Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide
Natriuretic peptides, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), have cardioprotective effects and regulate blood pressure in mammals. ANP and BNP are hormones secreted from the heart into the bloodstream in response to increase...
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MDPI AG
2022-09-01
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| author | Takeshi Tokudome Kentaro Otani |
| author_facet | Takeshi Tokudome Kentaro Otani |
| author_sort | Takeshi Tokudome |
| collection | DOAJ |
| description | Natriuretic peptides, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), have cardioprotective effects and regulate blood pressure in mammals. ANP and BNP are hormones secreted from the heart into the bloodstream in response to increased preload and afterload. Both hormones act through natriuretic peptide receptor 1 (NPR1). In contrast, CNP acts through natriuretic peptide receptor 2 (NPR2) and was found to be produced by the vascular endothelium, chondrocytes, and cardiac fibroblasts. Based on its relatively low plasma concentration compared with ANP and BNP, CNP is thought to function as both an autocrine and a paracrine factor in the vasculature, bone, and heart. The cytoplasmic domains of both NPR1 and NPR2 display a guanylate cyclase activity that catalyzes the formation of cyclic GMP. NPR3 lacks this guanylate cyclase activity and is reportedly coupled to G<sub>i</sub>-dependent signaling. Recently, we reported that the continuous infusion of the peptide osteocrin, an endogenous ligand of NPR3 secreted by bone and muscle cells, lowered blood pressure in wild-type mice, suggesting that endogenous natriuretic peptides play major roles in the regulation of blood pressure. Neprilysin is a neutral endopeptidase that degrades several vasoactive peptides, including natriuretic peptides. The increased worldwide clinical use of the angiotensin receptor-neprilysin inhibitor for the treatment of chronic heart failure has brought renewed attention to the physiological effects of natriuretic peptides. In this review, we provide an overview of the discovery of ANP and its translational research. We also highlight our recent findings on the blood pressure regulatory effects of ANP, focusing on its molecular mechanisms. |
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| format | Article |
| id | doaj.art-3db4dcf888b742cfbe6104c218c95987 |
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| issn | 2079-7737 |
| language | English |
| last_indexed | 2024-03-10T00:40:06Z |
| publishDate | 2022-09-01 |
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| series | Biology |
| spelling | doaj.art-3db4dcf888b742cfbe6104c218c959872023-11-23T15:08:04ZengMDPI AGBiology2079-77372022-09-01119135110.3390/biology11091351Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic PeptideTakeshi Tokudome0Kentaro Otani1Department of Pathophysiology of Heart Failure and Therapeutics, National Cerebral and Cardiovascular Center Research Institute, Suita 564-8565, JapanCenter for Regenerative Medicine, National Cerebral and Cardiovascular Center Research Institute, Suita 564-8565, JapanNatriuretic peptides, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and C-type natriuretic peptide (CNP), have cardioprotective effects and regulate blood pressure in mammals. ANP and BNP are hormones secreted from the heart into the bloodstream in response to increased preload and afterload. Both hormones act through natriuretic peptide receptor 1 (NPR1). In contrast, CNP acts through natriuretic peptide receptor 2 (NPR2) and was found to be produced by the vascular endothelium, chondrocytes, and cardiac fibroblasts. Based on its relatively low plasma concentration compared with ANP and BNP, CNP is thought to function as both an autocrine and a paracrine factor in the vasculature, bone, and heart. The cytoplasmic domains of both NPR1 and NPR2 display a guanylate cyclase activity that catalyzes the formation of cyclic GMP. NPR3 lacks this guanylate cyclase activity and is reportedly coupled to G<sub>i</sub>-dependent signaling. Recently, we reported that the continuous infusion of the peptide osteocrin, an endogenous ligand of NPR3 secreted by bone and muscle cells, lowered blood pressure in wild-type mice, suggesting that endogenous natriuretic peptides play major roles in the regulation of blood pressure. Neprilysin is a neutral endopeptidase that degrades several vasoactive peptides, including natriuretic peptides. The increased worldwide clinical use of the angiotensin receptor-neprilysin inhibitor for the treatment of chronic heart failure has brought renewed attention to the physiological effects of natriuretic peptides. In this review, we provide an overview of the discovery of ANP and its translational research. We also highlight our recent findings on the blood pressure regulatory effects of ANP, focusing on its molecular mechanisms.https://www.mdpi.com/2079-7737/11/9/1351atrial natriuretic peptidetranslational researchheart failureblood pressuremolecular mechanism |
| spellingShingle | Takeshi Tokudome Kentaro Otani Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide Biology atrial natriuretic peptide translational research heart failure blood pressure molecular mechanism |
| title | Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide |
| title_full | Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide |
| title_fullStr | Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide |
| title_full_unstemmed | Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide |
| title_short | Molecular Mechanism of Blood Pressure Regulation through the Atrial Natriuretic Peptide |
| title_sort | molecular mechanism of blood pressure regulation through the atrial natriuretic peptide |
| topic | atrial natriuretic peptide translational research heart failure blood pressure molecular mechanism |
| url | https://www.mdpi.com/2079-7737/11/9/1351 |
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