scholarly journals Regulation of angiotensin type 1 receptor and its gene expression: role in renal growth.

1997 ◽  
Vol 8 (2) ◽  
pp. 193-198
Author(s):  
D H Wang ◽  
Y Du ◽  
H Zhao ◽  
J P Granger ◽  
R C Speth ◽  
...  
Keyword(s):  
Salt Intake ◽  
Sodium Intake ◽  
Plasma Renin ◽  
At1 Receptor ◽  
Sodium Depletion ◽  
Renal Growth ◽  
Sodium Diet ◽  
Low Sodium ◽  
Low Salt ◽  
Losartan Treatment

Low sodium intake has been demonstrated to upregulate the gene expression of the predominant renal type 1 angiotensin II (Ang II) receptor (AT1), the AT1A subtype. The study presented here tests the hypothesis that the upregulation of renal AT1 mRNA induced by sodium depletion occurs conjointly with an elevation of the AT1 receptor that modulates renal growth. Seven-week-old male Wistar rats were divided into four groups and treated for 2 wk with normal sodium diet, normal sodium diet plus 3 mg/kg/day losartan, low sodium diet, or low sodium diet plus losartan. Body weight and MAP were not significantly different among the four groups. Plasma renin activity was significantly elevated by losartan treatment, low salt intake, or a combination of the two, compared with the plasma renin activity of the controls. Northern blot analysis indicated that renal AT1 mRNA levels were significantly increased-183% by losartan, 212% by low salt intake, and 227% by the combination of the two-compared with their levels in controls. Radioligand binding assays revealed that AT1 receptors were significantly increased by low salt intake but were significantly decreased by losartan treatment. Renal AT1 receptor binding in the rats subjected to sodium depletion plus losartan did not differ from that in control rats. Kidney weight, kidney weight/body weight ratio, and renal DNA and protein content were not altered by sodium depletion but were significantly lowered by losartan treatment with both normal and low sodium intake, compared with those of controls. The protein/DNA ratio was not significantly different among the four groups. Blockade of renal AT1 receptors with losartan was found to retard normal renal growth, indicating that Ang II is required for normal renal development. Low sodium intake was found to increase mRNA and expression of the renal AT1 receptor but to have no effect on renal growth, suggesting that an increase in renal mass above a normal level requires the activation of multiple factors. Blockade of the AT1 receptor by losartan was found to upregulate AT1 mRNA but to down-regulate the AT1 receptor, suggesting that AT1 receptor-mediated intracellular events are necessary to sustain functional AT1 receptor expression in the kidney.

Alterations in Cerebrospinal Fluid Angiotensin II by Sodium Intake in Patients with Essential Hypertension

1989 ◽  
Vol 77 (4) ◽  
pp. 389-394 ◽  
Author(s):  
Minoru Kawamura ◽  
Yuhei Kawano ◽  
Kaoru Yoshida ◽  
Masahito Imanishi ◽  
Satoshi Akabane ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Essential Hypertension ◽  
Sodium Intake ◽  
Ang Ii ◽  
Sodium Depletion ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. Angiotensin (ANG) levels were measured in the cerebrospinal fluid of 15 patients with essential hypertension on a high sodium diet for 1 week and on a low sodium diet for a further week. ANGs were determined using a system of extraction by Sep-Pak cartridges followed by h.p.l.c. combined with radioimmunoassay. 2. Sodium depletion resulted in increases of ANG II in the cerebrospinal fluid from 1.16 ± 0.38 (sem) to 1.83 ± 0.43 fmol/ml (P < 0.01) and of ANG III from 0.65 ± 0.11 to 0.86 ± 0.15 fmol/ml (P < 0.01). 3. The ANG II level in the cerebrospinal fluid was found to be unchanged and recovery of added ANG II was approximately 90%, even after incubation for 3 h, on both diets. Thus, it is unlikely that ANG II is produced or degraded in the cerebrospinal fluid in vitro. 4. There was no significant correlation between the cerebrospinal fluid and the plasma ANG II concentration on the low sodium diet. 5. These results suggest that the cerebrospinal fluid ANG II level increases with sodium depletion, and that the effect of the level of ANG II on the activity of the angiotensin-forming system in the central nervous system may be assessed by determination of ANG II in the cerebrospinal fluid in patients with essential hypertension.

The Effect of a Reduced Sodium Intake on Post-Renal Transplantation Hypertension in Rats

1984 ◽  
Vol 66 (3) ◽  
pp. 269-276 ◽  
Author(s):  
M. H. De Keijzer ◽  
A. P. Provoost ◽  
E. D. Wolff ◽  
W. J. Kort ◽  
I. M. Weijma ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Normal Diet ◽  
Transplant Recipients ◽  
Plasma Renin Concentration ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium

1. In an experimental model of post-renal transplantation hypertension in rats, we studied the effect of a reduction of sodium intake on the development of this type of hypertension. 2. Systolic blood pressure, plasma- renin concentration and renal function were measured regularly in recipients of an allogeneic kidney transplant that had previously undergone active immunological enhancement. 3. Transplant recipients on a normal diet showed a rise in systolic blood pressure during the second week after transplantation. The systolic blood pressure of recipients on a low sodium diet remained normotensive throughout the 15 weeks follow-up period. 4. The plasma renin concentration was low in the hypertensive recipients on a normal diet, as compared with unilaterally nephrectomized controls. Although the plasma renin concentration of recipients on a low sodium diet fell below that of unilaterally nephrectomized controls on a low sodium diet, it was higher than that of recipients on a normal diet. 5. The renal function of transplant recipients was greatly reduced compared with that of control rats. The glomerular filtration rate was reduced to a greater extent than the effective renal plasma flow. 6. In a separate experiment it was revealed that a similar reduction in the glomerular filtration rate of kidneys permanently damaged by temporary ischaemia did not result in an increase in the systolic blood pressure. 7. Survival up to 6 weeks after transplantation was the same for both groups of recipients. Recipients on a low sodium diet, however, showed a better 15 weeks survival, probably owing to the absence of hypertension in this group. 8. The prevention of the development of hypertension by means of a reduction of sodium intake, points to an involvement of sodium retention in this post-transplantation hypertension model.

Both high and low maternal salt intake in pregnancy alter kidney development in the offspring

2011 ◽  
Vol 301 (2) ◽  
pp. F344-F354 ◽  
Author(s):  
Nadezda Koleganova ◽  
Grzegorz Piecha ◽  
Eberhard Ritz ◽  
Luis Eduardo Becker ◽  
Annett Müller ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Kidney Development ◽  
Salt Intake ◽  
Sodium Intake ◽  
Adult Life ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Sodium Diet ◽  
Low Sodium ◽  
Arterial Blood

In humans, low glomerular numbers are related to hypertension, cardiovascular, and renal disease in adult life. The present study was designed 1) to explore whether above- or below-normal dietary salt intake during pregnancy influences nephron number and blood pressure in the offspring and 2) to identify potential mechanisms in kidney development modified by maternal sodium intake. Sprague-Dawley rats were fed low (0.07%)-, intermediate (0.51%)-, or high (3.0%)-sodium diets during pregnancy and lactation. The offspring were weaned at 4 wk and subsequently kept on a 0.51% sodium diet. The kidney structure was assessed at postnatal weeks 1 and 12 and the expression of proteins of interest at term and at week 1. Blood pressure was measured in male offspring by telemetry from postnatal month 2 to postnatal month 9. The numbers of glomeruli at weeks 1 and 12 were significantly lower and, in males, telemetrically measured mean arterial blood pressure after month 5 was higher in offspring of dams on a high- or low- compared with intermediate-sodium diet. A high-salt diet was paralleled by higher concentrations of marinobufagenin in the amniotic fluid and an increase in the expression of both sprouty-1 and glial cell-derived neutrophic factor in the offspring's kidney. The expression of FGF-10 was lower in offspring of dams on a low-sodium diet, and the expression of Pax-2 and FGF-2 was lower in offspring of dams on a high-sodium diet. Both excessively high and excessively low sodium intakes during pregnancy modify protein expression in offspring kidneys and reduce the final number of glomeruli, predisposing the risk of hypertension later in life.

scholarly journals Correlation of Salt Sensitivity, Plasma Renin Activity and Aldosterone in Hypertensive Patients

2017 ◽  
Vol 18 (s1) ◽  
pp. 55-60
Author(s):  
Nebojsa Tasic ◽  
Danijela Tasic ◽  
Dalibor Dragisic ◽  
Miroslav Mitrovic
Keyword(s):  
Blood Pressure ◽  
Essential Hypertension ◽  
Salt Intake ◽  
Plasma Renin ◽  
Salt Loading ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Resistant Group

Abstract Plasma-renin values vary in normotensive and hypertensive populations. Some studies consider renin to be a key factor in the aetiology of hypertension, but other studies note that renin is an important factor in cardiovascular homeostasis and functions more as a growth factor than as a pressor hormone. The aim of this study was to assess the PRA and aldosterone values under different salt intake regimes in patients with essential hypertension. The study group consisted of 50 untreated patients (27 women and 23 men; average age 42±9,2 yrs.; average BMI 27,91±4,6 kg/m2) with essential hypertension. All patients were put on a high-sodium diet (200 mmol NaCl per day) for one week after a week on a low-sodium diet (20 mmol NaCl per day). Sodium sensitivity (SS) was defined as a 10-mmHg increase in the mean blood pressure at the end of the high- vs. the low-sodium diet. The SS group consisted of 26 patients, and the sodiuminsensitive group consisted of 24 patients. The PRA and aldosterone levels were determined in 12 patients. PRA values in the SS group during rest were significantly lower compared with the salt-resistant group during all regimes of salt intake (F=10,56, p=0,0012). Salt loading in SS patients causes a significant decrease in PRA (in rest and effort) values in comparison to values during a low salt intake regime (rest: t=4,49, p<0,001; effort: t=3,45, p<0,01). The PRA values in the salt-resistant group did not vary significantly under the different salt intake regimes. The aldosterone values followed the pattern of the PRA values. It is necessary to distinguish investigations on salt intake effects based on incidence and value of blood pressure and investigations on salt restriction’s effects on of blood pressure levels (i.e., non-pharmacological hypertension therapy).

scholarly journals Remodeling and angiotensin II responses of the uterine arcuate arteries of pregnant rats are altered by low- and high-sodium intake

Reproduction ◽  
2006 ◽  
Vol 131 (2) ◽  
pp. 331-339 ◽  
Author(s):  
Jean St-Louis ◽  
Benoît Sicotte ◽  
Annie Beauséjour ◽  
Michèle Brochu
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Sodium Intake ◽  
High Salt ◽  
Pregnant Rats ◽  
High Sodium ◽  
Sodium Diet ◽  
Uterine Arteries ◽  
Low Sodium Diet ◽  
Low Sodium

Lowering and increasing sodium intake in pregnant rats evoke opposite changes in renin–angiotensin–aldosterone system (RAAS) activity and are associated with alterations of blood volume expansion. As augmented uterine blood flow during gestation is linked to increased circulatory volume, we wanted to determine if low- and high-sodium intakes affect the mechanical properties and angiotensin II (AngII) responses of the uterine vasculature. Non-pregnant and pregnant rats received a normal sodium (0.22% Na+) diet. On the 15th day of gestation some animals were moved to a low-sodium (0.03%) diet, whereas others were given NaCl supplementation as beverage (saline, 0.9% or 1.8%) for 7 days. All rats were killed after 7 days of treatment (eve of parturition). Uterine arcuate arteries (>100 μm) were set up in wire myographs under a tension equivalent to 50 mmHg transmural pressure. The pregnancy-associated increase in diameter of the uterine arteries was significantly attenuated on the low-sodium diet and 1.8% NaCl supplementation. The arcuate arteries of non-pregnant rats on the low-sodium diet showed markedly increased responses to AngII and phenylephrine (Phe). Pregnancy also resulted in heightened responses to AngII and Phe that were significantly reduced for the former agent in rats on the low-sodium diet. Sodium supplementation of non-pregnant rats did not affect the reactivity of the uterine arteries to AngII, but significantly reduced the effect of Phe (1 μmol/l). High salt also significantly diminished the elevated responses to AngII in the arteries of pregnant animals. It was observed that altered sodium intake affects the mechanical and reactive properties of the uterine arcuate arteries more importantly in pregnant than in non-pregnant rats. Low-salt intake similarly affected the reactivity of the uterine arcuate arteries to AngII and Phe, whereas high-salt intake more specifically affected AngII responses. These results showed that perturbations of sodium intake have major impacts on the structure and functions of the uterine arterial circulation, indicating RAAS involvement in uterine vascular remodeling and function during gestation.

scholarly journals No effect of the angiotensin receptor blocker candesartan on cerebrovascular autoregulation in rats during very high and low sodium intake

2019 ◽  
Vol 20 (3) ◽  
pp. 147032031987461
Author(s):  
Sigurdur T Sigurdsson ◽  
Peter Bie ◽  
Arne H Nielsen ◽  
Svend Strandgaard ◽  
Olaf B Paulson
Keyword(s):  
Blood Pressure ◽  
Angiotensin Receptor Blocker ◽  
Salt Intake ◽  
Sodium Intake ◽  
Receptor Blocker ◽  
Angiotensin Receptor ◽  
Sprague Dawley ◽  
Sodium Diet ◽  
Low Sodium ◽  
Renin Level

Autoregulation of cerebral blood flow (CBF) denotes that CBF is constant despite fluctuation of blood pressure within wide limits. Inhibition of the renin–angiotensin system (RAS) is known to decrease the lower and upper limits of CBF autoregulation. We have previously shown that this includes inhibition by the angiotensin receptor blocker (ARB) candesartan. In the present study we investigated the influence of the ARB candesartan on the lower limit of CBF autoregulation in two groups of Sprague-Dawley rats, on high (4.0% Na+) and low (0.004% Na+) sodium diet, respectively. Control animals were given the same diet, but no ARB. CBF was studied with the laser Doppler method. Blood pressure was lowered by controlled bleeding. Results revealed that both high and low sodium diet with low and high renin levels respectively block the influence of candesartan on CBF autoregulation. This was expected in rats on a high salt diet with a low renin level, but unexpected in rats with a low salt intake with a high renin level.

Effect of sodium depletion on peripheral vascular responses to heat stress in baboons

1987 ◽  
Vol 62 (4) ◽  
pp. 1538-1543 ◽  
Author(s):  
D. W. Proppe
Keyword(s):  
Salt Intake ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Sodium Depletion ◽  
Angiotensin System ◽  
Vascular Responses ◽  
Renal Vasoconstriction ◽  
Cutaneous Vasodilation ◽  
Low Salt ◽  
Renal Vascular

The cutaneous vasodilation and renal vasoconstriction in baboons during environmental heating (EH) appear to be produced predominantly by sympathetic vasoconstrictor withdrawal and activation of the renin-angiotensin system, respectively. Since these mechanisms may be influenced differently by sodium depletion, this study examined the hypothesis that sodium depletion would have a differential effect on cutaneous and renal vascular responses to EH. Sodium depletion was produced in chronically instrumented baboons by placing them on low-salt intake for 8–19 days along with diuretic administration. EH consisted of exposing the baboon to an ambient temperature of 40–42 degrees C until core temperature (Tc) reached 39.8–40.0 degrees C. Both control plasma renin activity (PRA) and the rise in PRA with Tc during EH were considerably larger in sodium-depleted baboons. However, the magnitudes of the progressive increases in iliac vascular conductance (used as an index of hindlimb cutaneous vasodilation) and renal vascular resistance with rising Tc during EH were unaltered by sodium depletion. Therefore, neither cutaneous nor renal vascular responses to EH are influenced by elevated PRA and other changes accompanying sodium depletion in the baboon.

Abstract 17541: An Education Intervention Focused on Self-monitoring for Symptom and Sodium Intake Improves Adherence to the Low Sodium Diet and Health Outcome in Patients with Heart Failure

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Eun Kyeung Song ◽  
Debra K Moser ◽  
Seok-Min Kang ◽  
Terry A Lennie
Keyword(s):  
Health Outcomes ◽  
Cox Regression ◽  
Sodium Intake ◽  
Control Group ◽  
Education Intervention ◽  
Self Monitoring ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Patients With Heart Failure

Background: Despite the clinical emphasis on recommending a low sodium diet (LSD), adherence to a LSD remains poor in patients with heart failure (HF). Additional research is needed to determine successful interventions to improve adherence to a LSD and health outcomes. Purpose: To determine the effect of an education intervention on adherence to a LSD and health outcomes. Method: A total of 109 HF patients (age 64±9 years, 29% female) who were non-adherent to LSD, indicating > 3g of 24-hour urinary sodium excretion (24hr UNa) at baseline, were randomly assigned to one of 3 groups: 1) symptom monitoring and restricted 3 gram sodium diet (SMART) group, 2) the telephone monitoring (TM) group, or 3) usual care control group. The SMART group received individualized teaching and guidance of self-monitoring for worsening symptom and sodium intake using symptom and food diary for 4 sessions over 8 weeks. Patients assigned to either of the 2 intervention groups (SMART or TM) received phone calls every 2 weeks over 8 weeks. At 6 months follow-up, adherence to a LSD was assessed using 24hr UNa. Patients were followed for 1 year to determine time to first event of hospitalization or death due to cardiac problems. Repeated measures ANOVA and Cox regression were used to determine the effect of intervention. Results: The SMART group (n=37) showed a significant reduction in sodium intake across time compared to the TM group (n=35) and control group (n=37) (p= .022). In the Cox regression, patients in the SMART group had longer cardiac event-free survival compared to the control group after controlling for age, gender, ejection fraction, angiotensin-converting enzyme inhibitor use, and better blocker use (p=.008). Conclusion: An education intervention focused on self-monitoring for symptom and sodium intake improved adherence to LSD and health outcomes in patients with HF. Helping patients engage in self-monitoring for symptom and sodium intake by themselves can promote better health outcome.

Abstract P614: Relationship Of Sodium Intake And Stress With Bone Health In Women

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Allison Jasti ◽  
Deborah L Stewart ◽  
Gregory A Harshfield
Keyword(s):  
Bone Health ◽  
Salt Intake ◽  
Sodium Intake ◽  
Target Organ Damage ◽  
African American Adolescents ◽  
Ang Ii ◽  
Mineral Density ◽  
High Sodium ◽  
Low Sodium ◽  
Relationship Of

Background: The skeleton is vital to sodium homeostasis, accounting for 40% of the body’s sodium. Research indicates stress and low sodium intake are independently associated with RAAS activation. In certain populations, stress can induce salt sensitivity, increasing the risk of hypertension and target organ damage, but the association of low versus high sodium intake with bone health is controversial. Purpose: This study sought out the relationship of low sodium and stress-induced RAAS activation with bone health. The tested hypothesis was those with lowest sodium intake would have lower total bone mineral density (TBMD) and content (TBMC) associated with stress-induced increases in angiotensin ii (Ang II) and aldosterone (Aldo). Methods: We compared effect of stress on Ang II, Aldo, TBMD and TMBC in healthy Caucasian and African-American adolescents. Subjects were grouped by quartiles based on sodium intake, assessed by urinary sodium excretion. Results: Due to females, overall significant inverse associations are observed between TBMD, TBMC, Ang II and Aldo in the lowest sodium intake quartile. Post-stress, women in the lowest sodium intake quartile showed that increases in both Ang II and Aldo correspond with lower TMBC and TMBD. There was no significance between Ang II, Aldo, TMBC and TMBD in the three highest quartiles of women nor in any male quartile. Conclusion: These data suggest Ang II and Aldo may reduce TMBC and TMBD in women. Stress-induced increases in Ang II and Aldo, with low sodium intake, may further reduce TBMD and TBMC in women. Ang II inhibition and/or moderated salt intake may be an efficacious prevention or treatment against the development of osteoporosis.

Role of brain serotonergic pathways and hypothalamus in regulation of renin secretion

1987 ◽  
Vol 253 (1) ◽  
pp. R179-R185
Author(s):  
E. Gotoh ◽  
K. Murakami ◽  
T. D. Bahnson ◽  
W. F. Ganong
Keyword(s):  
Plasma Renin ◽  
Dorsal Raphe ◽  
Raphe Nucleus ◽  
Renin Secretion ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Head Up Tilt ◽  
Dorsal Raphé

To investigate the role of brain serotonergic neurons in the regulation of renin secretion, we measured changes in plasma renin activity (PRA), and, in some instances, plasma renin concentration (PRC), plasma angiotensinogen, and plasma adrenocorticotropic hormone (ACTH) in rats with lesions of the dorsal raphe nucleus and lesions of the paraventricular nuclei, dorsomedial nuclei, and ventromedial nuclei of the hypothalamus. We also investigated the effects of p-chloroamphetamine (PCA), immobilization, head-up tilt, and a low-sodium diet in the rats with dorsal raphe, paraventricular, and dorsomedial lesions. Lesions of the dorsal raphe nucleus abolished the increase in PRA produced by PCA but had no effect on the increase produced by immobilization, head-up tilt, and a low-sodium diet. Paraventricular lesions, which abolish the increase in plasma ACTH produced by PCA, immobilization, and head-up tilt, decreased plasma angiotensinogen. The paraventricular lesions abolished the PRA and the PRC responses to PCA and the PRA but not PRC response to immobilization, head-up tilt, and a low-sodium diet. The ventromedial lesions abolished the PRA and PRC responses to PCA and did not reduce plasma angiotensinogen. The data suggest that paraventricular lesions depress angiotensinogen production by the liver and that the paraventricular and ventromedial nuclei are part of the pathway by which serotonergic discharges increase renin secretion. They also suggest that the serotonergic pathway does mediate the increases in renin secretion produced by immobilization, head-up tilt, and a low-sodium diet.

Sign in / Sign up

Export Citation Format

Share Document