parasympathetic nervous system Flashcards
cholinergic blockade: identify the consequences of cholinoceptor blockade and list the main clinical uses and unwanted effects of muscarinic cholinoceptor antagonists
where are nictotinic receptors located, and significance
between pre and post ganglionic neurones in ANS (or between neurone and adrenal medulla in one SNS pathway); present throughout so can affect all aspects of ANS
what are nicotinic receptor antagonists also called
ganglion blocking drugs
what 2 things do nicotinic receptor antagonists block
block actual receptor, or act as ion channel blockers (e.g. preventing Na+ influx)
2 examples of nicotinic receptor antagonists
hexamethonium (blocks ion channel; anti-hypertensives), trimetaphan (blocks receptor; most common)
what is a use-dependent block and to what type of antagonist does it apply to
use-dependent block: blocks ion channel incompletely, not receptor; more open channels are, more effective drug is; receptor block: more agonist, less effective antagonist; ion channel block: more agonist, more effective antagonist
antagonist vs ion channel blocker affinity
antagonists have affinity to block receptor, but if in channel pore just physical blockade of pore
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outcome of nicotinic recepor antagonist use
could block out all ANS; depends which system is dominant in that moment in time (if SNS dominant at time, that is the effect that is lost, and vice versa)
outcome of increased SNS activity (at rest = dominant PSNS) due to nicotinic receptor antagonist use
pupil, trachea and bronchiole dilation; glycogenolysis and gluconeogenesis; lipolysis; increased renin secretion; detrusor relaxation and constriction of trigone and sphincter; thick, viscous secretions; piloerection and increased sweating; increased heart rate and contractility (at rest PSNS has more effect so this effect is lost, increasing heart rate); decreased GI motility and tone with sphincter contraction; dilation of skeletal muscle blood vessels; constriction of blood vessels innervating skin, mucous membranes and splanchnic area
why do nicotinic receptor antagonists cause hypotension
heart, blood vessels, kidneys: heart rate will increase (PSNS dominant at rest), but dilation of blood vessels to GIT (SNS dominant at rest; decreased TPR) and stops renin secretion to kidney (SNS dominant at rest; reduced blood volume, Ang II and TPR)
effect of nicotinic receptor antagonists on smooth muscle at rest
pupil dilation, decreased GI tone, bladder dysfunction, bronchodilation
effect of nicotinic receptor antagonists on exocrine secretions
decrease secretions from salivary glands, GIT, skin and trachea and bronchioles
what nicotinic receptor antagonist was the first anti-hypertensive
hexamethonium
when is trimetaphan (nicotinic receptor antagonist) used
during surgery as an anti-hypertensive as short acting
how does a-bungarotoxin work
covalently binds to receptor and must be replaced to restore function; designed to target skeletal muscle as binds to somatic nervous system nicotinic receptor at NMJ