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Vascular versus myocardial effects of calcium antagonists

W C Little1, C P Cheng

  • 1Department of Medicine, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina.

Drugs
|January 1, 1994
PubMed

Insights

Felodipine, a calcium channel blocker, demonstrates high vascular selectivity, causing vasodilation without negative inotropic effects. Unlike other calcium antagonists, felodipine enhances myocardial relaxation and filling, indicating superior vasoselectivity.

Area of Science:

  • Cardiovascular Pharmacology
  • Calcium Channel Blockers
  • Myocardial Contractility

Background:

  • Calcium entry is crucial for vascular smooth muscle tone and myocardial contractility.
  • Calcium antagonists are potent vasodilators but may have negative inotropic effects.
  • Verapamil affects vascular and myocardial contraction similarly, while felodipine shows high vascular selectivity.

Purpose of the Study:

  • To evaluate the inotropic effects of felodipine in conscious dogs.
  • To compare the vasoselectivity of felodipine with amlodipine and nifedipine.
  • To determine if felodipine exhibits negative inotropic effects at clinically relevant doses.

Main Methods:

  • Utilized left ventricular (LV) pressure-volume analysis in conscious dogs.
  • Administered felodipine at a plasma concentration of 16 nmol/L.
  • Conducted studies with and without adrenergic blockade.

Main Results:

  • Felodipine caused a 25 mm Hg fall in arterial pressure and reduced peripheral vascular resistance by 10%.
  • No negative inotropic effects were observed; myocardial contractile performance was slightly enhanced.
  • Felodipine improved LV relaxation and early diastolic filling, unlike amlodipine and nifedipine.

Conclusions:

  • Felodipine exhibits significantly greater vasoselectivity compared to amlodipine and nifedipine.
  • Clinically relevant doses of felodipine do not appear to have negative inotropic effects.
  • Felodipine's unique profile enhances myocardial relaxation and diastolic filling.

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