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Cardiovascular Research 1998 40(3):538-545; doi:10.1016/S0008-6363(98)00195-3
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

Effects of prostaglandin F2{alpha} on intracellular pH, intracellular calcium, cell shortening and L-type calcium currents in rat myocytes

Su Fong Yew, Katherine A. Reeves and Brian Woodward*

Department of Pharmacy and Pharmacology, University of Bath, Bath BA2 7AY, UK

* Corresponding author. Tel.: +44-1225-323-206; fax: +44-1225-826-114; e-mail: b.woodward@bath.ac.uk

Objective: We have studied the mechanisms underlying the positive inotropic action of prostaglandin F2{alpha} (PGF2{alpha}) by monitoring intracellular calcium transients, intracellular pH, L-type calcium currents and cell shortening in isolated ventricular myocytes. Methods: Rat myocytes were loaded with fura-2AM for intracellular calcium measurements, or BCECF-AM for pH measurements. Cell shortening was recorded using an edge detection system, and L-type calcium currents measured using whole cell patch clamping. Results: PGF2{alpha}(3 nmol l–1–3 µmol l–1) increased single myocyte shortening and reduced resting cell length in a concentration-dependent manner. While myocyte shortening was increased by PGF2{alpha}, this was not associated with any change in the amplitude of intracellular calcium transients, diastolic calcium, or L-type calcium currents. However, the same myocytes were capable of responding to catecholamines with increases in calcium transient amplitude and L-type calcium currents. PGF2{alpha} (3 µmol l–1) caused a reversible rise in intracellular pH of 0.08±0.01 pH units (n=5, p<0.05). The Na+–H+ exchanger inhibitor, HOE 694 (10 µmol l–1), abolished the PGF2{alpha}-induced rise in pH and the increase in cell shortening. PGF2{alpha}-induced increases in cell shortening and intracellular pH were also attenuated by the protein kinase C (PKC) inhibitor, chelerythrine (2 µmol l–1). Conclusion: The positive inotropic action of PGF2{alpha} appears to be mediated via activation of the Na+–H+ exchanger with the possible involvement of PKC. This suggests that PGF2{alpha}_produces intracellular alkalosis, which then sensitizes cardiac myofilaments to calcium.

KEYWORDS Calcium; Contractile function; Na/H–exchanger; Prostaglandins; Rat


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