Effects of sympathomimetic drugs on the cardiovascular system Domina Petric, MD

Type of adrenergic receptor Tissue Effects on the tissue α1 Smooth musculature of innervated blood vessels Contraction Dilator pupillae muscle Contraction (mydriasis) Smooth musculature of hair pilomotors Heart Increased strength of contraction α2 Postsynaptic in the brain Multiple effects Thrombocytes Agregation Adrenergic and cholinergic presynaptic endings Inhibition of neurotransmitters release Fat cells Lipolysis inhibition

Type of adrenergic receptor Tissue Effects on the tissue β1 Heart, juxtaglomerular cells Increased strength and speed of contraction, increased renin release β2 Smooth musculature of bronchi, uterus and blood vessels Relaxation Sceletal muscles Increased potassium uptake Liver Activation of glycogenolysis β3 Fat cells Activation of lipolysis

Type of adrenergic receptor Tissue Effects on the tissue D1 Smooth muscles Dilatation of blood vessels D2 Nerve endings Modulation of transmitters release

Effects of α1 receptors activation These receptors are widely distributed in the vasculature. Their activation causes arterial and venous contraction. Clean α1-receptor agonists increase peripheral arterial resistance and decrease capacity of veins. Increase of blood pressure causes reflex bradicardia. Reflex bradicardia is due to activation of baroreceptors. Venous inflow is increased.

Alfa-receptor agonist MIDODRINE can be used to treat orthostatic hypotension. In the blood vessels of skin and abdominal organs there are mostly alfa-receptors so constriction is a consequence of adrenaline and noradrenaline release. Blood vessels in sceletal muscles have both alfa and beta adrenergic receptors so release of adrenaline and noradrenaline can cause both contriction and vasodilatation. Blood vessels in the nasal mucosa have alfa-receptors. That is why sympathomimetics are used as nasal decongestans (local vasoconstriction).

Effects of α2-receptors activation These receptors are present in all blood vessels. Their activation causes vasoconstriction when used locally (very fast intravenous infusion or high oral dose). Systemic use of α2-receptors agonists causes both central α2-receptors activation and peripheral α2-receptors activation. Activation of central α2-receptors causes decrease of sympathetic tonus and lowers blood pressure. α2-agonists are therefore used as sympatholytics in treatment of hypertension.

Effects of β-receptors activation Activation of β-receptors in the heart increases heart contractility and heart frequency. Activation of β2-receptors on the periphery causes vasodilatation in some blood vessels. Sympathomimetics effects in the heart Positive inotropic effect: increase of intrinsic heart activity. Contraction is stronger, relaxation is faster. Positive chronotropic effect: increase of heart frequency. Positive dromotropic effect: increase of conduction speed in the atrioventricular node. Positive bathmotropic effect: increased excitability of the heart.

Effect of dopamine receptors activation Intravenous aplication of dopamine causes vasodilatation of renal, visceral, coronary and cerebral arterioles via activation of D1-receptors. Activation of D1-receptors in renal blood vessels can increase natriuresis. Activation of presynaptic D2-receptors inhibits noradrenalin release. Dopamine activates β1-receptors in the heart.

Effect of dopamine receptors activation Low dose of dopamine decreases peripheral resistance. When given in high speed infusion activates α-receptors. High speed infusion of dopamine mimics affects of noradrenaline. Activation of α-receptors causes vasoconstriction, including renal vasoconstriction. Katzung, Masters, Trevor. Clinical pharmacology. DOPAMINE