Atrial natriuretic peptide (ANP) gene promoter variant and increased susceptibility to early development of hypertension in humans

Rubattu, Speranza; Evangelista, Anna; Barbato, Daniela; Barba, Gianvincenzo; Stanzione, Rosita; Iacone, Roberto; Volpe, Massimo; Strazzullo, Pasquale

doi:10.1038/sj.jhh.1002228

Cited by 20 publications

(11 citation statements)

References 12 publications

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“…2). In a European population, the G allele was associated with low plasma ANP levels and high risks of hypertension and cardiac hypertrophy (Rubattu et al, 2006; Rubattu et al, 2007). A similar finding was reported in a Japanese population (Kato et al, 2000).…”

Section: Nppa Variants In Cardiovascular Diseasementioning

confidence: 99%

Atrial natriuretic peptide in cardiovascular biology and disease (NPPA)

Song

Wang

2015

Gene

161

101

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Atrial natriuretic peptide (ANP) is a cardiac hormone that regulates salt-water balance and blood pressure by promoting renal sodium and water excretion and stimulating vasodilation. ANP also has an anti-hypertrophic function in the heart, which is independent of its systemic blood pressure-lowering effect. In mice, ANP deficiency causes salt-sensitive hypertension and cardiac hypertrophy. Recent studies have shown that ANP plays an important role in regulating vascular remodeling and energy metabolism. Variants in the human NPPA gene, encoding the ANP precursor, are associated with hypertension, stroke, coronary artery disease, heart failure (HF) and obesity. ANP and related peptides are used as biomarkers for heart disease. Recombinant proteins and small molecules that enhance the ANP pathway have been developed to treat patients with HF. In this review, we discuss the role of ANP in cardiovascular biology and disease.

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Section: Nppa Variants In Cardiovascular Diseasementioning

confidence: 99%

Atrial natriuretic peptide in cardiovascular biology and disease (NPPA)

Song

Wang

2015

Gene

161

101

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“…57 Candidate gene studies in Japanese and Italian individuals have associated a C-664G variant with lower circulating ANP, hypertension, and left ventricular hypertrophy. 58,59, 60 There are mixed data regarding another missense variant, rs5063, which results in a valine to methionine substitution and has been linked to lower blood pressure among Chinese individuals and participants in the Women’s Genome Health study, although this was not observed among Japanese individuals. 58, 61,62, 63 In other populations, the rs5063 variant was associated with an increased risk of hypertension or stroke.…”

Section: Biologic Effects Of Natriuretic Peptides: Clinical Evidencementioning

confidence: 99%

Natriuretic Peptides and Cardiometabolic Health

Gupta

Wang

2015

Circ J

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Natriuretic peptides are cardiac-derived hormones with a range of protective functions, including natriuresis, diuresis, vasodilation, lusitropy, lipolysis, weight loss, and improved insulin sensitivity. The actions are mediated through membrane bound guanylyl cyclases that lead to production of the intracellular second-messenger cGMP. A growing body of evidence demonstrates that genetic and acquired deficiencies of the natriuretic peptide system can promote hypertension, cardiac hypertrophy, obesity, diabetes mellitus, the metabolic syndrome, and heart failure. Clinically, natriuretic peptides are robust diagnostic and prognostic markers and augmenting natriuretic peptides is a target for therapeutic strategies in cardio-metabolic disease. This review will summarize current understanding and highlight novel aspects of natriuretic peptide biology.

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“…The increased frequency of hypertension in carriers of molecular variants of the ANP gene [57] supports the concept of a critical biological function of ANP in BP regulation. In particular, a contribution of an ANP gene variant to an increased predisposition to the early development of hypertension and its complications has been reported in a cohort of Caucasian subjects followed-up for 28 years [57].…”

Section: Cardiovascular Damage In Dysmetabolic Patients: Possible Invmentioning

confidence: 84%

Natriuretic peptides and cardiovascular damage in the metabolic syndrome: molecular mechanisms and clinical implications

et al. 2009

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Natriuretic peptides are endogenous antagonists of vasoconstrictor and salt- and water-retaining systems in the body's defence against blood pressure elevation and plasma volume expansion, through direct vasodilator, diuretic and natriuretic properties. In addition, natriuretic peptides may play a role in the modulation of the molecular mechanisms involved in metabolic regulation and cardiovascular remodelling. The metabolic syndrome is characterized by visceral obesity, hyperlipidaemia, vascular inflammation and hypertension, which are linked by peripheral insulin resistance. Increased visceral adiposity may contribute to the reduction in the circulating levels of natriuretic peptides. The dysregulation of neurohormonal systems, including the renin-angiotensin and the natriuretic peptide systems, may in turn contribute to the development of insulin resistance in dysmetabolic patients. In obese subjects with the metabolic syndrome, reduced levels of natriuretic peptides may be involved in the development of hypertension, vascular inflammation and cardio vascular remodelling, and this may predispose to the development of cardiovascular disease. The present review summarizes the regulation and function of the natriuretic peptide system in obese patients with the metabolic syndrome and the involvement of altered bioactive levels of natriuretic peptides in the pathophysiology of cardiovascular disease in patients with metabolic abnormalities.

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Atrial natriuretic peptide (ANP) gene promoter variant and increased susceptibility to early development of hypertension in humans

Cited by 20 publications

References 12 publications

Atrial natriuretic peptide in cardiovascular biology and disease (NPPA)

Atrial natriuretic peptide in cardiovascular biology and disease (NPPA)

Natriuretic Peptides and Cardiometabolic Health

Natriuretic peptides and cardiovascular damage in the metabolic syndrome: molecular mechanisms and clinical implications

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