scholarly journals Effects of Angiotensin II and Dietary Salt on Neurogenic Vasomotor Tone: Dose Dependancy

2006 ◽  
Vol 20 (4) ◽  
Author(s):  
Fiona Dianne McBryde ◽  
Carolyn J Barrett ◽  
Sarah‐Jane Guild ◽  
Simon C Malpas
Keyword(s):  
Angiotensin Ii ◽  
Dietary Salt ◽  
Vasomotor Tone

Inappropriately high circulating and intrarenal angiotensin II levels during dietary salt loading exacerbate hypertension in Cyp1a1–Ren-2 transgenic rats

2010 ◽  
Vol 28 (3) ◽  
pp. 495-509 ◽  
Author(s):  
Zuzana Husková ◽  
Zdeňka Vaňourková ◽  
Michaela Erbanová ◽  
Monika Thumová ◽  
Martin Opočenský ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dietary Salt ◽  
Transgenic Rats ◽  
Salt Loading

Effects of Dietary Salt Load and Salt Depletion on the Course of Hypertension and Angiotensin II Levels in Male and Female Heterozygous Ren-2 Transgenic Rats

2007 ◽  
Vol 30 (1) ◽  
pp. 45-55 ◽  
Author(s):  
Zuzana Husková ◽  
Herbert J. Kramer ◽  
Zdenka Vaňourková ◽  
Monika Thumová ◽  
Jan Malý ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Dietary Salt ◽  
Transgenic Rats ◽  
Male And Female ◽  
Salt Load ◽  
Salt Depletion

scholarly journals Effects of dietary salt on angiotensin peptides in kidney.

1995 ◽  
Vol 6 (4) ◽  
pp. 1209-1215
Author(s):  
Q C Meng ◽  
J Durand ◽  
Y F Chen ◽  
S Oparil
Keyword(s):  
Angiotensin Ii ◽  
Spontaneously Hypertensive Rats ◽  
Spontaneously Hypertensive Rat ◽  
Sprague Dawley ◽  
Dietary Salt ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Angiotensin Peptides ◽  
Sprague Dawley Rats ◽  
Wistar Kyoto

This study used a novel simple method for the extraction, separation, identification, and quantitation of angiotensin-like immunoactivity from tissue to examine the effects of altering dietary NaCl intake on intrarenal angiotensin I, II, and III levels in salt-sensitive, spontaneously hypertensive rats, salt-resistant Wistar-Kyoto rats, and Sprague-Dawley rats. Seven-week-old male spontaneously hypertensive rats, Wistar-Kyoto rats, and Sprague-Dawley rats were assigned randomly to a diet containing either 8% (high) or 1% (basal) salt and were maintained on these diets for 3 wk. Rats were then decapitated without prior anesthesia, and kidneys were rapidly (< 30 s) removed, snap frozen in liquid nitrogen, and stored at -80 degrees C. Frozen tissue was extracted in 2 M acetic acid and then subjected to solid-phase extraction with the cation exchange resin AG 50W X4. Angiotensin peptides were separated by reversed-phase high-performance liquid chromatography on a phenyl silica gel column with an eluent consisting of 20% acetonitrile in 0.1 M ammonium phosphate buffer, pH 4.9, and quantitated by radioimmunoassay. The elution of standard peptides under isocratic conditions revealed clear resolution of angiotensin I, II, and III and the (1-7) and (3-8) peptides. Recoveries of both labeled and unlabeled angiotensin peptide standards from the extraction step were > 90%. Renal angiotensin II stores were significantly higher in spontaneously hypertensive rats than in Wistar-Kyoto or Sprague-Dawley rats, independent of diet. Renal angiotensin II and III were further suppressed during dietary salt supplementation in both salt-resistant strains but not in the spontaneously hypertensive rat. These findings are consistent with an enhanced (compared with Wistar-Kyoto and Sprague-Dawley rats) role for angiotensin II in the kidney of the salt-sensitive, spontaneously hypertensive rat, particularly under conditions of dietary salt supplementation.

Angiotensin II-based hypertension and the sympathetic nervous system: the role of dose and increased dietary salt in rabbits

2007 ◽  
Vol 92 (5) ◽  
pp. 831-840 ◽  
Author(s):  
Fiona D. McBryde ◽  
Sarah-Jane Guild ◽  
Carolyn J. Barrett ◽  
John W. Osborn ◽  
Simon C. Malpas
Keyword(s):  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Dietary Salt ◽  
Sympathetic Nervous

scholarly journals Aldosterone Is Essential for Angiotensin II-Induced Upregulation of Pendrin

2017 ◽  
Vol 29 (1) ◽  
pp. 57-68 ◽  
Author(s):  
Daigoro Hirohama ◽  
Nobuhiro Ayuzawa ◽  
Kohei Ueda ◽  
Mitsuhiro Nishimoto ◽  
Wakako Kawarazaki ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mineralocorticoid Receptor ◽  
Intercalated Cells ◽  
Wild Type ◽  
Dietary Salt ◽  
Renin Angiotensin Aldosterone System ◽  
Salt Restriction ◽  
Salt Diet ◽  
Low Salt ◽  
Dietary Salt Restriction

The renin-angiotensin-aldosterone system has an important role in the control of fluid homeostasis and BP during volume depletion. Dietary salt restriction elevates circulating angiotensin II (AngII) and aldosterone levels, increasing levels of the Cl−/HCO3− exchanger pendrin in β-intercalated cells and the Na+-Cl− cotransporter (NCC) in distal convoluted tubules. However, the independent roles of AngII and aldosterone in regulating these levels remain unclear. In C57BL/6J mice receiving a low-salt diet or AngII infusion, we evaluated the membrane protein abundance of pendrin and NCC; assessed the phosphorylation of the mineralocorticoid receptor, which selectively inhibits aldosterone binding in intercalated cells; and measured BP by radiotelemetry in pendrin-knockout and wild-type mice. A low-salt diet or AngII infusion upregulated NCC and pendrin levels, decreased the phosphorylation of mineralocorticoid receptor in β-intercalated cells, and increased plasma aldosterone levels. Notably, a low-salt diet did not alter BP in wild-type mice, but significantly decreased BP in pendrin-knockout mice. To dissect the roles of AngII and aldosterone, we performed adrenalectomies in mice to remove aldosterone from the circulation. In adrenalectomized mice, AngII infusion again upregulated NCC expression, but did not affect pendrin expression despite the decreased phosphorylation of mineralocorticoid receptor. By contrast, AngII and aldosterone coadministration markedly elevated pendrin levels in adrenalectomized mice. Our results indicate that aldosterone is necessary for AngII-induced pendrin upregulation, and suggest that pendrin contributes to the maintenance of normal BP in cooperation with NCC during activation of the renin-angiotensin-aldosterone system by dietary salt restriction.

scholarly journals Dietary Salt With Nitric Oxide Deficiency Induces Nocturnal Polyuria via Hyperactivation of Intrarenal Angiotensin Ⅱ-SPAK-NCC Pathway

2021 ◽  
Author(s):  
Yosuke Sekii ◽  
Hiroshi Kiuchi ◽  
Kentaro Takezawa ◽  
Takahiro Imanaka ◽  
Sohei Kuribayashi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiotensin Ii ◽  
Salt Intake ◽  
Underlying Mechanism ◽  
High Salt ◽  
Common Disease ◽  
No Production ◽  
Nocturnal Polyuria ◽  
Dietary Salt ◽  
High Salt Intake

Abstract Nocturnal polyuria is the most frequent cause of nocturia, a common disease associated with a compromised quality of life and increased mortality. Its pathogenesis is complex, and the detailed underlying mechanism remains unknown. Herein, we report that concomitant intake of a high-salt diet and reduced nitric oxide (NO) production achieved through Nω-Nitro-L-arginine methyl ester hydrochloride (L-NAME) administration in mice resulted in nocturnal polyuria recapitulating the clinical features in humans. High salt intake under reduced NO production overactivated the angiotensin II-SPAK (STE20/SPS1-related proline–alanine-rich protein kinase)-NCC (sodium chloride co-transporter) pathway in the kidney, resulting in the insufficient excretion of sodium during the day and its excessive excretion at night. Excessive Na excretion at night in turn leads to nocturnal polyuria due to osmotic diuresis. Our study identified a central role for the intrarenal angiotensin II-SPAK-NCC pathway in the pathophysiology of nocturnal polyuria, highlighting its potential as a promising therapeutic target.

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