Proctolin and an endogenous proctolin-like peptide act as inotropic modulators of the Limulus heart by directly enhancing muscle fiber contractility without altering cardiac ganglion electrical activity.
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Animal data on proctolin inotropy should not yet change practice; leaves open hypothesis of similar mechanisms in mammalian hearts.
Synthetic proctolin increases the force but not the rate of heart contractions of Limulus in a time- and dose-dependent manner. The threshold of this effect is 3 X 10−10M and the EDS0 is approximately 10−10M. At concentrations up to 10−7 M, proctolin has no effect on the rhythmic electrical activity of the isolated cardiac ganglion, and it does not change the simple and compound postsynaptic potentials recorded at the cardiac neuromuscular junction. Proctolin acts directly on the cardiac muscle fibres. Electrically stimulated myocardia show a proctolin-induced increase in contraction amplitude with the same concentration dependence as the intact heart. A compound with an apparent molecular weight of 700–800 occurs in the Limulus nervous system, particularly in the cardiac ganglion. This compound resembles proctolin in being heat-stable, resistant to trypsin and chymotrypsin cleavage, and losing activity in a time-dependent manner in response to treatment with leucine aminopeptidase or pronase. This peptide induces spontaneous contractions and a contracture of the cockroach hindgut in a manner similar to proctolin. Moreover, the Limulus inotropic peptide, like proctolin, increases the force of contraction of the Limulus heart without affecting beat frequency. It is concluded that an endogenous, proctolin-like peptide is an inotropic modulator of the Limulus heart, acting directly on the muscle fibres and not affecting cardiac ganglion activity.
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Watson et al. (1983) studied this question.
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