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Molecular biology of hypertension.

Publication ,  Journal Article
Krieger, JE; Dzau, VJ
Published in: Hypertension
September 1991

Hypertension results from abnormalities of the control systems that normally regulate blood pressure. These control systems include vascular, cardiogenic, renal, neurogenic, and endocrine mechanisms that interact in a complex but integrated manner to achieve blood pressure homeostasis. Multiple endogenous biologically active substances participate in the regulation of these control systems. Evidence suggests that abnormalities of these regulatory mechanisms resulting from altered genetic and environmental interactions play an important role in the pathogenesis of primary hypertension. Once hypertension develops, it tends to be self-perpetuating via amplifying mechanisms mediated by secondary structural changes in the blood vessels, heart, and kidney. These adaptative structural changes amplify and perpetuate hypertension by increasing systemic vascular resistance, enhancing cardiac output, and impairing renal sodium and water excretion. The long-term sequelae of hypertensive structural changes in these end organs are complications of atherosclerotic vascular disease, cardiac hypertrophy and failure, stroke, and renal failure. With the tools of molecular biology, our understanding of the molecular mechanisms underlying these abnormalities has increased enormously and continues to grow at a rapid pace, as illustrated by the discussion that follows. Our review of the molecular biology of hypertension will address systematically four key areas: 1) molecular biology of the control systems, 2) molecular mechanisms of cardiovascular structural changes, 3) genetics of hypertension, and 4) application of transgenic technology in studies of hypertension.

Duke Scholars

Published In

Hypertension

DOI

ISSN

0194-911X

Publication Date

September 1991

Volume

18

Issue

3 Suppl

Start / End Page

I3 / 17

Location

United States

Related Subject Headings

  • Renin-Angiotensin System
  • RNA, Messenger
  • Hypertension
  • Humans
  • Growth Substances
  • Genes
  • Gene Expression Regulation
  • Endothelins
  • Disease Models, Animal
  • Cardiovascular System & Hematology
 

Citation

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Krieger, J. E., & Dzau, V. J. (1991). Molecular biology of hypertension. Hypertension, 18(3 Suppl), I3-17. https://doi.org/10.1161/01.hyp.18.3_suppl.i3
Krieger, J. E., and V. J. Dzau. “Molecular biology of hypertension.Hypertension 18, no. 3 Suppl (September 1991): I3-17. https://doi.org/10.1161/01.hyp.18.3_suppl.i3.
Krieger JE, Dzau VJ. Molecular biology of hypertension. Hypertension. 1991 Sep;18(3 Suppl):I3-17.
Krieger, J. E., and V. J. Dzau. “Molecular biology of hypertension.Hypertension, vol. 18, no. 3 Suppl, Sept. 1991, pp. I3-17. Pubmed, doi:10.1161/01.hyp.18.3_suppl.i3.
Krieger JE, Dzau VJ. Molecular biology of hypertension. Hypertension. 1991 Sep;18(3 Suppl):I3-17.

Published In

Hypertension

DOI

ISSN

0194-911X

Publication Date

September 1991

Volume

18

Issue

3 Suppl

Start / End Page

I3 / 17

Location

United States

Related Subject Headings

  • Renin-Angiotensin System
  • RNA, Messenger
  • Hypertension
  • Humans
  • Growth Substances
  • Genes
  • Gene Expression Regulation
  • Endothelins
  • Disease Models, Animal
  • Cardiovascular System & Hematology