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

2. 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

3. 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

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

5. 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.

6. 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).

7. 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.

8. 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.

9. 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.

10. 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