What role do  - and  -adrenoceptors play in the regulation of the heart?

Abstract

Ahlquist described the existence of beta-adrenoceptors as structures mediating the positive effects of sympathetic nerve stimulation in the heart. Recently, the role of alpha-adrenoceptors has also been investigated by both biological and radioligand binding studies. The presence of alpha-adrenoceptors has now been demonstrated in the hearts of various mammalian species including man. Stimulation of beta-adrenoceptors causes positive ino-, chrono-, dromo- and bathmotropic effects while that of alpha-adrenoceptors is restricted to positive inotropic effects. Analysis of the effects mediated by alpha-stimulation as carried out in our department showed a clear-cut difference between the mechanisms underlying stimulation of beta- and of alpha-adrenoceptors: that evoked by beta-adrenoceptors is connected to an increase in cAMP, whereas that by alpha-adrenoceptors is not. Moreover, the effect of alpha-stimulation is evidently more dependent on heart rate and on the presence of Ca2+ than that of beta-stimulation. The nature of cardiac alpha-adrenoceptors is apparently distinct from that of other organs as they are stimulated by dopamine and adrenaline but not by the transmitter noradrenaline. Since the alpha-receptor-mediated increase in force of contraction is obviously less energy consuming than that via beta-receptors the heart gains a greater adaptability in adrenergic regulation especially in emergency situations such as myocardial infarction.

Do both adrenaline and noradrenaline stimulate cardiac α‐adrenoceptors to induce positive inotropy of rat atria?

“…This conclusion supports the results of early studies by Wagner & Schumann (Schumann, 1983) who found that in the presence of fiadrenoceptor blockade, phentolamine displaced the concentration-response curves for adrenaline but not for noradrenaline in rabbit and human cardiac muscle. The result is, however, at variance with those of Aass and co-workers who found a-adrenoceptormediated responses to noradrenaline in human atria (Skomedal et al, 1985), human ventricle (Aass et al, 1986) and rabbit papillary muscle (Aass et al, 1983).…”

Bone Marrow Oct3/4 + Cells Differentiate Into Cardiac Myocytes via Age-Dependent Paracrine Mechanisms

“…The cardiac myocyte differentiation of the bone marrow cells was associated with the expression of ␤ 1 -and ␤ 2 -adrenergic receptors, which are critical in the regulation of cardiac chronotropic function ( Figure 1C and 1D). 20 Indeed, this cardiac gene profile correlated with observational studies of spontaneous chronotropy (Videos 1 and 2 in the online data supplement) in the newly formed CCMs (60.1Ϯ12.2 contractions per minute).…”

Is There Still a Place for Vasopressors in the Treatment of Cardiac Arrest?

“…Th e α-receptors mediate mainly vasoconstriction, while β-receptors are responsible for stimulating eff ects on the heart (β 1 ) along with vasodilatation in some vascular beds (β 2 ) [10]. Th e vasoconstrictor α eff ect represents the scope of the administration of epinephrine during CPR, whereas cardiac stimulation from β eff ects is not benefi cial in this context, because the heart is not contracting and cardiac output depends essentially on chest compression.…”