2-Adrenergic drugs

They cause mydriasis (dilatation of the pupil).

Acts centrally at the nucleus tractus solitarius to decrease sympathetic outflow.

They relax the urinary bladder.

Post-synaptic excitatory, causing contraction except in the gastrointestinal tract.

It makes the compound water-soluble and leads to rapid degradation by MAO and COMT.

Orally or via patch.

By releasing norepinephrine (NE) from presynaptic stores at adrenergic terminals.

A drug that relaxes the uterus to treat premature labor.

Haemostatic, mydriatic, and nasal decongestant.

A reduction of response after repeated administration due to depletion of vesicles from stored NE.

Nasal rebound.

To produce effects similar to stimulation of the sympathetic nervous system.

A natural catecholamine and CNS transmitter.

Metabolized by COMT, resulting in a short duration of action.

Induces lipolysis and hyperglycemia.

Non-selective adrenergic receptors (α1, α2, β1, β2, β3).

They cause bronchodilation.

Absorbed orally.

They increase the conversion of glycogen to glucose, leading to hyperglycemia.

They stimulate adrenergic receptors by increasing norepinephrine release or inhibiting its uptake.

As a nasal and ocular decongestant and in flu remedies.

Dopamine, as it increases blood pressure without causing renal impairment.

It causes contraction of the urinary bladder's sphincter, leading to urinary retention.

Tachycardia, arrhythmias, headache, and hypertension.

A synthetic imidazoline and alpha-2 agonist.

Bronchodilation for acute attacks of asthma and COPD.

Psychic and physical dependence, psychosis, and it is not used therapeutically anymore.

Norepinephrine, which acts on alpha and beta receptors.

Increases heart rate (+ chronotropic effect) and can cause tachycardia.

They inhibit norepinephrine release through a negative feedback mechanism.

It decreases insulin (α1) and increases glucagon (β2).

Sympathomimetics.

A non-selective β agonist.

Severe vasoconstriction via α1 receptors.

It is not destroyed by monoamine oxidase (MAO).

It has a prolonged duration of action since it is not inactivated by COMT.

Agents that have both direct and indirect stimulation of adrenergic receptors, such as ephedrine and pseudoephedrine.

Vasoconstriction and hypertension, with little effect on heart rate.

Synthetic non-catecholamines like ephedrine and amphetamine.

To reduce intraocular pressure in glaucoma.

They relax the uterus, delaying premature labor.

Agents that stimulate adrenergic receptors directly, such as adrenaline, noradrenaline, and dopamine.

Acts directly on receptors and indirectly by releasing NE from adrenergic nerve endings.

D1 > β1 > α1 (in order).

Only by intravenous (I.V) route.

From postganglionic adrenergic fibers.

Mainly in cardiac arrest and rarely in acute asthma attacks.

Given parentally by infusion or orally.

They target specific adrenergic receptor subtypes, such as phenylephrine for alpha-1 and clonidine for alpha-2.

It is involved in the production of angiotensin II, a potent vasoconstrictor.

It can lead to hypotension by stimulating β2 receptors.

It causes bronchodilation (β2).

Congestive heart disease, hyperthyroidism, and closed-angle glaucoma.

Treatment of nasal stuffiness.

Hyperthyroidism and congestive heart disease.

Absorbed orally, not destroyed by MAO or catechol-O-methyltransferase (COMT), leading to prolonged action.

Hypertension.

It increases inotropic, chronotropic, and dromotropic activity (β1).

They increase heart rate.

They inhibit peristalsis and secretion.

Increases blood pressure and induces reflex bradycardia.

Mental alertness, wakefulness, concentration, self-confidence, depression, fatigue, euphoria, appetite loss, and increased energy expenditure.

Increases force of contraction but decreases heart rate.

Pseudoephedrine has less pressor effects compared to ephedrine.

In acute heart failure.

Adrenergic neurons as the primary neurotransmitter.

Due to its weak β2 activity, which does not induce bronchodilation.

Vasodilation of mesenteric, coronary, and renal blood vessels, leading to improved blood flow and diuresis.

Fast onset and short duration of action.

Adrenaline, given subcutaneously.

They can become non-selective.

+ve inotropic and +ve chronotropic effects, increasing blood pressure.

Intravenously (IV), subcutaneously (SC), inhalation, and topically.

Alpha (α) and Beta (β) adrenoceptors.

Adrenergic agonists that lack a catechol ring, are lipid-soluble, and can be administered orally.

Blood glucose levels increase (hyperglycemia) due to decreased insulin and increased glycogenolysis.

Excitatory function mainly present in the heart, increasing heart rate and force of contraction.

Natural catecholamines like norepinephrine and epinephrine.

It constricts skin and peripheral vessels (α1) and dilates coronary and skeletal vessels (β2).

Adrenergic agonists that have a catechol ring, are water-soluble, and have a short half-life.

They can increase blood pressure through vasoconstriction.

They cause relaxation, including in the uterus and bronchial smooth muscles.

It is inactivated by intestinal enzymes.

It decreases motility (β2) and contracts sphincters (α1).

Systolic blood pressure increases and diastolic blood pressure decreases.

As a hemostatic agent and combined with local anesthetics.