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Are alpha-adrenoceptors involved in positive inotropic effects of phenylephrine in chick ventricles?
K Nakazawa1, Y Kasuya, K Shigenobu
1Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.
Insights
Phenylephrine enhances chick heart contraction and Ca-action potentials, suggesting a role for beta-adrenergic mechanisms. Further research is needed to fully understand its effects on cardiac function.
Area of Science:
- Cardiology
- Pharmacology
- Developmental Biology
Background:
- Alpha-adrenergic mechanisms in cardiac function are not fully understood.
- Phenylephrine's role in chick ventricular contractility requires clarification.
Purpose of the Study:
- To investigate the effects of phenylephrine on chick ventricular contraction and Ca-action potentials.
- To determine if alpha-adrenergic mechanisms contribute to phenylephrine's effects in chick ventricles.
Main Methods:
- Isolated ventricles from embryonic and hatched chicks were used.
- Contractile force and Ca-action potentials were measured.
- Pharmacological antagonists (phentolamine, sotalol, prazosin, yohimbine) were employed.
Main Results:
- Phenylephrine increased ventricular contractile force in a dose-dependent manner.
- Methoxamine did not affect contractility.
- Phenylephrine enhanced maximum upstroke velocity of Ca-action potentials.
- Sotalol, but not phentolamine, blocked phenylephrine's effect on action potentials.
Conclusions:
- Phenylephrine's positive inotropic effect is partially mediated by beta-adrenergic actions.
- Increased Ca-influx through sarcolemma plays a role in phenylephrine's effects.
- Additional mechanisms, not strictly alpha-adrenergic, may contribute to phenylephrine's cardiac actions.
Abstract:
Effects of phenylephrine on contraction and Ca-action potentials were investigated to clarify whether the alpha-adrenergic mechanism may play a role in chick ventricles. Phenylephrine increased the contractile force of the ventricles isolated from both embryonic and hatched chicks, while methoxamine did not affect their contractility. Developmental changes in the sensitivity to phenylephrine, i.e., increase with age from late embryonic to early neonatal stages, were quite similar to those to a beta-agonist, isoproterenol. The positive inotropism of phenylephrine was antagonized by phentolamine and sotalol, but not antagonized by prazosin or yohimbine. Isobutylmethylxanthine augmented the effect of phenylephrine. Maximum upstroke velocity of Ca-action potentials recorded in partially depolarized ventricles were enhanced by phenylephrine, and the enhancement was eliminated by sotalol but not by phentolamine. The results suggested that the beta-adrenergic action of phenylephrine may be involved in part of its positive inotropic effect, which is mediated by increased Ca-influx through sarcolemma. Another mechanism may also participate in the effects of phenylephrine, but may not necessarily be classified as an "alpha-adrenergic effect".