Natriuretic Peptides and Salt Sensitivity

Villarreal, Daniel; Freeman, Ronald H.

doi:10.1007/978-1-4612-3960-4_14

Cited by 5 publications

(2 citation statements)

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“…Several lines of evidence indicate that ANP is involved in the pathogenesis of salt-sensitive hypertension (29). Chronic blockade of endogenous ANP with a monoclonal antibody accelerates the development and exacerbates the severity of hypertension in strokeprone, spontaneously hypertensive rats (SHR-SP) and DOCA-salt hypertensive rats (8).…”

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confidence: 99%

Dietary salt supplementation selectively downregulates NPR-C receptor expression in kidney independently of ANP

Sun

Chen

Majid-Hasan

et al. 2002

American Journal of Physiology-Renal Physiology

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Atrial natriuretic peptide (ANP) has negative modulatory effects on a variety of pathophysiological mechanisms; i.e., it inhibits hypoxia-induced pulmonary vasoconstriction and vascular remodeling and facilitates natriuresis and vasorelaxation in NaCl-supplemented subjects. We have previously demonstrated organ-selective potentiation of ANP in the pulmonary circulation of hypoxia-adapted animals by local downregulation of its clearance receptor (NPR-C; Li H, Oparil S, Meng QC, Elton T, and Chen Y-F. Am J Physiol Lung Cell Mol Physiol 268: L328-L335, 1995). The present study tested the hypothesis that NPR-C expression is attenuated selectively in kidneys of NaCl-supplemented subjects. Adult male wild-type (ANPϩ/ϩ) and homozygous mutant (ANPϪ/Ϫ) mice were studied after 5 wk of normal or high-salt diets. Mean arterial pressure (MAP) and left (LV) and right ventricular (RV) mass were greater in ANPϪ/Ϫ mice than in ANPϩ/ϩ mice fed the normal-salt diet; salt supplementation induced increases in plasma ANP in ANPϩ/ϩ mice and in MAP and LV, RV, and renal mass in ANPϪ/Ϫ mice but not in ANPϩ/ϩ mice. NPR-C mRNA levels were selectively and significantly reduced (Ͼ60%) in kidney, but not in lung, brain, LV, or RV, by dietary salt supplementation in both genotypes. NPR-A mRNA levels did not differ among diet-genotype groups in any organ studied. cGMP content was significantly increased in kidney, but not in lung or brain, by dietary salt supplementation in both genotypes. These findings suggest that selective downregulation of NPR-C in the kidney in response to dietary salt supplementation may contribute to local elevation in ANP levels and may be functionally significant in attenuating the development of salt-sensitive hypertension.salt-sensitive hypertension; atrial natriuretic peptide; clearance receptor; atrial natriuretic peptide knockout mice; kidney ATRIAL NATRIURETIC PEPTIDE (ANP) is a peptide hormone that has potent natriuretic, diuretic, vasodilator, sympatholytic, and renin-and aldosterone-suppressing activities and is involved in the regulation of volume and electrolyte balance and blood pressure (3-5, 25). The biological functions of ANP are mediated through activation of the NPR-A receptor and increases in intracellular cGMP (6). Circulating levels of ANP are regulated by binding to and inactivation by NPR-C, a membrane-bound receptor that functions as a clearance receptor to eliminate ANP from the circulation (16,19), as well as hydrolysis by neutral endopeptidase 24.11 (NEP) (7).Several lines of evidence indicate that ANP is involved in the pathogenesis of salt-sensitive hypertension (29). Chronic blockade of endogenous ANP with a monoclonal antibody accelerates the development and exacerbates the severity of hypertension in strokeprone, spontaneously hypertensive rats (SHR-SP) and DOCA-salt hypertensive rats (8). Dietary salt supplementation in normotensive salt-resistant rats is associated with increased plasma ANP levels (11), whereas salt-sensitive SHR do not increase plasma ANP levels appropriately in res...

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mentioning

confidence: 99%

Dietary salt supplementation selectively downregulates NPR-C receptor expression in kidney independently of ANP

Sun

Chen

Majid-Hasan

et al. 2002

American Journal of Physiology-Renal Physiology

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“…In the kidneys, a combination of hemodynamic and tubular transport effects seem to be responsible for ANP-BNP/NPRA-induced natriuresis and diuresis, exerting both direct and indirect effects on tubules, including the proximal tubules, as well as cortical and innermedullary collecting ducts ( Sonnenberg et al, 1986 ; Brenner et al, 1990 ; Zhao et al, 2010 ; Prieto et al, 2012 ). ANP actions facilitate the excretion of salt and water with an increase in GFR and RBF in the kidneys ( Burnett et al, 1984 ; Camarago et al, 1984 ; Freeman et al, 1985 ; Meyer and Forsmann, 1997 ; Villrreal and Freeman, 1997 ; Melo et al, 2000 ; Shi et al, 2003 ; Pandey, 2008 ; Zhao et al, 2010 ). ANP- and BNP-induced natriuresis and diuresis causes a direct inhibition of tubular transport processes.…”

Section: Nps and Their Receptors In Cardiovascular Disordersmentioning

confidence: 99%

Molecular Signaling Mechanisms and Function of Natriuretic Peptide Receptor-A in the Pathophysiology of Cardiovascular Homeostasis

Pandey

2021

Front. Physiol.

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The discovery of atrial, brain, and C-type natriuretic peptides (ANP, BNP, and CNP) and their cognate receptors has greatly increased our knowledge of the control of hypertension and cardiovascular homeostasis. ANP and BNP are potent endogenous hypotensive hormones that elicit natriuretic, diuretic, vasorelaxant, antihypertrophic, antiproliferative, and antiinflammatory effects, largely directed toward the reduction of blood pressure (BP) and cardiovascular diseases (CVDs). The principal receptor involved in the regulatory actions of ANP and BNP is guanylyl cyclase/natriuretic peptide receptor-A (GC-A/NPRA), which produces the intracellular second messenger cGMP. Cellular, biochemical, molecular, genetic, and clinical studies have facilitated understanding of the functional roles of natriuretic peptides (NPs), as well as the functions of their receptors, and signaling mechanisms in CVDs. Transgenic and gene-targeting (gene-knockout and gene-duplication) strategies have produced genetically altered novel mouse models and have advanced our knowledge of the importance of NPs and their receptors at physiological and pathophysiological levels in both normal and disease states. The current review describes the past and recent research on the cellular, molecular, genetic mechanisms and functional roles of the ANP-BNP/NPRA system in the physiology and pathophysiology of cardiovascular homeostasis as well as clinical and diagnostic markers of cardiac disorders and heart failure. However, the therapeutic potentials of NPs and their receptors for the diagnosis and treatment of cardiovascular diseases, including hypertension, heart failure, and stroke have just begun to be expanded. More in-depth investigations are needed in this field to extend the therapeutic use of NPs and their receptors to treat and prevent CVDs.

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Physiology of Natriuretic Peptides and Their Receptors

Pandey¹

2007

Hypertension and Hormone Mechanisms

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Natriuretic Peptides and Salt Sensitivity

Cited by 5 publications

References 62 publications

Dietary salt supplementation selectively downregulates NPR-C receptor expression in kidney independently of ANP

Dietary salt supplementation selectively downregulates NPR-C receptor expression in kidney independently of ANP

Molecular Signaling Mechanisms and Function of Natriuretic Peptide Receptor-A in the Pathophysiology of Cardiovascular Homeostasis

Physiology of Natriuretic Peptides and Their Receptors

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