Calcium handling by vascular myocytes in hypertension

R. C.A. Tostes, D. W. Wilde, L. M. Bendhack, R. C. Webb

Research output: Contribution to journalArticle

21 Citations (Scopus)

Abstract

Calcium ions (Ca2+) trigger the contraction of vascular myocytes and the level of free intracellular Ca2+ within the myocyte is precisely regulated by sequestration and extrusion mechanisms. Extensive evidence indicates that a defect in the regulation of intracellular Ca2+ plays a role in the augmented vascular reactivity characteristic of clinical and experimental hypertension. For example, arteries from spontaneously hypertensive rats (SHR) have an increased contractile sensitivity to extracellular Ca2+ and intracellular Ca2+ levels are elevated in aortic smooth muscle cells of SHR. We hypothesize that these changes are due to an increase in membrane Ca2+ channel density and possibly function in vascular myocytes from hypertensive animals. Several observations using various experimental approaches support this hypothesis: 1) the contractile activity in response to depolarizing stimuli is increased in arteries from hypertensive animals demonstrating increased voltage-dependent Ca2+ channel activity in hypertension; 2) Ca2+ channel agonists such as Bay K 8644 produce contractions in isolated arterial segments from hypertensive rats and minimal contraction in those from normotensive rats; 3) intracellular Ca2+ concentration is abnormally increased in vascular myocytes from hypertensive animals following treatment with Ca2+ channel agonists and depolarizing interventions, and 4) using the voltage-clamp technique, the inward Ca2+ current in arterial myocytes from hypertensive rats is nearly twice as large as that from myocytes of normotensive rats. We suggest that an alteration in Ca2+ channel function and/or an increase in Ca2+ channel density, resulting from increased channel synthesis or reduced turnover, underlies the increased vascular reactivity characteristic of hypertension.

Original languageEnglish (US)
Pages (from-to)315-323
Number of pages9
JournalBrazilian Journal of Medical and Biological Research
Volume30
Issue number3
DOIs
StatePublished - Mar 1997

Fingerprint

Muscle Cells
Blood Vessels
Rats
Hypertension
Calcium
Animals
Inbred SHR Rats
Arteries
3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester
Clamping devices
Electric potential
Patch-Clamp Techniques
Ion Channels
Smooth Muscle Myocytes
Extrusion
Muscle
Cells
Ions
Membranes
Defects

Keywords

  • Bay K 8644
  • Calcium
  • Hypertension
  • Vascular reactivity
  • Vascular smooth muscle
  • Voltage-operated calcium channels

ASJC Scopus subject areas

  • Biophysics
  • Neuroscience(all)
  • Biochemistry
  • Physiology
  • Immunology
  • Pharmacology, Toxicology and Pharmaceutics(all)
  • Cell Biology

Cite this

Calcium handling by vascular myocytes in hypertension. / Tostes, R. C.A.; Wilde, D. W.; Bendhack, L. M.; Webb, R. C.

In: Brazilian Journal of Medical and Biological Research, Vol. 30, No. 3, 03.1997, p. 315-323.

Research output: Contribution to journalArticle

Tostes, R. C.A. ; Wilde, D. W. ; Bendhack, L. M. ; Webb, R. C. / Calcium handling by vascular myocytes in hypertension. In: Brazilian Journal of Medical and Biological Research. 1997 ; Vol. 30, No. 3. pp. 315-323.
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