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

Contraction

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

Effects of α1 receptors activation

➝ These receptors are widely distributed in thevasculature.

➝ Their activation causes arterial and venouscontraction.

➝ Clean α1-receptor agonists increase peripheralarterial resistance and decrease capacity of veins.

➝ Increase of blood pressure causes reflexbradicardia.

➝ Reflex bradicardia is due to activation ofbaroreceptors.

➝ Venous inflow is increased.

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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).

These receptors are present in all bloodvessels.

Their activation causes vasoconstriction when used locally (very fast intravenous infusion or high oral dose).

Systemic use of α2-receptors agonists causesboth central α2-receptorsactivation and peripheralα2-receptors activation.

Effects of α2-receptors activation

Activation of centralα2-receptors causesdecrease ofsympathetic tonus and lowers bloodpressure.

α2-agonists are therefore used as sympatholytics intreatment ofhypertension.

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Effects of β-receptors activation

Activation ofβ-receptorsin the heartincreasesheartcontractilityand heartfrequency.

Activation ofβ2-receptorson theperipherycausesvasodilatationin some bloodvessels.

Sympathomimetics effects in the heart1) Positive inotropic effect:

increase of intrinsic heartactivity. Contraction is stronger, relaxation is faster.

2) Positive chronotropic effect: increase of heart frequency.

3) Positive dromotropic effect: increase of conduction speedin the atrioventricular node.

4) Positive bathmotropic effect: increased excitability of theheart.

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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.

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Effect of dopamine receptors activation

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Low dose ofdopaminedecreasesperipheralresistance.

When givenin highspeed

infusionactivates α-receptors.

High speedinfusion ofdopamine

mimicsaffects of

noradrenaline.

Activation of α-receptors causesvasoconstriction,

including renalvasoconstriction.

DOPAMINE