Role of ETA receptors in experimental ANG II-induced hypertension in rats

2001 ◽  
Vol 281 (1) ◽  
pp. R150-R154 ◽  
Author(s):  
Jennifer R. Ballew ◽  
Gregory D. Fink
Keyword(s):  
Mean Arterial Pressure ◽  
Salt Intake ◽  
Sodium Intake ◽  
Male Rats ◽  
Ang Ii ◽  
High Sodium ◽  
High Sodium Intake ◽  
Induced Hypertension ◽  
Baseline Levels

The objectives were to determine if ANG II-induced hypertension is maintained by activation of endothelin type A (ETA) receptors by endogenous ET-1 and if this effect is influenced by salt intake. Male rats were maintained on high sodium intake (HS; 6 meq/day) or on normal sodium intake (NS; 2 meq/day). Hypertension was produced by intravenous infusion of ANG II (5 ng/min) for 15 days. Five-day oral dosing with the selective ETA-receptor antagonist ABT-627 (∼2 mg · kg−1 · day−1) reduced mean arterial pressure (MAP) to baseline levels in rats on HS receiving ANG II infusion, but it did not affect MAP in normotensive HS controls. In rats on NS, ABT-627 only transiently decreased MAP in rats receiving ANG II and slightly reduced MAP in normotensive controls. ABT-627 produced mild retention of sodium and water in NS rats receiving ANG II, but not in any other group. These results indicate that ET-1 plays a role in ANG II-induced hypertension via activation of ETAreceptors and that this role is more prominent in rats on HS.

Role of endothelin ETB receptor activation in angiotensin II-induced hypertension: effects of salt intake

2001 ◽  
Vol 281 (5) ◽  
pp. H2218-H2225 ◽  
Author(s):  
Jennifer R. Ballew ◽  
Gregory D. Fink
Keyword(s):  
Arterial Pressure ◽  
Receptor Antagonist ◽  
Salt Intake ◽  
Receptor Activation ◽  
Salt Sensitivity ◽  
Male Rats ◽  
Ang Ii ◽  
High Salt Intake ◽  
Induced Hypertension

We showed recently that endothelin (ET)A receptors are involved in the salt sensitivity of ANG II-induced hypertension. The objective of this current study was to characterize the role of endothelin ETB receptor activation in the same model. Male rats on fixed normal (2 meq/day) or high (6 meq/day) salt intake received a continuous intravenous infusion of ANG II or salt only for 15 days. During the middle 5 days of the infusion period, rats were given either the selective ETB receptor antagonist A-192621 or the nonselective endothelin receptor antagonist A-182086 (both at 24 mg · kg−1 · day−1intra-arterially). Infusion of ANG II caused a greater rise in arterial pressure in rats on high-salt intake. The administration of A-192621 increased arterial pressure further in all rats. The chronic hypertensive effect of A-192621 was not significantly affected by salt intake or ANG II. The administration of A-182086 lowered arterial pressure chronically only in rats on normal salt intake receiving ANG II. Thus the salt sensitivity of ANG II-induced hypertension is not caused by changes in ETB receptor function.

Role of aldosterone in angiotensin II-induced hypertension in rats

1990 ◽  
Vol 259 (1) ◽  
pp. R102-R109 ◽  
Author(s):  
N. L. Kanagy ◽  
C. M. Pawloski ◽  
G. D. Fink
Keyword(s):  
Angiotensin Ii ◽  
Sodium Intake ◽  
Chronic Administration ◽  
Plasma Aldosterone ◽  
Ang Ii ◽  
Plasma Aldosterone Concentration ◽  
High Sodium ◽  
High Sodium Intake ◽  
Induced Hypertension ◽  
Commercial Radio

Initial experiments demonstrated that a 1-h infusion of 10 ng/min angiotensin II (ANG II) into rats causes an increase in plasma aldosterone concentration (PAC) and that chronic administration of aldosterone alone to rats on increased sodium intake causes hypertension. We therefore hypothesized that a portion of the hypertensive effect of chronic ANG II infusion is accompanied by and dependent on chronic release of aldosterone. To test this hypothesis, 10 ng/min ANG II or saline was infused into chronically instrumented rats housed in metabolism cages. Fifteen rats were maintained on a high sodium intake (6 meq/day); 10 received ANG II and 5 received saline. Ten other rats were maintained on a normal sodium intake (2 meq/day); five received ANG II and five received saline. PAC was measured using a commercial radio-immunoassay kit. Mean arterial pressure (MAP), heart rate, water intake, urine output, and urine electrolytes were measured daily during 3-day control, 16- or 28-day infusion, and 4-day recovery periods. Compared with saline-infused rats, ANG II-infused rats on high sodium intake had normal values for all variables except MAP, which was significantly elevated during ANG II infusion. In the normal sodium group, none of the variables were consistently different during ANG II infusion compared with control. These results suggest that ANG II-induced hypertension in the rat is sodium dependent, that plasma aldosterone does not play a major role in ANG II-induced hypertension in the rat, and that a small chronic increase in circulating ANG II does not necessarily lead to a detectable sustained increase in PAC.

Pressure natriuresis and angiotensin II in reduced kidney mass, salt-induced hypertension

1992 ◽  
Vol 262 (1) ◽  
pp. R61-R71 ◽  
Author(s):  
J. E. Hall ◽  
H. L. Mizelle ◽  
M. W. Brands ◽  
D. A. Hildebrandt
Keyword(s):  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Sodium Intake ◽  
Renal Perfusion ◽  
Sodium Balance ◽  
Ang Ii ◽  
High Sodium ◽  
High Sodium Intake ◽  
Induced Hypertension ◽  
Pressure Natriuresis

In normal subjects, high sodium intake causes little change in mean arterial pressure (MAP). However, MAP is sodium sensitive after reduction of kidney mass. The present study examined the role of increased renal artery pressure and decreased angiotensin II (ANG II) formation in maintaining sodium balance during high sodium intake in dogs with reduced kidney mass. In seven dogs with pressure natriuresis intact, increasing sodium intake from 36 to 466 meq/day for 7 days raised MAP from 91 +/- 2 to 106 +/- 2 mmHg. Sodium excretion increased promptly and cumulative sodium balance increased by only 80 +/- 26 meq after 7 days of high sodium intake. When renal perfusion pressure was servo-controlled to prevent pressure natriuresis, comparable increases in sodium intake raised MAP from 88 +/- 2 to 128 +/- 4 mmHg after 7 days. Sodium excretion rose to match intake, but cumulative sodium balance increased by 226 +/- 34 meq after 7 days. In dogs in which ANG II levels were held constant by converting enzyme inhibition and constant ANG II infusion (2 ng.kg-1.min-1 iv), raising sodium intake for 7 days elevated MAP from 126 +/- 2 to 146 +/- 4 mmHg after 7 days while increasing cumulative sodium balance by 212 +/- 29 meq. When renal perfusion pressure was servo-controlled and ANG II levels held constant, raising sodium intake elevated MAP from 125 +/- 3 to 166 +/- 11 mmHg and increased cumulative sodium balance by 399 +/- 128 meq. These data indicate that pressure natriuresis and decreased ANG II formation are important in minimizing sodium retention and hypertension during high sodium intake. However, other mechanisms can increase sodium excretion independent of pressure natriuresis and suppression of ANG II during salt-induced hypertension.

scholarly journals High Na intake increases renal angiotensin II levels and reduces expression of the ACE2-AT2R-MasR axis in obese Zucker rats

2012 ◽  
Vol 303 (3) ◽  
pp. F412-F419 ◽  
Author(s):  
Preethi Samuel ◽  
Quaisar Ali ◽  
Rifat Sabuhi ◽  
Yonnie Wu ◽  
Tahir Hussain
Keyword(s):  
Sodium Intake ◽  
Zucker Rats ◽  
Kidney Cortex ◽  
Complex Nature ◽  
Ang Ii ◽  
Pronounced Increase ◽  
High Sodium ◽  
High Sodium Intake ◽  
Obese Rats ◽  
Obese Zucker Rats

High sodium intake is known to regulate the renal renin-angiotensin system (RAS) and is a risk factor for the pathogenesis of obesity-related hypertension. The complex nature of the RAS reveals that its various components may have opposing effects on natriuresis and blood pressure regulation. We hypothesized that high sodium intake differentially regulates and shifts a balance between opposing components of the renal RAS, namely, angiotensin-converting enzyme (ACE)-ANG II-type 1 ANG II receptor (AT1R) vs. AT2-ACE2-angiotensinogen (Ang) (1–7)-Mas receptor (MasR), in obesity. In the present study, we evaluated protein and/or mRNA expression of angiotensinogen, renin, AT1A/BR, ACE, AT2R, ACE2, and MasR in the kidney cortex following 2 wk of a 8% high-sodium (HS) diet in lean and obese Zucker rats. The expression data showed that the relative expression pattern of ACE and AT1BR increased, renin decreased, and ACE2, AT2R, and MasR remained unaltered in HS-fed lean rats. On the other hand, HS intake in obese rats caused an increase in the cortical expression of ACE, a decrease in ACE2, AT2R, and MasR, and no changes in renin and AT1R. The cortical levels of ANG II increased by threefold in obese rats on HS compared with obese rats on normal salt (NS), which was not different than in lean rats. The HS intake elevated mean arterial pressure in obese rats (27 mmHg) more than in lean rats (16 mmHg). This study suggests that HS intake causes a pronounced increase in ANG II levels and a reduction in the expression of the ACE2-AT2R-MasR axis in the kidney cortex of obese rats. We conclude that such changes may lead to the potentially unopposed function of AT1R, with its various cellular and physiological roles, including the contribution to the pathogenesis of obesity-related hypertension.

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.

scholarly journals Országos Táplálkozás és Tápláltsági Állapot Vizsgálat – OTÁP2014. III. A magyar lakosság makroelem-bevitele

2017 ◽  
Vol 158 (17) ◽  
pp. 653-661 ◽  
Author(s):  
Barbara Nagy ◽  
Zsuzsanna Nagy-Lőrincz ◽  
Márta Bakacs ◽  
Éva Illés ◽  
Eszter Sarkadi Nagy ◽  
...  
Keyword(s):  
Dietary Habits ◽  
Salt Intake ◽  
Sodium Intake ◽  
Public Awareness ◽  
Adult Population ◽  
Age Group ◽  
High Sodium ◽  
Potassium Intake ◽  
Awareness Campaigns ◽  
High Sodium Intake

Abstract: Introduction and aim: The Hungarian Diet and Nutritional Status Survey examined the dietary habits of the Hungarian adult population. The aim of the study is to present the macroelement intake of the population. Method: The study represents the macrolement intake of the population with age 18 or over on the day of 31 December 2013, of those who are non-institutionalised. Results: Salt intake decreased compared to the findings of the previous study in 2009 but it is still extremely high (15.9 g in men and 11.2 g in women). The potassium intake is below the recommendation, which together with a high sodium intake increases the risk of high blood pressure. Calcium intake in the youngest age group reached the recommendations, whereas the intake in the oldest age group was well below the references. Magnesium intake complied with the recommendation, the intake of phosphorus however exceeded it. High sodium intake still represents substantial public health risk. Conclusion: The reduction that occured in the population’s salt intake since 2009 demonstrates the effectiveness of implemented prevention programs, cooperation with the industry and public awareness campaigns. Orv Hetil. 2017; 158(17): 653–661.

scholarly journals Brain “ouabain,” ANG II, and sympathoexcitation by chronic central sodium loading in rats

1998 ◽  
Vol 274 (4) ◽  
pp. H1269-H1276 ◽  
Author(s):  
Bing S. Huang ◽  
Shereeni J. Veerasingham ◽  
Frans H. H. Leenen
Keyword(s):  
Wistar Rats ◽  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Baroreflex Control ◽  
Spontaneously Hypertensive ◽  
High Sodium ◽  
High Sodium Intake ◽  
Fab Fragments ◽  
Γ Globulins

Both brain ouabain-like activity (“ouabain”) and brain angiotensin II (ANG II) contribute to the sympathoexcitatory and pressor responses to high sodium intake in spontaneously hypertensive (SHR) and Dahl salt-sensitive (Dahl S) rats. To assess whether increases in cerebrospinal fluid (CSF) sodium can mimic this pattern of changes, Wistar rats were chronically infused with artificial CSF (aCSF) or sodium-rich aCSF (0.8 or 1.2 M sodium) intracerebroventricularly through osmotic minipumps for 14 days. Sodium-rich aCSF (0.8 M) was also infused intracerebroventricularly for 2 wk concomitantly with either antibody Fab fragments that bind ouabain and related steroids with high affinity, γ-globulins as control (200 μg/day for both), or the AT1blocker losartan (1 mg ⋅ kg−1 ⋅ day−1). Sodium-rich aCSF increased CSF sodium from 146 ± 2 to 152 ± 2 (0.8 M) and 160 ± 3 (1.2 M) mmol/l, and increased brain “ouabain” in the hypothalamus, pituitary, and pons. In conscious rats, sodium-rich aCSF increased baseline mean arterial pressure (MAP), enhanced MAP, heart rate (HR), and renal sympathetic nerve activity (RSNA) responses to intracerebroventricular α2-adrenoceptor agonist guanabenz and air stress, and desensitized arterial and cardiopulmonary baroreflex control of HR and RSNA. These effects were largely prevented by intracerebroventricular Fab fragments or losartan. Thus, in Wistar rats, both brain “ouabain” and the brain renin-angiotensin system contribute to sympathoexcitation, impairment of baroreflexes, and hypertension caused by chronically increased CSF sodium. The similar patterns of changes caused by CSF sodium in Wistar rats and by high sodium intake in SHR and Dahl S rats indicate that if high sodium intake increases central sodium, such changes may contribute to sympathoexcitation and hypertension.

ANG II in median preoptic nucleus and pressor responses to CSF sodium and high sodium intake in SHR

2001 ◽  
Vol 281 (3) ◽  
pp. H1210-H1216 ◽  
Author(s):  
Adam S. Budzikowski ◽  
Frans H. H. Leenen
Keyword(s):  
Wistar Rats ◽  
Sodium Intake ◽  
High Salt ◽  
Ang Ii ◽  
Preoptic Nucleus ◽  
High Sodium ◽  
Median Preoptic Nucleus ◽  
High Sodium Intake ◽  
Air Jet ◽  
Pressor Responses

Pressor responses to increases in cerebrospinal fluid (CSF) sodium in Wistar rats and to high salt intake in spontaneously hypertensive rats (SHR) involve both brain ouabainlike activity (“ouabain”) and the brain renin-angiotensin system (RAS). Because some of the effects of “ouabain” are mediated by the median preoptic nucleus (MnPO) and this nucleus contains all elements of the RAS, the present study assessed possible interactions of “ouabain” and ANG II in this nucleus. In conscious Wistar rats, injection of ANG II into the MnPO significantly increased mean arterial pressure (MAP) and heart rate (HR). This response was not affected by pretreatment with a subpressor dose of ouabain. MAP and HR increases by ouabain in the MnPO were significantly attenuated by MnPO pretreatment with losartan. In Wistar rats, losartan in the MnPO also abolished pressor and HR responses to intracerebroventricular 0.3 M NaCl and attenuated MAP and HR responses to intracerebroventricular ouabain. Five weeks of a high-salt diet in SHRs resulted in exacerbation of hypertension and increased responses to air-jet stress and intracerebroventricular guanabenz. Losartan injected into the MnPO reversed the salt-sensitive component of the hypertension and normalized the depressor response to guanabenz but did not change responses to air-jet stress. We conclude that in the MnPO, ANG II via AT1 receptors mediates cardiovascular responses to an acute increase in CSF sodium as well as the chronic pressor responses to high sodium intake in SHR.

The passive role of calcium in hypertension: A position statement as of August 20,1985

1986 ◽  
Vol 64 (6) ◽  
pp. 808-811 ◽  
Author(s):  
Herbert G. Langford
Keyword(s):  
Sodium Intake ◽  
Position Statement ◽  
Ionized Calcium ◽  
Calcium Excretion ◽  
Laboratory Studies ◽  
Hypertensive Patients ◽  
High Sodium ◽  
High Sodium Intake ◽  
Natriuretic Effect

Epidemiologic data suggest that calcium intake is lower in hypertensive individuals than in normotensive individuals. Moreover, hypertensive patients and rats excrete more calcium in their urine than normotensives, and laboratory studies (low ionized calcium, high parathyroid hormone (PTH)) suggest that the hypertensive is somewhat calcium depleted. However, both the low ionized calcium and elevated PTH should tend to lower pressure rather than raise it, leaving only the presumed and poorly documented natriuretic effect of calcium as a hypotensive mechanism. The evidence is better for a high sodium intake producing a conditioned deficiency of calcium by increasing calcium excretion than for a low intake of calcium raising blood pressure.

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