Catecholamines are important regulators of peripheral vascular resistance and venous capacitance. α-ARs increase arterial smooth muscle tone, whereas β₂-ARs relax vascular smooth muscle . Skin and splanchnic vessels have mainly α-ARs and, thus, constrict in response to catecholamines, whereas skeletal muscle vessels have both α- and β₂-ARs and can either constrict or dilate, respectively, after catecholamine stimulation (Table 1.1; [1, 6]). Renal, splanchnic, coronary, and cerebral vessels also have dopaminergic D₁ receptors, and they dilate in response to dopamine (the third endogenous catecholamine hormone) activation [13]. This mediates, in large part, the natriuresis (through increase of the resultant renal glomerular filtration rate) and the hypotension usually observed upon systemic administration of low doses of dopamine (the so-called renal dose of dopamine) .

Endogenous catecholamines are extremely important in the regulation of cardiac contractile function primarily through their actions via cardiostimulatory β-ARs (Table 1.1; [1, 11, 13–15]). β₁-ARs are the primary subtype in the heart, comprising 75–80 % of total myocardial β-ARs. The remaining cardiac β-ARs are largely made up of β₂-ARs, with a minor component of β₃-ARs found in human myocardium [1]. β-AR activation results in increased pacemaker activity (at the sinoatrial node and in the Purkinje fibers) and conduction velocity at the atrioventricular node, whereas it decreases the refractory period [1]. All these actions lead to positive chronotropy (Table 1.1). Cardiac contractility is enhanced (positive inotropy), and the relaxation is accelerated (positive lusitropy; Table 1.1). The end result is a cardiomyocyte twitch response of increased tension but reduced duration. The intraventricular pressure of the intact heart rises and falls more rapidly, and the ejection time is decreased. These effects are clearer in the absence of reflexes to blood pressure changes . These normal reflexes usually confound the direct effects of catecholamines on the heart, and the resultant net effect on the heart depends on the relative balance between the actions of these reflexes and the direct actions of catecholamines on cardiac muscle [1, 11, 15–16].

Catecholamines are also very important regulators of systemic blood pressure. Their effects on blood pressure are a function of three parameters: (a) their direct effects on the heart; (b) their effects on peripheral vascular resistance; and (c) on the venous return (Table 1.1). A pure α₁-AR agonist like phenylephrine increases peripheral arterial resistance and decreases venous capacitance . Therefore, systemic blood pressure rises, which then evokes a baroreceptor-mediated reflex increase in vagal tone in order to slow the heart rate . Cardiac output usually does not change, despite the reduction of heart rate, owing to the resultant increase in venous return (Frank–Starling effect on cardiac contractility) and to a minor positive inotropic effect of direct cardiac α₁-AR stimulation. These reflex responses are usually undetectable in hypotensive patients, in whom α₁-AR agonists are given to normalize blood pressure .

Specific catecholamine responses follow the previously discussed characteristics. Epi, which activates all ARs, is a very potent vasoconstrictor and cardiac stimulant. It raises systolic blood pressure by increasing the heart rate and force of contraction (cardiac β-AR effect) and peripheral vascular resistance (α₁-AR effect). However, it also dilates some peripheral vessels (mainly skeletal muscle vessels) via stimulation of β₂-ARs; thus, it might actually decrease peripheral resistance and diastolic pressure. This skeletal muscle vessel dilation contributes to increased skeletal blood flow during exercise. NE shares the activity of Epi at α-ARs but lacks significant β₂-AR activity. Consequently, it increases peripheral resistance (via α₁-ARs), heart rate, and force of contraction (cardiac β₁-AR effect), thus raising both systolic and diastolic blood pressures. Vagal reflexes usually counteract the positive chronotropic but not inotropic effects of NE. A simple β-AR agonist like isoproterenol markedly increases cardiac output, contractility, and rate of contraction (cardiac β-AR effects) while decreasing peripheral resistance by inducing β₂-AR-mediated peripheral vasodilation. Therefore, the net effect on blood pressure is a fall in diastolic and mean arterial pressures in combination with a slight increase (or no change) in systolic blood pressure [6, 15–16] .