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Postnatal developmental changes in the sensitivity of L-type Ca2+ channel to inhibition by verapamil in a mouse heart

Hironori Sagawa1, Shinsuke Hoshino2, Kengo Yoshioka1

  • 1Department of Physiology, Shiga University of Medical Science, Otsu, Shiga, Japan.

Pediatric Research
|March 20, 2018
PubMed

Insights

Verapamil more potently inhibits cardiac L-type Ca2+ channels in young mice. This age-dependent sensitivity may explain why verapamil causes hypotension in human neonates and infants.

Area of Science:

  • Cardiovascular Pharmacology
  • Developmental Physiology

Background:

  • Verapamil is contraindicated in neonates and infants due to risks of hypotension and bradyarrhythmia.
  • The age-dependent sensitivity of cardiac L-type Ca2+ channels to verapamil remains unclear.

Purpose of the Study:

  • To investigate age-dependent differences in the sensitivity of cardiac L-type Ca2+ channel current (ICa,L) to verapamil.
  • To compare verapamil's potency with other L-type Ca2+ channel antagonists across different age groups.

Main Methods:

  • Ventricular myocytes were isolated from mice at six different age groups (0 to 15 weeks).
  • Whole-cell patch-clamp technique was used to assess ICa,L inhibition by verapamil, nifedipine, and diltiazem.

Main Results:

  • Verapamil, nifedipine, and diltiazem all concentration-dependently blocked ventricular ICa,L in all age groups.
  • Nifedipine and diltiazem showed similar potency across all ages.
  • Verapamil was more potent in inhibiting ICa,L in younger mice (0-21 days) compared to older mice (28 days and 10-15 weeks).

Conclusions:

  • Ventricular ICa,L in pre-weaning mice (<21 days) exhibits higher sensitivity to verapamil.
  • This enhanced sensitivity may contribute to verapamil-induced hypotension observed in human neonates and infants.

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