Hypertension, cardiac hypertrophy, and sudden death in mice lacking natriuretic peptide receptor A

DOI Web Site 被引用文献40件
  • Paula M. Oliver
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Jennifer E. Fox
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Ron Kim
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Howard A. Rockman
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Hyung-Suk Kim
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Robert L. Reddick
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Kailash N. Pandey
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Sharon L. Milgram
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Oliver Smithies
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912
  • Nobuyo Maeda
    Department of Pathology, University of North Carolina, 710 Brinkhous-Bullitt Building, Chapel Hill, NC 27599-7525; Departments of Medicine and Physiology, University of North Carolina, Chapel Hill, NC 27599; Department of Pathology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78284; and Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, GA 30912

抄録

<jats:p> Natriuretic peptides, produced in the heart, bind to the natriuretic peptide receptor A (NPRA) and cause vasodilation and natriuresis important in the regulation of blood pressure. We here report that mice lacking a functional <jats:italic>Npr1</jats:italic> gene coding for NPRA have elevated blood pressures and hearts exhibiting marked hypertrophy with interstitial fibrosis resembling that seen in human hypertensive heart disease. Echocardiographic evaluation of the mice demonstrated a compensated state of systemic hypertension in which cardiac hypertrophy and dilatation are evident but with no reduction in ventricular performance. Nevertheless, sudden death, with morphologic evidence indicative in some animals of congestive heart failure and in others of aortic dissection, occurred in all 15 male mice lacking <jats:italic>Npr1</jats:italic> before 6 months of age, and in one of 16 females in our study. Thus complete absence of NPRA causes hypertension in mice and leads to cardiac hypertrophy and, particularly in males, lethal vascular events similar to those seen in untreated human hypertensive patients. </jats:p>

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