Before we leave the adrenergic activators, it is useful to consider in detail the cardiovascular actions of epinephrine, norepinephrine, and isoproterenol. Some textbooks also consider dopamine in this context. Consider the effects of these agents on heart rate, cardiac output, total peripheral resistance, and mean arterial pressure. If you find these effects easy enough to remember, try adding their effects on systolic and diastolic blood pressure to your mental database.
Norepinephrine increases total peripheral resistance and mean arterial pressure.
Through stimulation of α receptors, norepinephrine causes constriction of all major vascular beds. This, in turn, causes an increase in resistance and pressure. The increase in blood pressure causes a reflex increase in parasympathetic output to the heart, which acts to slow the heart down. Therefore, heart rate often decreases after administration of norepinephrine in spite of direct activation of β1 receptors.
Epinephrine predominantly affects the heart through β1 receptors, causing an increase in heart rate and cardiac output.
Although epinephrine activates all α and β receptors, if given systemically its effects are predominated by effects on the heart. It increases heart rate, stroke volume, and cardiac output. The effects of epinephrine on blood pressure and peripheral resistance are dose dependent. At low doses, there is a fall in peripheral resistance as a result of vasodilation in the skeletal muscle beds (β2 effect). At higher doses, there is some vasoconstriction (α1) balancing the vasodilation (β2), resulting in little or no change in peripheral resistance. At even higher doses, the vasoconstriction (α1) will predominate, resulting in an increase in peripheral resistance and blood pressure.
Isoproterenol causes a marked decrease in total peripheral resistance and an increase in heart rate and cardiac output.
Remember that isoproterenol is an agonist at all β receptors. Therefore, it does not cause vasoconstriction of the vascular smooth muscle (α1). The vasodilation in the skeletal muscle beds (β2) is unopposed. This results in a net decrease in peripheral resistance. Isoproterenol also stimulates β1 receptors in the heart, resulting in an increase in heart rate and stroke volume.
Find graphs of these changes in your textbook and make sure that you understand them.