scholarly journals Klotho Gene in Human Salt-Sensitive Hypertension

2020 ◽  
Vol 15 (3) ◽  
pp. 375-383 ◽  
Author(s):  
Lorena Citterio ◽  
Simona Delli Carpini ◽  
Sara Lupoli ◽  
Elena Brioni ◽  
Marco Simonini ◽  
...  
Keyword(s):  
Salt Intake ◽  
Sodium Intake ◽  
Salt Sensitivity ◽  
Single Nucleotide ◽  
Related Disorder ◽  
Klotho Gene ◽  
A Genome ◽  
Treatment Naïve ◽  
Pressure Natriuresis ◽  
Salt Sensitive Hypertension

Background and objectivesHypertension is a common aging-related disorder. Salt intake is one of the main environmental factors contributing to the development of hypertension. Transgenic mice with one-half Klotho deficiency displayed a spontaneous BP increase and salt-sensitive hypertension in response to high sodium intake. Usually circulating levels of α-Klotho decrease with age, and this reduction may be stronger in patients with several aging-related diseases. This study aimed at exploring the association of Klotho with salt sensitivity in humans.Design, setting, participants, & measurementsThe role of Klotho polymorphisms and α-Klotho serum levels was evaluated in patients with hypertension who were treatment naive and underwent an acute salt-sensitivity test (discovery n=673, intravenous 2 L of 0.9% saline in 2 hours). Salt sensitivity was defined as a mean BP increase of >4 mm Hg at the end of the infusion. A total of 32 single nucleotide polymorphisms in the Klotho gene (KL), previously identified with a genome-wide association study, were used in the genetic analysis and studied for a pressure-natriuresis relationship.ResultsOf the patients with hypertension, 35% were classified as salt sensitive. The most relevant polymorphism associated with pressure natriuresis was the common missense single nucleotide polymorphism rs9536314, and the GG and GT genotypes were more represented among patients who were salt sensitive (P=0.001). Those carrying the G allele showed a less steep pressure-natriuresis relationship, meaning that a significant increase in mean BP was needed to excrete the same quantity of salt compared with patients who were salt resistant. KL rs9536314 also replicated the pressure-natriuresis association in an independent replication cohort (n=193) and in the combined analysis (n=866). There was an inverse relationship between circulating Klotho and mean BP changes after the saline infusion (r=−0.14, P=0.03). Moreover, circulating α-Klotho was directly related to kidney function at baseline eGFR (r=0.22, P<0.001).ConclusionsKL rs9536314 is associated with salt-sensitive hypertension in patients with hypertension who are treatment naive. Moreover, circulating α-Klotho levels were mainly related to diastolic BP changes at the end of a salt load and to eGFR as an expression of kidney aging.

Responsiveness vs. basal activity of plasma ANG II as a determinant of arterial pressure salt sensitivity

2003 ◽  
Vol 285 (5) ◽  
pp. H2142-H2149 ◽  
Author(s):  
John W. Osborn ◽  
Pilar Ariza-Nieto ◽  
John P. Collister ◽  
Sandra Soucheray ◽  
Benjamin Zimmerman ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Salt Intake ◽  
Enzyme Inhibitor ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Salt Sensitivity ◽  
Saline Control ◽  
Ang Ii ◽  
Sprague Dawley ◽  
Salt Sensitive Hypertension

Infusion of angiotensin II (ANG II) causes salt-sensitive hypertension. It is unclear whether this is due to the body's inability to suppress ANG II during increased salt intake or, rather, an elevated basal level of plasma ANG II itself. To distinguish between these mechanisms, Sprague-Dawley rats were instrumented with arterial and venous catheters for measurement of arterial pressure and infusion of drugs, respectively. The sensitivity of arterial pressure to salt was measured in four groups with the following treatments: 1) saline control (Con, n = 12); 2) administration of the angiotensin-converting enzyme inhibitor enalapril to block endogenous ANG II (ANG-Lo, n = 10); 3) administration of enalapril and 5 ng · kg–1 · min–1 ANG II to clamp plasma ANG II at normal levels (ANG-Norm, n = 10); and 4) administration of enalapril and 20 ng · kg–1 · min–1 ANG II to clamp ANG II at high levels (ANG-Hi, n = 10). Rats ingested a 0.4% NaCl diet for 3 days and then a 4.0% NaCl diet for 11 days. Arterial pressure of rats fed the 0.4% NaCl diet was lower in ANG-Lo (84 ± 2 mmHg) compared with Con (101 ± 3 mmHg) and ANG-Norm (98 ± 4 mmHg) groups, whereas ANG-Hi rats were hypertensive (145 ± 4 mmHg). Salt sensitivity was expressed as the change in arterial pressure divided by the change in sodium intake on the last day of the 4.0% NaCl diet. Salt sensitivity (in mmHg/meq Na) was lowest in Con rats (0.0 ± 0.1) and progressed from ANG-Lo (0.8 ± 0.2) to ANG-Norm (1.5 ± 0.5) to ANG-Hi (3.5 ± 0.5) rats. We conclude that the major determinant of salt sensitivity of arterial pressure is the basal level of plasma ANG II rather than the responsiveness of the renin-angiotensin system.

scholarly journals Effects of AT1A receptor deletion on blood pressure and sodium excretion during altered dietary salt intake

2002 ◽  
Vol 283 (3) ◽  
pp. F447-F453 ◽  
Author(s):  
Amy J. Mangrum ◽  
R. Ariel Gomez ◽  
Victoria F. Norwood
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Wild Type ◽  
Compensatory Mechanisms ◽  
Wide Range ◽  
Blood Pressures ◽  
Pressure Natriuresis

The present study was performed to investigate the role of type 1A ANG II (AT1A) receptors in regulating sodium balance and blood pressure maintenance during chronic dietary sodium variations in AT1A receptor-deficient (−/−) mice. Groups of AT1A (−/−) and wild-type mice were placed on a low (LS)-, normal (NS)-, or high-salt (HS) diet for 3 wk. AT1A(−/−) mice on an LS diet had high urinary volume and low blood pressure despite increased renin and aldosterone levels. On an HS diet, (−/−) mice demonstrated significant diuresis, yet blood pressure increased to levels greater than control littermates. There was no effect of dietary sodium intake on systolic blood pressures in wild-type animals. The pressure-natriuresis relationship in AT1A (−/−) mice demonstrated a shift to the left and a decreased slope compared with wild-type littermates. These studies demonstrate that mice lacking the AT1A receptor have blood pressures sensitive to changes in dietary sodium, marked alterations of the pressure-natriuresis relationship, and compensatory mechanisms capable of maintaining normal sodium balance across a wide range of sodium intakes.

scholarly journals Distinct effects on long-term function of injured and contralateral kidneys following unilateral renal ischemia-reperfusion

2012 ◽  
Vol 302 (5) ◽  
pp. F625-F635 ◽  
Author(s):  
David P. Basile ◽  
Ellen C. Leonard ◽  
Deoye Tonade ◽  
Jessica L. Friedrich ◽  
Shreevrat Goenka
Keyword(s):  
Sodium Intake ◽  
Ischemia Reperfusion ◽  
Kidney Injury ◽  
Dietary Sodium ◽  
Vascular Density ◽  
Contralateral Kidney ◽  
Direct Injury ◽  
Pressure Natriuresis ◽  
Salt Sensitive Hypertension ◽  
Injured Kidney

Salt-sensitive hypertension and chronic kidney disease (CKD) following recovery from acute kidney injury (AKI) may occur secondary to incomplete repair, or by activation of circulating factors stimulated by injury. We created two types of renal injury induced by unilateral ischemia-reperfusion (I/R); in a direct/ipsilateral AKI group, rats were subjected to unilateral I/R and the untouched contralateral kidney was removed by unilateral nephrectomy after 5 wk to isolate effects on the injured kidney. In the remote/contralateral AKI group, the injured kidney was removed after 5 wk to isolate effects on the untouched kidney. When these animals were subsequently challenged with elevated dietary sodium for an additional 4 wk (0.4 to 4%), both remote/contralateral and direct/ipsilateral AKI rats manifested a significant increase in blood pressure relative to sham-operated controls. Similarly, in acute studies, both ipsilateral and contralateral kidneys had impaired pressure natriuresis and hemodynamic responses. Reductions in vascular density were observed following direct/ipsilateral injury, but were not observed in the remote/contralateral kidney. However, both remote/contralateral and direct/ipsilateral kidneys contained interstitial cells, some of which were identified as activated (low CD62L/CD4+) T lymphocytes. In contrast, only the direct/ipsilateral AKI group demonstrated significant CKD following exposure to elevated salt. This was characterized by a significant reduction in creatinine clearance, an increase in albuminuria, and a dramatic expansion of interstitial inflammation. Taken together, these data suggest that the salt-sensitive features of AKI on hypertension and CKD are segregable such that effects on hemodynamics and hypertension occur independent of direct renal damage. However, prior direct injury to the kidney is required to elicit the full manifestation of CKD induced by elevated sodium intake.

scholarly journals Genetically, dietary sodium intake is causally associated with salt-sensitive hypertension risk in a community-based cohort study: a Mendelian randomization approach

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
J.R Choi
Keyword(s):  
Mendelian Randomization ◽  
Salt Intake ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Funding Source ◽  
Dietary Salt ◽  
Community Based ◽  
Dietary Salt Intake ◽  
Hypertension Risk ◽  
Salt Sensitive Hypertension

Abstract   Excessive dietary salt intake is associated with an increased risk of hypertension. Salt sensitivity, i.e., an elevation in blood pressure in response to high dietary salt intake, has been associated with a high risk of cardiovascular disease and mortality. We investigated whether a causal association exists between dietary sodium intake and hypertension risk using Mendelian randomization (MR). We performed an MR study using data from a large genome-wide association study comprising 15,034 Korean adults in a community-based cohort study. A total of 1,282 candidate single nucleotide polymorphisms associated with dietary sodium intake, such as rs2960306, rs4343, and rs1937671, were selected as instrumental variables. The inverse variance weighted method was used to assess the evidence for causality. Higher dietary sodium intake was associated with salt-sensitive hypertension risk. The variants of SLC8E1 rs2241543 and ADD1 rs16843589 were strongly associated with increased blood pressure. In the logistic regression model, after adjusting for age, gender, smoking, drinking, exercise, and body mass index, the GRK4 rs2960306TT genotype was inversely associated with hypertension risk (OR = 0.356, 95% CI = 0.236–0.476). However, the 2350GG genotype (ACE rs4343) exhibited a 2.11-fold increased hypertension risk (OR = 2.114, 95% CI = 2.004–2.224) relative to carriers of the 2350AA genotype, after adjusting for confounders. MR analysis revealed that the odds ratio for hypertension per 1 mg/day increment of dietary sodium intake was 2.24 in participants with the PRKG1 rs12414562 AA genotype. Our findings suggest that dietary sodium intake may be causally associated with hypertension risk. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): This research was supported by the Basic Science Research Program through the National Research Foundation of Korea (NRF), funded by the Ministry of Education (2017R1D1A3B03034119, 2014M3C9A3064552), and the KRIBB Initiative program. This research was also supported by the Medical Research Center Program (2017R1A5A2015369). This work was supported (in part) by the Yonsei University Research Fund 2017. Bioresources for this study were provided by the National Biobank of Korea and the Centers for Disease Control and Prevention, Republic of Korea (2017-009).

scholarly journals High-salt intake enhances superoxide activity in eNOS knockout mice leading to the development of salt sensitivity

2010 ◽  
Vol 299 (3) ◽  
pp. F656-F663 ◽  
Author(s):  
Libor Kopkan ◽  
Arthur Hess ◽  
Zuzana Husková ◽  
Luděk Červenka ◽  
L. Gabriel Navar ◽  
...  
Keyword(s):  
Salt Intake ◽  
Salt Sensitivity ◽  
High Salt ◽  
No Production ◽  
Wild Type ◽  
Total N ◽  
High Salt Intake ◽  
Excretion Rates ◽  
Salt Sensitive Hypertension

A deficiency in nitric oxide (NO) generation leads to salt-sensitive hypertension, but the role of increased superoxide (O2−) in such salt sensitivity has not been delineated. We examined the hypothesis that an enhancement in O2− activity induced by high-salt (HS) intake under deficient NO production contributes to the development of salt-sensitive hypertension. Endothelial NO synthase knockout (eNOS KO; total n = 64) and wild-type (WT; total n = 58) mice were given diets containing either normal (NS; 0.4%) or high-salt (HS; 4%) for 2 wk. During this period, mice were chronically treated with a O2− scavenger, tempol (400 mg/l), or an inhibitor of NADPH oxidase, apocynin (1 g/l), in drinking water or left untreated ( n = 6–8 per group). Blood pressure was measured by radiotelemetry and 24-h urine samples were collected in metabolic cages. Basal mean arterial pressure (MAP) in eNOS KO was higher (125 ± 4 vs. 106 ± 3 mmHg) compared with WT. Feeding HS diet did not alter MAP in WT but increased it in eNOS KO to 166 ± 9 mmHg. Both tempol and apocynin treatment significantly attenuated the MAP response to HS in eNOS KO (134 ± 3 and 139 ± 4 mmHg, respectively). Basal urinary 8-isoprostane excretion rates (UIsoV), a marker for endogenous O2− activity, were similar (2.8 ± 0.2 and 2.4 ± 0.3 ng/day) in both eNOS KO and WT mice. However, HS increased UIsoV more in eNOS KO than in WT (4.6 ± 0.3 vs. 3.8 ± 0.2 ng/day); these were significantly attenuated by both tempol and apocynin treatment. These data indicate that an enhancement in O2− activity contributes substantially to the development of salt-sensitive hypertension under NO-deficient conditions.

scholarly journals Association of Single Nucleotide Polymorphisms in Salt Taste Receptor Genes With Dietary Salt Intake and Blood Pressure Among Iranian Adults Population

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 945-945
Author(s):  
Noushin Mohammadifard ◽  
Mojgan Gharipour ◽  
Faezeh Moazeni
Keyword(s):  
Blood Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Taste Receptors ◽  
Urine Collection ◽  
Nucleotide Polymorphisms ◽  
Dietary Salt ◽  
Single Nucleotide ◽  
Dietary Salt Intake ◽  
Salt Taste

Abstract Objectives So far, few researches has examined how genetic variation in salt taste receptors affects food intake in Iranian population. Thus, in this study, we aimed to investigate associations of single nucleotide polymorphisms (SNPs) in salt taste receptors genes with dietary salt intake and blood pressure. Methods This cross-sectional study was carried out among 116 randomly selected adults aged 18 years and over in Isfahan city, Iran. Subjects with diabetes insipidus, renal insufficiency, a special dietary regimen, fasting or menstruating on the day of sampling, using diuretics and oral contraceptives or pregnant and lactating women as well as participants who had incomplete 24-h urine collection were excluded. A 24-h urine collection and blood pressure measurement were done. Whole blood was collected to extract DNA and measure SNP rs239345 in the ENaC and rs224534, rs4790151 and rs8065080 in the TRPV1 gene. Results Homozygous carriers of the T allele for rs239345 were found to consume significantly more sodium (4414.7 ± 1943.8 mg/day) compared to the AA genotype (3887.4 ± 1709.1 mg/day). Further, they also had higher diastolic blood pressure compared to subjects with the AA genotype (81.3 ± 9.7 vs. 75.3 ± 8.3 mmHg). Compared to subjects with the CC genotype, those with homozygous carriers of the T allele for rs8065080 in the TRPV1 had higher sodium intake (3592.6 ± 1645.2 mg/day vs. 4604.2 ± 2013.5 mg/day) and systolic blood pressure (118.1 ± 11.3 mmHg vs. 123.4 ± 11.5 mmHg). No differences were found in dietary sodium intake and blood pressure with the rs224534 and rs4790151 SNPs. Conclusions These findings suggest that genetic variation in the ENaC and TRPV1 genes may contribute to inter-individual differences in salt intake and blood pressure. Funding Sources The National Institute for Medical Research Development (NIMAD) was funded this study via grant number of 977,549.

Abstract 135: PVN Galphai2 Protein Over Expression Attenuates Dahl Salt Sensitive Hypertension and GNAI2 Polymorphic Variance Represents a Clinical Biomarker of the Salt Sensitivity of Blood Pressure

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Richard D Wainford ◽  
Xiaoling Zhang
Keyword(s):  
Viral Vector ◽  
Salt Intake ◽  
Critical Role ◽  
Salt Sensitivity ◽  
Over Expression ◽  
Protein Levels ◽  
Neuron Activation ◽  
High Salt Intake ◽  
The Individual ◽  
Salt Sensitive Hypertension

Aim: We hypothesize that a) in the DSS rat, which in contrast to the normotensive DSR rat fails to up regulate PVN Gαi 2 proteins on a high salt intake (Wainford et al, Hypertension 2015), PVN specific Gαi 2 protein over expression will attenuate the development of salt sensitive hypertension (HTN) and, b) SNPs in the GNAI2 gene, which are associated with HTN in Japanese and Italian populations, represent a biomarker of the salt-sensitivity of BP. Methods: Male DSS rats instrumented with a radiotelemetry probe (DSI; PA-C40) received a bilateral PVN shuttle or Gαi 2 expressing lenti-viral vector microinjection (2x10 9 infectious units per ml/60nl/side) and were maintained on a 7-day normal 0.4% (NS) intake for baseline BP prior to 21 day high 4% NaCl (HS) intake. On day 21 rats were sacrificed to assess PVN Gαi 2 protein expression (immunoblotting), plasma NE content (ELISA) or underwent a 5% volume expansion (VE) prior to cardiac perfusion and c-fos IHC to assess PVN neuron activation (N=4/gp/study). SNPs in the GNAI2 gene were examined in GenSalt (N=968) for associations with the salt sensitivity of BP (increase in systolic BP of 5mmHg or greater during HS intake, N=326 are salt sensitive: 172 Female, 154 male). Results: Bilateral lenti-virus increased PVN Gαi 2 protein levels 3 fold (p<0.05) on both NS and HS intake, attenuated HTN (Day 21 HS MAP [mmHg] shuttle 160±3 vs. Gαi 2 144±4, P<0.05), abolished Na + evoked global and renal sympathoexcitation (Day 21 HS plasma NE [nmol/L] shuttle 82±5 vs. Gαi 2 50±4, P<0.05). PVN Gαi 2 over expression increased VE-evoked natriuresis (peak natriuresis (UNaV; [μeq/min] shuttle NS 43±3, shuttle HS 16±3, Gαi 2 HS 31±3, P<0.05) and PVN sympathoinhibitory parvocellular neuron activation (medial parvocellular c-Fos positive cells shuttle NS 67±8, shuttle HS 29±3, Gαi 2 vector HS 48±6, P<0.05). 3 GNAI2 SNPs are present in GenSalt - rs9852677 and rs2282751 did not associate with the salt sensitivity of BP. SNP rs10510755 positively correlated with the salt sensitivity of BP (MAF:6%, Z-score: 1.94, p<0.05) independently of sex. Conclusion: These data suggest a critical role of PVN Gαi 2 proteins in countering the pathophysiology of salt sensitive HTN and that GNAI2 polymorphic variance represents a biomarker of the individual salt sensitivity of BP.

scholarly journals Activation of the Sympathetic Nervous System Promotes Blood Pressure Salt-Sensitivity in C57BL6/J Mice

Hypertension ◽  
2021 ◽  
Vol 77 (1) ◽  
pp. 158-168
Author(s):  
Ailsa F. Ralph ◽  
Celine Grenier ◽  
Hannah M. Costello ◽  
Kevin Stewart ◽  
Jessica R. Ivy ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Function ◽  
Salt Intake ◽  
Salt Sensitivity ◽  
High Salt ◽  
Sodium Balance ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Salt Intake ◽  
Pressure Natriuresis

Global salt intake averages >8 g/person per day, over twice the limit advocated by the American Heart Association. Dietary salt excess leads to hypertension, and this partly mediates its poor health outcomes. In ≈30% of people, the hypertensive response to salt is exaggerated. This salt-sensitivity increases cardiovascular risk. Mechanistic cardiovascular research relies heavily on rodent models and the C57BL6/J mouse is the most widely used reference strain. We examined the effects of high salt intake on blood pressure, renal, and vascular function in the most commonly used and commercially available C57BL6/J mouse strain. Changing from control (0.3% Na + ) to high salt (3% Na + ) diet increased systolic blood pressure in male mice by ≈10 mm Hg within 4 days of dietary switch. This hypertensive response was maintained over the 3-week study period. Returning to control diet gradually reduced blood pressure back to baseline. High-salt diet caused a rapid and sustained downregulation in mRNA encoding renal NHE3 (sodium-hydrogen-exchanger 3) and EnaC (epithelial sodium channel), although we did not observe a suppression in aldosterone until ≈7 days. During the development of salt-sensitivity, the acute pressure natriuresis relationship was augmented and neutral sodium balance was maintained throughout. High-salt diet increased ex vivo sensitivity of the renal artery to phenylephrine and increased urinary excretion of adrenaline, but not noradrenaline. The acute blood pressure–depressor effect of hexamethonium, a ganglionic blocker, was enhanced by high salt. Salt-sensitivity in commercially sourced C57BL6/J mice is attributable to sympathetic overactivity, increased adrenaline, and enhanced vascular sensitivity to alpha-adrenoreceptor activation and not sodium retention or attenuation of the acute pressure natriuresis response.

scholarly journals Sensory Afferent Renal Nerve Activated Gαi2 Subunit Proteins Mediate the Natriuretic, Sympathoinhibitory and Normotensive Responses to Peripheral Sodium Challenges

2021 ◽  
Vol 12 ◽  
Author(s):  
Jesse D. Moreira ◽  
Kayla M. Nist ◽  
Casey Y. Carmichael ◽  
Jill T. Kuwabara ◽  
Richard D. Wainford
Keyword(s):  
Blood Pressure ◽  
Volume Expansion ◽  
Salt Intake ◽  
Sodium Intake ◽  
Salt Sensitivity ◽  
Dietary Sodium ◽  
Whole Body ◽  
Renal Nerves ◽  
Acute Administration ◽  
Resistant Phenotype

We have previously reported that brain Gαi2 subunit proteins are required to maintain sodium homeostasis and are endogenously upregulated in the hypothalamic paraventricular nucleus (PVN) in response to increased dietary salt intake to maintain a salt resistant phenotype in rats. However, the origin of the signal that drives the endogenous activation and up-regulation of PVN Gαi2 subunit protein signal transduction pathways is unknown. By central oligodeoxynucleotide (ODN) administration we show that the pressor responses to central acute administration and central infusion of sodium chloride occur independently of brain Gαi2 protein pathways. In response to an acute volume expansion, we demonstrate, via the use of selective afferent renal denervation (ADNX) and anteroventral third ventricle (AV3V) lesions, that the sensory afferent renal nerves, but not the sodium sensitive AV3V region, are mechanistically involved in Gαi2 protein mediated natriuresis to an acute volume expansion [peak natriuresis (μeq/min) sham AV3V: 43 ± 4 vs. AV3V 45 ± 4 vs. AV3V + Gαi2 ODN 25 ± 4, p &lt; 0.05; sham ADNX: 43 ± 4 vs. ADNX 23 ± 6, AV3V + Gαi2 ODN 25 ± 3, p &lt; 0.05]. Furthermore, in response to chronically elevated dietary sodium intake, endogenous up-regulation of PVN specific Gαi2 proteins does not involve the AV3V region and is mediated by the sensory afferent renal nerves to counter the development of the salt sensitivity of blood pressure (MAP [mmHg] 4% NaCl; Sham ADNX 124 ± 4 vs. ADNX 145 ± 4, p &lt; 0.05; Sham AV3V 125 ± 4 vs. AV3V 121 ± 5). Additionally, the development of the salt sensitivity of blood pressure following central ODN-mediated Gαi2 protein down-regulation occurs independently of the actions of the brain angiotensin II type 1 receptor. Collectively, our data suggest that in response to alterations in whole body sodium the peripheral sensory afferent renal nerves, but not the central AV3V sodium sensitive region, evoke the up-regulation and activation of PVN Gαi2 protein gated pathways to maintain a salt resistant phenotype. As such, both the sensory afferent renal nerves and PVN Gαi2 protein gated pathways, represent potential targets for the treatment of the salt sensitivity of blood pressure.

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