Role of blood pressure in mediating the influence of salt intake on renin expression in the kidney

2012 ◽  
Vol 302 (10) ◽  
pp. F1278-F1285 ◽  
Author(s):  
Katharina Machura ◽  
Björn Neubauer ◽  
Dominik Steppan ◽  
Ramona Kettl ◽  
Andreas Groβ ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Distribution Pattern ◽  
Salt Intake ◽  
Salt Content ◽  
Similar Distribution ◽  
High Salt Intake ◽  
Low Salt ◽  
Afferent Arterioles ◽  
Similar Distribution Pattern

The salt intake of an organism controls the number of renin-producing cells in the kidney by yet undefined mechanisms. This study aimed to assess a possible mediator role of preglomerular blood pressure in the control of renin expression by oral salt intake. We used wild-type (WT) mice and mice lacking angiotensin II type 1a receptors (AT1a−/−) displaying an enhanced salt sensitivity to renin expression. In WT kidneys, we found renin-expressing cells at the ends of all afferent arterioles. A low-salt diet (0.02%) led to a moderate twofold increase in renin-expressing cells along afferent arterioles. In AT1a−/− mice, lowering of salt content led to a 12-fold increase in renin expression. Here, the renin-expressing cells were distributed along the preglomerular vascular tree in a typical distal-to-proximal distribution gradient which was most prominent at high salt intake and was obliterated at low salt intake by the appearance of renin-expressing cells in proximal parts of the preglomerular vasculature. While lowering of salt intake produced only a small drop in blood pressure in WT mice, the marked reduction of systolic blood pressure in AT1a−/− mice was accompanied by the disappearance of the distribution gradient from afferent arterioles to arcuate arteries. Unilateral renal artery stenosis in AT1a−/− mice on a normal salt intake produced a similar distribution pattern of renin-expressing cells as did low salt intake. Conversely, increasing blood pressure by administration of the NOS inhibitor N-nitro-l-arginine methyl ester or of the adrenergic agonist phenylephrine in AT1a−/− mice kept on low salt intake produced a similar distribution pattern of renin-producing cells as did normal salt intake alone. These findings suggest that changes in preglomerular blood pressure may be an important mediator of the influence of salt intake on the number and distribution of renin-producing cells in the kidney.

scholarly journals SUN-LB94 Impact of the Gut Microbiome and Renin-Angiotensin-Aldosterone System in Hypertensive Patients With Low-Salt Intake

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Kouki Taniguchi ◽  
Satoshi Nagase ◽  
Shigehiro Karashima ◽  
Mitsuhiro Kometani ◽  
Daisuke Aono ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Gut Microbiome ◽  
Salt Intake ◽  
High Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Hypertensive Patients ◽  
Renin Angiotensin ◽  
High Salt Intake ◽  
Low Salt ◽  
The Impact

Abstract Salt intake is one of most important environmental factors responsible for triggering the onset of hypertension. Renin-angiotensin-aldosterone system (RAAS) plays a key role in adjusting sodium homeostasis and blood pressure. Recently, the potential role of the gut microbiome (GM) in altering the health of the host has drawn considerable attention. We investigated the impact of intestinal microflora and RAAS in hypertensive patients with low-salt or high-salt intake using an observational study. A total of 239 participants were enrolled and their GMs and clinical backgrounds examined, including the renin-angiotensin-aldosterone system and inflammatory cytokine levels. On the basis of enterotypes—determined by cluster analysis—and salt intake, the participants were classified into four groups, low salt/GM enterotype 1, low salt/GM enterotype 2, high salt/GM enterotype 1, and high salt/GM enterotype 2. The prevalence of hypertension was significantly lower in the low-salt intake (low salt/GM enterotype 1 = 47% vs low salt/GM enterotype 2 = 27%, p = 0.04) groups. No significant difference in the prevalence of hypertension was observed for the two GM enterotype groups with high-salt intake (GM enterotype 1 = 50%, GM enterotype 2 = 47%; p = 0.83). Plasma aldosterone concentration was significantly different among the four groups (p < 0.01). Furthermore, the relative abundance of Blautia, Bifidobacterium, Escherichia-Shigella, Lachnoclostridium, and Clostridium sensu stricto was also significantly different among these enterotypes. This suggested in certain individuals (with specific gut bacteria composition) changing dietary habits—to low salt—would be ineffective for regulating hypertension through RAAS. Our findings provide a new strategy for controlling blood pressure and preventing the development of hypertension through restoring GM homeostasis.

Blood pressure and fluid-electrolyte balance in mice with reduced or absent ANP

1996 ◽  
Vol 271 (1) ◽  
pp. R109-R114 ◽  
Author(s):  
S. W. John ◽  
A. T. Veress ◽  
U. Honrath ◽  
C. K. Chong ◽  
L. Peng ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Volume ◽  
Volume Expansion ◽  
Salt Intake ◽  
High Salt ◽  
High Salt Diet ◽  
Salt Diet ◽  
Blood Volume Expansion ◽  
High Salt Intake ◽  
Low Salt

Atrial natriuretic peptide (ANP)-gene knockout mice of three genotypes (+/+, +/-, and -/-) were maintained on a low-salt diet (0.008% NaCl). They were then fed either the same low-salt diet or a high-salt diet (8% NaCl) for 1 wk. No differences were found among genotypes in daily food and water intakes or in urinary volume and electrolyte excretions. Arterial blood pressures measured in anesthetized animals at the end of the dietary regimen were significantly and similarly increased in -/- compared with +/+ mice on each diet. Renal excretion of fluid and electrolytes was measured in anesthetized mice before and after acute blood volume expansion. No genotype differences were observed before volume expansion. After volume expansion the wild-type (+/+) mice had much greater saluretic responses than either the heterozygous (+/-) or the homozygous mutant (-/-) animals on the low-salt diet but not on the high-salt diet. We conclude that ANP lowers blood pressure in the absence of detected changes in renal function; ANP is not essential for normal salt balance, even on high-salt intake; and ANP is essential for the natriuretic response to acute blood volume expansion on a low-salt but not high-salt intake.

Role of Vasopressin in Blood Pressure Control of Spontaneously Hypertensive Rats

1978 ◽  
Vol 55 (s4) ◽  
pp. 247s-250s ◽  
Author(s):  
Jan Möhring ◽  
Jacqueline Kintz ◽  
Josiane Schoun
Keyword(s):  
Blood Pressure ◽  
Blood Pressure Control ◽  
Spontaneously Hypertensive Rats ◽  
Salt Intake ◽  
Renin Angiotensin System ◽  
Pressure Control ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
High Salt Intake

1. The role of arginine—vasopressin (AVP) and of angiotensin in blood pressure control of spontaneously hypertensive rats (SH rats, stroke-prone strain) was studied. 2. In SH rats, which drank water or 1% NaCl, plasma AVP concentrations were elevated during the benign course of hypertension and increased further when the animals entered the malignant phase. Blood pressure correlated significantly with plasma AVP concentrations in SH rats on water, but not in SH rats on saline. 3. The injection of a specific AVP antiserum lowered blood pressure significantly in SH rats on water and in SH rats on saline. 4. When the correlation between blood pressure and plasma AVP of SH rats on water was compared with the respective correlation obtained during infusion of AVP into normotensive rats, a marked shift to the left became apparent, the factor of displacement amounting to more than 1000. 5. Saralasin did not affect blood pressure of SH rats on water, except for two rats with malignant hypertension. However, in SH rats on saline, saralasin lowered blood pressure significantly. 6. It is concluded that in SH rats AVP plays an important vasopressor role in blood pressure control and that sensitization to the vasopressor effect of AVP occurs in these animals. The renin—angiotensin system is significantly involved in blood pressure control of SH rats only when they are subjected to high salt intake.

scholarly journals High Salt Intake Increases Blood Pressure in Normal Rats: Putative Role of 20-HETE and No Evidence on Changes in Renal Vascular Reactivity

2015 ◽  
Vol 40 (3) ◽  
pp. 323-334 ◽  
Author(s):  
A. Walkowska ◽  
M. Kuczeriszka ◽  
J. Sadowski ◽  
K.H. Olszyñski ◽  
L. Dobrowolski ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Reactivity ◽  
Salt Intake ◽  
High Salt ◽  
Putative Role ◽  
High Salt Intake ◽  
Renal Vascular

Blunted hypertensive effect of combined fructose and high-salt diet in gene-targeted mice lacking functional serum- and glucocorticoid-inducible kinase SGK1

2006 ◽  
Vol 290 (4) ◽  
pp. R935-R944 ◽  
Author(s):  
Dan Yang Huang ◽  
Krishna M. Boini ◽  
Björn Friedrich ◽  
Marco Metzger ◽  
Lothar Just ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Flow Rate ◽  
Fluid Intake ◽  
Salt Intake ◽  
Control Diet ◽  
High Salt ◽  
Urinary Flow Rate ◽  
Urinary Flow ◽  
High Salt Intake

Serum- and glucocorticoid-inducible kinase (SGK1) is transcriptionally upregulated by mineralocorticoids and activated by insulin. The kinase stimulates the renal epithelial Na+ channel and may thus participate in blood pressure regulation. Hyperinsulinemia is triggered by dietary fructose, which sensitizes blood pressure for salt intake. The role of SGK1 in hypertensive effects of combined fructose and high-salt intake was thus explored in SGK1 knockout mice ( sgk1−/−) and their wild-type littermates ( sgk1+/+). Renal SGK1 transcript levels of sgk1+/+ mice were significantly elevated after fructose diet. Under control diet, fluid intake, urinary flow rate, urinary Na+, K+, and Cl− excretion, and blood pressure were similar in sgk1−/− and sgk1+/+ mice. Addition of 10% fructose to drinking water increased fluid intake and urinary flow rate in both genotypes, and did not significantly alter urinary Na+, K+, and Cl− output in either genotype. Additional high NaCl diet (4% NaCl) did not significantly alter fluid intake and urine volume but markedly increased urinary output of Na+ and Cl−, approaching values significantly ( P < 0.05) larger in sgk1−/− than in sgk1+/+ mice (Na+: 2,572 ± 462 vs. 1,428 ± 236; Cl−: 2,364 ± 388 vs. 1,379 ± 225 μmol/24 h). Blood pressure was similar in sgk1+/+ and sgk1−/− mice at control diet or fructose alone but increased only in sgk1+/+ mice (115 ± 1 vs. 103 ± 0.7 mmHg, P < 0.05) after combined fructose and high-salt intake. Acute intravenous insulin infusion (during glucose clamp) caused antinatriuresis in sgk1+/+ mice, an effect significantly blunted in sgk1−/− mice. The observations reveal a pivotal role of SGK1 in insulin-mediated sodium retention and the salt-sensitizing hypertensive effect of high fructose intake.

scholarly journals Epithelial Sodium Channel and Salt-Sensitive Hypertension

Hypertension ◽  
2021 ◽  
Vol 77 (3) ◽  
pp. 759-767
Author(s):  
Stephanie M. Mutchler ◽  
Annet Kirabo ◽  
Thomas R. Kleyman
Keyword(s):  
Blood Pressure ◽  
Sodium Channel ◽  
Salt Intake ◽  
Extracellular Fluid ◽  
Pressure Rise ◽  
Epithelial Sodium Channel ◽  
Sodium Reabsorption ◽  
High Salt Intake ◽  
Salt Sensitive Hypertension

The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodium intake while others experience almost no change. These differences are, in part, attributable to genetic variation in pathways involved in sodium handling and excretion. ENaC (epithelial sodium channel) is one of the key transporters responsible for the reabsorption of sodium in the distal nephron. This channel has an important role in the regulation of extracellular fluid volume and consequently blood pressure. Herein, we review the role of ENaC in the development of salt-sensitive hypertension, and present mechanistic insights into the regulation of ENaC activity and how it may accelerate sodium-induced damage and dysfunction. We discuss the traditional role of ENaC in renal sodium reabsorption and review work addressing ENaC expression and function in the brain, vasculature, and immune cells, and how this has expanded the implications for its role in the initiation and progression of salt-sensitive hypertension.

Effect of naloxone on hypertension in Dahl salt-sensitive rats

1992 ◽  
Vol 262 (1) ◽  
pp. H162-H167 ◽  
Author(s):  
M. D. Johnson ◽  
B. K. Richmond
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Salt Content ◽  
Chronic Administration ◽  
High Salt ◽  
Acute Administration ◽  
Developmental Phase ◽  
Dietary Salt ◽  
Low Salt ◽  
Blood Pressures

Experiments were conducted to test the hypothesis that chronic administration of an opioid receptor antagonist, naloxone, would affect the outcome of the developmental phase of hypertension in Dahl salt-sensitive (S/JR strain) rats. Accordingly, S/JR rats were maintained on either a low-salt (0.45% NaCl) or a high-salt (7% NaCl) diet for 4 wk. Half of the animals of each dietary group were treated with naloxone (100-130 micrograms/h) by osmotic minipump. Food and water intakes of the high-salt animals were measured for the first 25 days, and blood pressure was measured at the end of the 4 wk via an indwelling femoral arterial catheter. Naloxone treatment slightly but significantly reduced the level of hypertension attained in the high-salt animals (158 +/- 2 mmHg in naloxone-treated animals vs. 168 +/- 3 mmHg in control animals; P less than 0.05) and also attenuated food (and hence salt) and water intakes. Naloxone did not affect the blood pressure of the low-salt animals. To determine whether the slight attenuation of hypertension might be secondary to a reduction of salt intake, a group of control S/JR animals were fed a moderately high-salt diet (2% NaCl), and naloxone-treated S/JR animals were salt-intake matched to this group by daily adjustment of the dietary salt content. Blood pressures after 4 wk of treatment were not different between these two groups. Finally, acute administration of 1 and 30 mg/kg of naloxone failed to lower blood pressure of animals with established hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Knowledge and behaviors regarding salt intake according to urinary Na excretion and blood pressure

2020 ◽  
Vol 30 (Supplement_5) ◽  
Author(s):  
T Silva-Santos ◽  
P Moreira ◽  
P Padrão ◽  
S Abreu ◽  
O Pinho ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Sodium Excretion ◽  
Salt Intake ◽  
Disease Risk ◽  
Salt Content ◽  
Urinary Sodium Excretion ◽  
Processed Foods ◽  
Salt Reduction ◽  
High Salt Intake ◽  
And Behaviors

Abstract Background Understanding salt-related knowledge, attitudes and behaviors can help the design of effective health interventions. Therefore, our objective was to describe knowledge and behaviors related to salt intake according to urinary sodium excretion and blood pressure in University workers. Methods We performed our study in a subsample of the participants of the iMC Salt project (n = 60 subjects, 60.5% women, mean age 48±9.5 years). Sodium excretion were measured by one 24-h urinary collection, validated by creatinine excretion and participants were grouped according to the WHO sodium recommendations (&lt;2.0 g/day; high, ≥2.0 g/day). Subjects were classified as hypertensive if the systolic blood pressure was ≥130 mmHg and/or diastolic blood pressure was ≥80mmHg. Knowledge and behaviors regarding salt intake were assessed by the WHO Stepwise Approach to Chronic Disease Risk Factor Surveillance. Results About 74.6% of the participants reported that reducing salt in their diet was very important and 93.2% think that salt is harmful to health. However, 76.3% always add salt during cooking, 42.4% said that they always or often consume processed foods high in salt, 79.7% reported that they don't look at the salt on food labels, 50.8% don't buy low salt alternatives and 30.5% don't use spices as one substitute for salt when cooking. Hypertensive subjects had a higher mean sodium excretion (3710±1508mg/day vs 2478±871mg/day, p = 0.002) and reported a significant higher frequency of consumption of processed foods high in salt (53.1% vs 29.6%, p = 0.024). No significant differences were found with the other variables. Conclusions Most university workers were aware that high salt intake can cause health problems, but they reported low adherence to behaviors to control their salt intake. Hypertensive subjects recognized that frequently consume processed foods high in salt, so reduce salt content on those products could have important impact on their daily salt consumption. Key messages This study provides evidence on knowledge and behaviors regarding salt intake to guide salt reduction policies. Hypertensive participants reported a higher frequency of eating processed foods rich in salt.

Abstract MP70: Aldosterone And Inverse Salt Sensitivity Of Blood Pressure

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Peng Xu ◽  
John J Gildea ◽  
Mahabuba Akhter ◽  
Robert M Carey ◽  
Wei Yue ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Salt Sensitivity ◽  
High Salt ◽  
Sodium Reabsorption ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Salt Intake ◽  
Low Salt ◽  
Harmful Effects

Salt sensitivity affects approximately 20% of adults worldwide and has similar mortality and morbidity sequalae as hypertension. Research has focused on the harmful effects of a high salt diet but have not focused on the harmful effects of a low salt diet. Inverse salt sensitive (ISS) individuals require high salt intake in order to maintain a normal blood pressure. Aldosterone increases ENaC and sodium reabsorption via the mineralocorticoid receptor (MR). We previously reported that αENaC was significantly lower in ISS renal tubule cells isolated from urine (uRTC), while these cells showed higher ENaC like activities under trypsin stimulation. We hypothesized that aldosterone may act as a stimulus and play a role in ISS high blood pressure on a low salt diet (LSD). Plasma aldosterone was significantly increased on LSD in all salt study participants, and ISS individuals showed the highest aldosterone level (ISS HS 3.8±0.38, n=26; ISS LS 35±3.38, n=22; SR HS 4.34±0.18, n=180; SR LS 32.62±1.6, n=152; SS HS 4.65±0.35, n=43; SS LS 26.08±2.18, n=38; HS Vs LS, p<0.001, two-way ANOVA). Moreover, both aldosterone and plasma renin activity (PRA) were significantly lower in salt sensitive (SS) individuals on LSD (PRA LS: ISS 6.05±0.87, n=17; SR 5.94±0.36, n=108; SS 4.43±0.57, n=34; p<0.05, one-way ANOVA), indicating LSD was protective to SS individuals. Treatment of uRTCs with 1 μM aldosterone increased MR and αENaC expression in ISS but not in SR (salt resistant) cells (MR: SR VEH 12164±213; SR Aldosterone 12327±128; ISS VEH 12128±40 vs ISS Aldosterone 13506±128, n=3, p<0.001, two-way ANOVA; αENaC: SR VEH 5023±46; SR Aldosterone 4895±55; ISS VEH 4270±21 vs ISS Aldosterone 5013±113, n=3, p<0.001, two-way ANOVA). High salt treatment further decreased MR in ISS but not in SR cells (ISS: 142mM 11066±188 vs 192mM 10425±74; p<0.05, n=3 two-way ANOVA). These results are consistent with the hypothesis that ISS individuals retain excess Na + and exhibit decreased BP when compared to SR or SS individuals under high salt diet, but reabsorb more sodium and exhibit elevated blood pressure under low salt diet. Higher circulating aldosterone and ex-vivo urine derived renal cell aldosterone sensitivity under low salt conditions may be a novel diagnostic test to identify ISS individuals.

Sign in / Sign up

Export Citation Format

Share Document