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Attenuated microvascular alterations in coarctation hypertension.

D L Stacy1, R L Prewitt

  • 1Department of Physiology, Eastern Virginia Medical School, Norfolk 23501.

The American Journal of Physiology
|January 1, 1989
PubMed
Summary

Chronic hypertension causes arteriolar changes. This study in cremaster muscle suggests these alterations, including reduced diameter and density, are pressure or flow dependent, unlike in renal hypertension.

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Area of Science:

  • Physiology
  • Vascular Biology
  • Hypertension Research

Background:

  • Chronic hypertension is linked to arteriolar vasoconstriction, diameter reduction, and rarefaction.
  • The pressure or flow dependence of these microvascular changes in hypertension remains unclear.

Purpose of the Study:

  • To investigate the pressure and flow dependence of arteriolar functional and structural changes during developing and chronic coarctation hypertension.
  • To compare these alterations with those seen in renal hypertension models.

Main Methods:

  • Coarctation hypertension was induced in rats using a silver clip on the abdominal aorta.
  • Arteriolar diameters, vascular tone, medial-intimal area, and arteriole density were measured in the cremaster muscle at 2, 4, and 8 weeks post-intervention.

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  • Measurements were compared between hypertensive and control rats.

    • Main Results:

    • Reduced resting diameters were observed in second-, third-, and fourth-order arterioles in hypertensive rats.
    • Elevated vascular tone was noted in second-, third-, and fourth-order arterioles.
    • No significant increase in medial-intimal area was found.
    • A 20% reduction in small arteriole density occurred at 8 weeks of hypertension.

    Conclusions:

    • Arteriolar diameter reductions and rarefaction in coarctation hypertension are attenuated compared to one-kidney, one-clip hypertension.
    • These findings suggest that microvascular alterations in hypertension are largely dependent on pressure and flow levels.