cardiac hypertrophy. The way in which sodium intake and the operation of the renin-angiotensin-aldosterone system interact in the pathogenesis of cardiac hypertrophy is poorly understood. The aims of this study were to investigate the cardiac effects of the renin-angiotensin system (RAS) blockade in the spontaneously hypertensive rat (SHR), using co-treatment with an angiotensin II receptor blocker (ARB) and an angiotensin-converting enzyme (ACE) inhibitor with different sodium intakes. Our experiments with SHR show that, at high levels of sodium intake (4.0%), aggressive RAS blockade treatment with candesartan (3 mg/kg) and perindopril (6 mg/kg) does not result in regression of cardiac hypertrophy. In contrast, RAS blockade coupled with reduced sodium diet (0.2%) significantly regresses cardiac hypertrophy, impairs animal growth and is associated with elevated plasma renin and dramatically suppressed plasma angiotensinogen levels. Histological analyses indicate that the differential effect of reduced sodium on heart growth during RAS blockade is not associated with any change in myocardial interstitial collagen, but reflects modification of cellular geometry. Dimensional measurements of enzymatically-isolated ventricular myocytes show that, in the RAS blocked, reduced sodium group, myocyte length and width were decreased by about 16—19% compared with myocytes from the high sodium treatment group. Our findings highlight the importance of `titrating' sodium intake with combined RAS blockade in the clinical setting to optimise therapeutic benefit.

scholarly journals Maternal high-sodium intake alters the responsiveness of the renin–angiotensin system in adult offspring

Life Sciences ◽  
2012 ◽  
Vol 90 (19-20) ◽  
pp. 785-792 ◽  
Author(s):  
Débora R. Ramos ◽  
Nauilo L. Costa ◽  
Karen L.L. Jang ◽  
Ivone B. Oliveira ◽  
Alexandre A. da Silva ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Adult Offspring ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
High Sodium ◽  
High Sodium Intake

Abstract 84: Angiotensin II Type 1a Receptor in the Subfornical Organ is Essential for Blood Pressure Regulation and Hydromineral Effects in Mouse Models of Elevated Brain Renin-Angiotensin System Activity.

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Aline Hilzendeger ◽  
Deborah R Davis ◽  
Martin D Cassell ◽  
Allyn L Mark ◽  
Justin L Grobe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Intake ◽  
Dna Recombination ◽  
Renin Angiotensin System ◽  
Cre Recombinase ◽  
Subfornical Organ ◽  
Specific Expression ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Conditional Allele

Elevated brain renin-angiotensin system (RAS) activity is necessary to increase blood pressure in many animal models of hypertension. We tested the hypothesis that AT1A receptors (AT1AR) within the subfornical organ (SFO) are required for the phenotypes that result from an increased brain RAS. We examined the effect of SFO-targeted Cre-recombinase mediated ablation of AT1A in mice treated with DOCA-salt (deoxycorticosterone acetate, 50 mg s.c. + ad lib 0.15 M NaCl). Mice homozygous for a conditional allele of the endogenous AT1A gene (AT1ARflox) were administered an adenovirus encoding Cre-recombinase and eGFP (AdCre), or eGFP alone (AdGFP) into the lateral cerebral ventricle, then treated for 3 weeks with DOCA-salt. AdCre reduced DOCA-salt hypertension (AdGFP baseline: 108±3 mmHg; AdGFP pre-DOCA: 104±3; AdGFP post-DOCA: 136±6 vs AdCre baseline: 116±2; Adcre pre-DOCA: 109±3, Adre post-DOCA: 118±5; P≤0.01), polydipsia (AdGFP+DOCA: 20.6±2.1 mL/day; AdCre+DOCA: 11.6±1.1, P<0.05), and sodium intake (AdGFP+DOCA: 2.6±0.3 mEq/day; AdCre+DOCA: 1.8±0.2, P<0.05). AdCre reduced AT1AR mRNA in the SFO (0.4±0.3 fold of AdGFP), without significant effect in the paraventricular or arcuate nuclei, or cortex; this was paralleled by SFO-specific AT1AR genomic DNA recombination. AdCre also caused SFO-specific recombination in ROSA-TdTomato reporter mice. Complementing the DOCA-salt model, we also examined the effect of AT1AR ablation in the SFO of double-transgenic sRA mice. sRA mice exhibit life-long brain-specific angiotensin overproduction via expression of human angiotensinogen via its own promoter and neuron-specific expression of human renin via the synapsin promoter. In sRA mice bred onto the AT1A conditional genetic background, AdCre significantly attenuated the polydipsia (AdGFP: -0.2±2; AdCre: -9.7±2.6 mL/day) and sodium intake (AdGFP: +0.2±0.7; AdCre: -1.3±0.4 mEq/day). Blood pressure measures are in progress. Together, these data highlight the involvement of SFO AT1A receptors in blood pressure in DOCA-salt model and additionally in hydromineral balance in two different models of increased brain RAS activity.

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