Key result
Methoxamine produced a dose-related increase in force development of cat papillary muscle that was selectively blocked by alpha-adrenergic receptors, without direct effects on adenyl cyclase activity.
Why the study?
Does methoxamine increase force development in cat ventricular myocardium via alpha-adrenergic receptors?
Does methoxamine increase force development in cat ventricular myocardium via alpha-adrenergic receptors?
Methoxamine exerts a positive inotropic effect on cat ventricular myocardium that is mediated by alpha-adrenergic receptors, independent of adenyl cyclase activity.
Answers are grounded in this paper and cite their sources.
Alpha-adrenergic inotropy independent of adenyl cyclase supported in feline myocardium; leaves open human translation.
The present study was undertaken to evaluate the effects of methoxamine on force development and adenyl cyclase activity in cat ventricular myocardium. Methoxamine produced a dose-related increase in force development of isometrically contracting cat papillary muscles. The positive inotropic effects of methoxamine were not altered by beta-adrenergic blockade (propranolol), or catecholamine depletion by prior reserpinization, but were completely prevented by alpha-adrenergic blockade (phentolamine or ergotamine). Neither ergotamine, phentolamine, nor methoxamine had any direct effects on adenyl cyclase activity. Phentolamine did not attenuate the increase in force development produced by paired electrical stimulation, suggesting that it does not block the entry of calcium into the muscle. In summary, methoxamine produced a dose-related increase in force development of the cat papillary muscle that was selectively blocked by alpha-adrenergic receptors in ventricular myocardium.
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Rabinowitz et al. (1975) studied Cat ventricular myocardium (animal model). Methoxamine vs. Alpha- and beta-adrenergic blockade was evaluated on Force development and adenyl cyclase activity. Methoxamine produced a dose-related increase in force development of cat papillary muscle that was selectively blocked by alpha-adrenergic receptors, without direct effects on adenyl cyclase activity.
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