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Vascular smooth muscle function and its changes in hypertension

  • D. F. Bohr
    ,
  • R. C. Webb
  • University of Michigan, Ann Arbor
Scholary Output:
Contribution to journal
Review article
Peer-review

Abstract

The contractile state of vascular smooth muscle influences arterial blood pressure and regulates organ blood flow. Current evidence suggests that the contractile apparatus of vascular smooth muscle is composed of thin and thick filaments, and that force generated between these two filaments provides the mechanism for cell shortening. The molecular events that initiate the interaction between these filaments are dependent upon the free sarcoplasmic concentration of activator calcium, which is regulated by the cell membrane and at subcellular sites. Changes in electrical activity of the cell membrane and interaction of pharmacologic agents with membrane receptor alter the cell, causing either a decrease or increase in sarcoplasmic calcium concentration and thus changing the contractile state of the vascular smooth muscle cell. Alterations in the cellular mechanisms that regulate intracellular calcium concentration may contribute to abnormal vascular function in pathologic states. In this brief review, the normal mechanism of vascular smooth muscle contraction is described, and the evidence that indicates that components of the contractile process change in hypertension is examined.

Publication Information

Output type

Scholary Output:
Contribution to journal
Review article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 3-16 (14 pages)

Journal (Volume, Issue Number)

American Journal of Medicine (Volume 77, Issue 4 A)

Publication milestones

  • Published - 1984

Publication status

Published - 1984

ISSN

0002-9343

Publication IDs

  • Scopus: 0021674529
  • PubMed: 6091449

Publication metrics

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Fractional count
1
Fractional count
0.50
Fractional count
1
Fractional count
0.50
Fractional count
1
Fractional count
1
Scopus
citations

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Citation count
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Funding Details

From the Department of Physiology, University of Michigan Medical School, Ann Arbor, Michigan. This work was supported by grants from the National Institutes of Health (HL-18575 and HL-27020). Requests for reprints should be addressed to Dr. David F. Bohr, Department of Physiology, 7710 Med. Sci. II, University of Michigan, Ann Arbor, Michigan 48109. *Recipient of a Research Career Development Award from the National Institutes of Health.
FundersFunding numbers
NIH
HL-18575
NHLBI
R01HL027020