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Mechanical load opposes angiotensin-mediated decrease in vascular alpha 1-adrenoceptors

M L Clements1, J E Faber

  • 1Department of Physiology, University of North Carolina, Chapel Hill 27599-7545, USA.

Hypertension (Dallas, Tex. : 1979)
|May 1, 1997
PubMed
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Angiotensin II reduces alpha 1B-adrenergic receptors in vascular smooth muscle, an effect blunted by mechanical loading. This interaction influences cell growth and receptor expression, potentially impacting hypertension.

Area of Science:

  • Cardiovascular Physiology
  • Molecular Pharmacology
  • Hypertension Research

Background:

  • Alpha 1-adrenergic receptor activity in vascular smooth muscle is elevated by angiotensin II and in hypertension.
  • The direct impact of angiotensin II on alpha 1-adrenoceptor subtype expression remains unclear.
  • Previous work indicated mechanical load doesn't alter alpha 1B/1D-adrenoceptor expression, but hypertension may involve a humoral factor reducing alpha 1B-receptors.

Purpose of the Study:

  • To investigate the effect of angiotensin II, alone and with mechanical loading, on alpha 1D- and alpha 1B-adrenergic receptor mRNA and density in cultured rat aortic smooth muscle cells.
  • To determine if angiotensin II directly modulates alpha 1-adrenoceptor subtype expression.
  • To explore the interplay between angiotensin II and mechanical load on vascular smooth muscle cells.

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Main Methods:

  • Cultured rat aortic smooth muscle cells were exposed to varying concentrations of angiotensin II for different durations.
  • Alpha 1D and alpha 1B-adrenergic receptor mRNA levels and alpha 1-receptor density were quantified.
  • Cells were subjected to cyclic mechanical loading, and the effects of angiotensin type 1 receptor antagonist losartan were assessed.

Main Results:

  • Angiotensin II caused a time- and dose-dependent decrease in alpha 1B-adrenergic receptor mRNA and overall alpha 1-receptor density.
  • Alpha 1D mRNA levels transiently decreased with angiotensin II exposure.
  • Mechanical loading counteracted angiotensin II-induced cellular hypertrophy and the reduction in alpha 1B mRNA and receptor density. Losartan blocked these effects.

Conclusions:

  • Angiotensin II selectively downregulates alpha 1B-adrenergic receptor expression in vascular smooth muscle cells.
  • Mechanical loading mitigates the effects of angiotensin II on alpha 1B-receptor expression and cell growth.
  • Angiotensin II and intravascular pressure interact to modulate vascular smooth muscle cell growth and alpha 1B-adrenergic receptor expression, offering insights into hypertension mechanisms.