Key result
PGE1 and PGE2 inhibit cardiac sympathetic neurotransmission dose-dependently by reducing adrenergic transmitter release.
Why the study?
The effects of prostaglandins E1, E2, and F2α on sympathetic neurotransmission in the heart were not fully characterized.
Population
Isolated perfused, sympathetically innervated rabbit heart
Comparison
Infusion of prostaglandins E1, E2, and F2α at concentrations from 3×10‐9M to 1.5×10‐6M
Design
Preclinical experimental study
Authors
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Suggests prostaglandin modulation of cardiac sympathetic activity; leaves open translation to human physiology or therapy.
PGE1 and PGE2, but not PGF2α, inhibit sympathetic neurotransmission in the rabbit heart primarily by reducing noradrenaline release from adrenergic nerve terminals.
Hedqvist et al. (1971) studied this question. Prostaglandins E1, E2 and F2α was evaluated on Chronotropic, inotropic and noradrenaline overflow responses to sympathetic nerve stimulation. PGE1 and PGE2, but not PGF2α, inhibited sympathetic neurotransmission in the rabbit heart in a dose-dependent manner, mainly by reducing transmitter release from adrenergic nerve terminals.
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