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Statin treatment in hypercholesterolemic men does not attenuate angiotensin II-induced venoconstriction

Christoph Schindler1, Kristina Guenther2, Cosima Hermann2

  • 1Clinical Research Center Hannover & Institute of Clinical Pharmacology, Hannover Medical School, Hannover, Germany; Institute of Clinical Pharmacology, Medical Faculty, Technical University Dresden, Dresden, Germany.

Plos One
|September 30, 2014
PubMed

Insights

Statins did not significantly alter angiotensin II-mediated vasoconstriction in hypercholesterolemic patients. However, statin treatment showed a modest increase in angiotensin-(1-7) levels, suggesting complex effects on vascular regulation.

Area of Science:

  • Cardiovascular Pharmacology
  • Endocrinology
  • Vascular Biology

Background:

  • Experimental studies indicate statins may affect vascular angiotensin II type 1 (AT1) receptor responsiveness.
  • Hypercholesterolemia is associated with an exaggerated pressor response to angiotensin II, which may be normalized by statins.

Purpose of the Study:

  • To investigate the effect of atorvastatin on angiotensin II-mediated vasoconstriction in hypercholesterolemic patients.
  • To assess changes in plasma angiotensin II and angiotensin-(1-7) levels following statin treatment.

Main Methods:

  • A randomized, cross-over study involving 12 hypercholesterolemic patients.
  • Patients received either atorvastatin (40 mg) or irbesartan (150 mg) daily for 30 days.
  • Angiotensin II-induced venoconstriction was measured using a linear variable differential transducer; plasma angiotensin levels were quantified.

Main Results:

  • Atorvastatin treatment did not significantly alter angiotensin II-mediated venoconstriction (65%±11% before vs. 73%±11% after).
  • Irbesartan significantly reduced venoconstriction (59%±10% before vs. 28%±9% after; P<0.05).
  • Atorvastatin showed a modest increase in angiotensin-(1-7) levels (24±9 to 32±8 pg/mL; P=0.023) but no significant change in angiotensin II levels.
  • Irbesartan significantly increased both angiotensin II and angiotensin-(1-7) levels.

Conclusions:

  • Statin treatment does not appear to significantly affect angiotensin II-mediated venoconstriction in hypercholesterolemic patients.
  • The modest increase in angiotensin-(1-7) suggests statins may influence the renin-angiotensin system differently than AT1 receptor blockers.
  • Discrepancies between vascular and systemic responses may indicate statin interference with blood pressure buffering reflexes.
Abstract

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