The Renin-Angiotensin System and Body Function

Reid, Ian A.

doi:10.1001/archinte.1985.00360080153023

Cited by 38 publications

(8 citation statements)

References 18 publications

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“…However, if the adipose ISF compartment was ϳ5% of the intracellular compartment by weight, a 20-fold greater plasma level than adipose tissue (ISF plus cells) would not be unreasonable if plasma and adipose ISF AGT were in diffusion equilibrium. The ISF of adipose tissue has been reported to be in the range of 3-15% of tissue weight (23).…”

Section: Discussionmentioning

confidence: 99%

“…Renin concentration is the primary rate-limiting step in this plasma cascade (7), although changes in plasma AGT levels can also influence the generation of angiotensins. Functional consequences are mediated primarily through Ang II binding to the Ang II type Ia receptor AT 1 R, which acts within the kidney, brain, adrenal glands, and vasculature to mediate increased blood volume and total peripheral resistance, thereby maintaining blood pressure (23).…”

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confidence: 99%

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Renin dynamics in adipose tissue: adipose tissue control of local renin concentrations

Fowler¹,

Krueth²,

Bernlohr³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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The renin-angiotensin system (RAS) has been implicated in a variety of adipose tissue functions, including tissue growth, differentiation, metabolism, and inflammation. Although expression of all components necessary for a locally derived adipose tissue RAS has been demonstrated within adipose tissue, independence of local adipose RAS component concentrations from corresponding plasma RAS fluctuations has not been addressed. To analyze this, we varied in vivo rat plasma concentrations of two RAS components, renin and angiotensinogen (AGT), to determine the influence of their plasma concentrations on adipose and cardiac tissue levels in both perfused (plasma removed) and nonperfused samples. Variation of plasma RAS components was accomplished by four treatment groups: normal, DOCA salt, bilateral nephrectomy, and losartan. Adipose and cardiac tissue AGT concentrations correlated positively with plasma values. Perfusion of adipose tissue decreased AGT concentrations by 11.1%, indicating that adipose tissue AGT was in equilibrium with plasma. Cardiac tissue renin levels positively correlated with plasma renin concentration for all treatments. In contrast, adipose tissue renin levels did not correlate with plasma renin, with the exception of extremely high plasma renin concentrations achieved in the losartan-treated group. These results suggest that adipose tissue may control its own local renin concentration independently of plasma renin as a potential mechanism for maintaining a functional local adipose RAS.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Renin dynamics in adipose tissue: adipose tissue control of local renin concentrations

Fowler¹,

Krueth²,

Bernlohr³

et al. 2009

American Journal of Physiology-Endocrinology and Metabolism

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“…Inadequate functioning of the renin–angiotensin system contributes substantially to the development of hypertension and cardiovascular and renal pathology (including left ventricular hypertrophy, structural alternations of the vasculature, neointima formation, nephrosclerosis, etc.) [2].…”

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confidence: 99%

Comparison of the solution structures of angiotensin I & II

Spyroulias¹,

Nikolakopoulou²,

Tzakos

et al. 2003

European Journal of Biochemistry

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Conformational analysis of angiotensin I (AI) and II (AII) peptides has been performed through 2D 1 H-NMR spectroscopy in dimethylsulfoxide and 2,2,2-trifluoroethanol/H 2 O. The solution structural models of AI and AII have been determined in dimethylsulfoxide using NOE distance and 3 J HNHa coupling constants. Finally, the AI family of models resulting from restrained energy minimization (REM) refinement, exhibits pairwise rmsd values for the family ensemble 0.26 ± 0.13 Å , 1.05 ± 0.23 Å , for backbone and heavy atoms, respectively, and the distance penalty function is calculated at 0.075 ± 0.006 Å 2 . Comparable results have been afforded for AII ensemble (rmsd values 0.30 ± 0.22 Å , 1.38 ± 0.48 Å for backbone and heavy atoms, respectively; distance penalty function is 0.029 ± 0.003 Å 2 ). The two peptides demonstrate similar N-terminal and different C-terminal conformation as a consequence of the presence/absence of the His9-Leu10 dipeptide, which plays an important role in the different biological function of the two peptides. Other conformational variations focused on the side-chain orientation of aromatic residues, which constitute a biologically relevant hydrophobic core and whose inter-residue contacts are strong in dimethylsulfoxide and are retained even in mixed organic-aqueous media. Detailed analysis of the peptide structural features attempts to elucidate the conformational role of the C-terminal dipeptide to the different binding affinity of AI and AII towards the AT 1 receptor and sets the basis for understanding the factors that might govern free-or bounddepended AII structural differentiation.Keywords: angiotensin; NMR; renin-angiotensin system; solid phase peptide synthesis; solution structure.The octapeptide angiotensin-II (H-Asp-Arg-Val-Tyr-IleHis-Pro-Phe-OH, AII) is one of the oldest peptide hormones, known for its multiplicity of biological actions related to endocrine or connected to the central and peripheral nervous system. It is produced by the conversion of angiotensin-I (H-Asp-Arg-Val-Tyr-Ile-His-Pro-PheHis-Leu-OH, AI) to AII by the action of the angiotensin-I converting enzyme (ACE) of the vascular endothelium. AI is generated in the circulation by the action of rennin from the kidneys on its substrate, called alpha 2 -globulin or angiotensinogen, produced in the liver [1].AII is a potent pressor agent, which has a vital role in the regulation of blood pressure, in the conservation of total blood volume and salt homeostasis. Furthermore, it is involved in the release of alcohol dehydrogenase (ADH), cell growth and the stimulation of the sympathetic system. Several antagonists of AII are efficient antipressor agents. Inadequate functioning of the reninangiotensin system contributes substantially to the development of hypertension and cardiovascular and renal pathology (including left ventricular hypertrophy, structural alternations of the vasculature, neointima formation, nephrosclerosis, etc.) [2].Structure-activity relationships studies from several laboratories have revealed the to...

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“…Renin cleaves its substrate angiotensinogen to generate the angiotensin I, which is converted to angiotensin II by angiotensin I‐converting enzyme. Angiotensin II stimulates aldosterone secretion through the adrenal cortex and also partially suppresses renin secretion by a direct effect on the juxtaglomerular cells (14). Aldosterone increases sodium reabsorption and potassium excretion in the distal tubule and the collecting duct of the nephron.…”

Section: Basic Principles Of Sodium Balancementioning

confidence: 99%

Diagnosis and management of hyponatraemia in hospitalised patients

Reddy¹,

Mooradian²

2009

International Journal of Clinical Practice

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Summary Hyponatraemia is a commonly encountered electrolyte abnormality in hospitalised patients and is associated with significant morbidity and mortality. The fact that most cases of hyponatraemia are the result of water imbalance rather than sodium imbalance underscores the role of antidiuretic hormone (ADH) in the pathophysiology. Hyponatraemia can be classified according to the measured plasma osmolality as isotonic, hypertonic or hypotonic. Hyponatraemia with a normal plasma osmolality usually indicates pseudohyponatraemia, while hyponatraemia because of a high plasma osmolality is typically caused by hyperglycaemia. After excluding isotonic and hypertonic causes, hypotonic hyponatraemia is further classified according to the volume status of the patient as hypovolaemic, hypervolaemic or euvolaemic. Hypovolaemic hyponatraemia is accompanied by extracellular fluid (ECF) volume deficit, while hypervolaemic hyponatraemia manifests with ECF volume expansion. The syndrome of inappropriate ADH (SIADH) should be suspected in any patient with euvolaemic hyponatraemia with a urine osmolality above 100 mOsm/kg and urine sodium concentration above 40 mEq/l. In the management of any hyponatraemia regardless of the patient’s volume status, it is advised to restrict free water and hypotonic fluid intake. Hypertonic saline and vasopressin antagonists can be used to correct symptomatic hyponatraemia. The rate of correction is dependent upon the duration, degree of hyponatraemia and the presence or absence of symptoms. Symptomatic acute hyponatraemia (< 48 h) is a medical emergency requiring rapid correction to prevent the worsening of brain oedema. In asymptomatic patients with chronic hyponatraemia (> 48 h or unknown duration), fluid restriction and close monitoring alone are sufficient, while a slow correction by 0.5 mEq/l/h may be attempted in symptomatic patients. Excessive rapid correction should be avoided in both acute and chronic hyponatraemia, because it can lead to irreversible neurological complications including central osmotic demyelination.

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The Renin-Angiotensin System and Body Function

Cited by 38 publications

References 18 publications

Renin dynamics in adipose tissue: adipose tissue control of local renin concentrations

Renin dynamics in adipose tissue: adipose tissue control of local renin concentrations

Comparison of the solution structures of angiotensin I & II

Diagnosis and management of hyponatraemia in hospitalised patients

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