Key result
The synthetic peptide L-calchin reduced peak systolic and developed pressure in isolated rat hearts and caused a voltage-independent block of L-type Ca2+ channel currents in rabbit myocytes.
Population
Isolated rat heart Langendorff preparations and whole-cell patch-clamped rabbit ventricular myocytes
Design
Preclinical
Authors
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May guide peptide-based L-type Ca2+ channel modulator design; leaves open therapeutic translation in cardiovascular disease.
The synthetic peptide L-calchin exhibits L-type Ca2+ channel blocking properties, confirming the functional binding site of calciseptine and FS2 and the role of flanking proline residues.
Kini et al. (1998) studied this question. L-calchin was evaluated on L-type Ca2+ channel blocking properties (peak systolic and developed pressure, L-type Ca2+ channel currents). The synthetic peptide L-calchin reduced peak systolic and developed pressure in isolated rat hearts and caused a voltage-independent block of L-type Ca2+ channel currents in rabbit myocytes.
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