L4 Sympathetic nervous system and adrenergic neurotransmission

Acetylcholine is the neurotransmitter at all ganglia, sympathetic or parasympathetic, and acts at nicotinic (N1) receptors.

Most sympathetic post ganglionic nerve endings have [blank_start]adrenergic[blank_end] receptors (adrenoceptors), which come in 2 types, [blank_start]alpha and beta[blank_end]. There are subtypes [blank_start]1 and 2[blank_end] for both alpha and beta receptors. Catecholamines act on several R types. Noradrenaline acts on [blank_start]alpha 1 and beta 1[blank_end]. Adrenaline acts on [blank_start]all adrenergic receptors[blank_end].

Select all the systems on which catecholamines have inhibitory actions.

Sympathetic affects on the heart, via [blank_start]beta 1[blank_end] receptor stimulation: • [blank_start]increased[blank_end] heart rate and contractility • [blank_start]increased[blank_end] AV node conduction • [blank_start]increased[blank_end] cardiac output Sympathetic affects on the lungs, via [blank_start]beta 2[blank_end] receptor stimulation: • [blank_start]decreased[blank_end] secretions • [blank_start]increased[blank_end] airway diameter (relaxed bronchial muscle) Sympathetic affects on the bladder: • Relaxation of the detrusor muscle (via [blank_start]beta[blank_end] receptors) • Contraction of the sphincter (via [blank_start]alpha 2[blank_end] receptors)

Blood vessels express alpha, beta, dopamine, histamine, and muscarinic receptors. SNS activation releases noradrenaline, adrenaline, and dopamine. Alpha 1 activation [blank_start]vasoconstricts[blank_end] vessels (arterioles) and [blank_start]decreases[blank_end] blood flow to unnecessary organs, so more blood can flow to where it's needed. Beta 2 [blank_start]vasodilates[blank_end] skeletal muscle beds and decreases overall vascular [blank_start]resistance[blank_end], increasing [blank_start]blood flow[blank_end] to muscles.

Dopamine (DA) has 3 different concentration-dependent mechanisms: - Low [DA]: acts at [blank_start]dopamine 1[blank_end] receptors to dilate renal [blank_start]artery[blank_end], and increase [blank_start]kidney perfusion[blank_end]. - Med [DA]: stimulates [blank_start]beta 2[blank_end] receptors to dilate [blank_start]skeletal muscle bed[blank_end], and decreases systemic vascular [blank_start]resistance[blank_end] - High [DA]: stimulates [blank_start]alpha 1[blank_end] receptors to cause vessel constriction and increase [blank_start]blood pressure[blank_end]. All levels of dopamine [blank_start]increase[blank_end] kidney perfusion.

Which of these is not a side effect of drugs that activate the SNS?

Sympathomimetic drugs are drugs that mimic the action of the [blank_start]sympathetic[blank_end] nervous system and are adrenergic [blank_start]agonists[blank_end]. They can be [blank_start]direct[blank_end] acting, and therefore selective for specific adrenergic receptors(or non-selective). They can also be [blank_start]indirect[blank_end] acting, by increasing the availability of [blank_start]noradrenaline/adrenaline[blank_end] to stimulate adrenoceptors.

Entacapone and selegine are directly acting sympathomimetic drugs used to treat Parkinson's disease.

Adrenergic [blank_start]antagonists[blank_end] are sympatholytics, i.e. they break the effects of the SNS. Many drugs [blank_start]interfere[blank_end] with the function of the SNS, and affect the [blank_start]physiology[blank_end] of sympathetically innervated organs. Several of these are important for the treatment of [blank_start]cardiovascular[blank_end] diseases(e.g. Beta blockers such as [blank_start]metoprolol[blank_end].)