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26 Cards in this Set
- Front
- Back
Parasympathetic control of the heart
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Vagus nerve releases ACh that binds to M2 receptors on cardiac muscle to tonic regulatory activity.
Increased Vagal activation of M2 receptors is inhibitory and decreases HR |
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Sympathetic control of the heart
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Mostly by vascular compensatory effects, some by cardiac nerves directly:
NE released by postganglionic sympathetic fibers bind to β1 receptors = increase HR and stroke volume (SV) = Increase cardiac output (CO) |
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Baroreceptor reflex for low BP
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Baroreceptors on aortic arch detect dec BP -> Nucleus of Solitary Tract -> inhibit PS and promote sympathetic activity = vasoconstriction and increased cardiac output
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Main action of α1 receptor and compensatory effect
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Main action is vasoconstriction (inc TPR)
Increasing TPR (and BP) causes compensatory dec in HR |
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Main action of α2 receptor and compensatory effect
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Main action is through CNS control to decrease TPR - no compensatory response usually because it is CNS controlled
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Main action of β1 receptor and compensatory effect
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Main action is increasing cardiac muscle contractility that increase HR and SV = inc CO
no compensatory effect of the heart is possible |
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Main action of β2 receptor and compensatory effect
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Main action is vasodilation (dec TPR)
Decreasing TPR (and BP) causes compensatory inc in HR |
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Where is the α1 receptor in the cardiovascular system, what is the biological action, and what preference for endogenous ligands?
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Vascular smooth muscle, especially small arterioles in skin, mucous membranes and kidneys
Vasoconstriction increases MAP NE >> Epi |
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Where is the β1 receptor in the cardiovascular system, what is the biological action, and what preference for endogenous ligands?
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Cardiac tissue and myocardium
Increasing Cardiac output increases MAP NE = Epi |
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Where is the β2 receptor in the cardiovascular system, what is the biological action, and what preference for endogenous ligands?
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Coronary arteries and skeletal muscle arterioles
Vasodilation increases perfusion of cardiac and skeletal muscles Epi >>> NE |
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Sympathetic control of urinary bladder
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Tonic control of urine retention
α1 receptors contract internal sphincter, β2 receptors inhibit detrusor muscle, presynaptic α2 receptors inhibit PS influence |
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Parasympathetic control of urinary bladder
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Ability to micturate with voluntary input
M2 receptors allow contraction of detrusor and relaxation of the internal sphincter by inhibiting sympathetic inputs |
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Sympathetic control of the eye
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α1 receptors on pupillary dilator = mydriasis
β2 receptors on ciliary muscle = relax lens for far vision (minor role) Dilated pupil |
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Parasympathetic control of the eye
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M2 receptors inhibit dilator muscles = miosis
M3 receptors on ciliary muscle = fatten lens for close focus Constricted pupil *Dominant tonic input |
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How can two different drugs acting on separately on the sympathetic and parasympathetic systems both cause mydriasis?
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α1 receptor agonist (symp)
Muscarinic antagonist (PS) |
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Which autonomic system has the greater control of ganglia in the ARTERIOLES and what would be the effect of a blockade of that ganglia?
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Sympathetic
Blockade = vasodilation and dec BP |
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Which autonomic system has the greater control of ganglia in the VEINS and what would be the effect of a blockade of that ganglia?
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Sympathetic
Blockade = vasodilation, dec venous return |
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Which autonomic system has the greater control of ganglia in the HEART and what would be the effect of a blockade of that ganglia?
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Parasympathetic
Blockade = tachycardia |
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Which autonomic system has the greater control of ganglia in the PUPIL/IRIS and what would be the effect of a blockade of that ganglia?
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Parasympathetic
Blockade = mydriasis |
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Which autonomic system has the greater control of ganglia in the CILIARY MUSCLE and what would be the effect of a blockade of that ganglia?
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Parasympathetic
Blockade = inability to accomadate and focus |
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Which autonomic system has the greater control of ganglia in the GI AND BLADDER and what would be the effect of a blockade of that ganglia?
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Parasympathetic
Blockade = constipation and urinary retention |
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Which autonomic system has the greater control of ganglia in the SWEAT GLANDS and what would be the effect of a blockade of that ganglia?
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Sympathetic
Blockade = anhidrosis (inability to sweat) |
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Major peripheral actions of catecholamines/sympathomimetics (8)
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contract blood vessels, increase HR and cardiac output, sweating, bronchodilation, increased blood flow to skeletal muscle, relax smooth muscle in gut, increase glycogen breakdown in liver/muscle, liberate fatty acids from adipose tissue
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Major CNS actions of catecholamines/sympathomimetics (3)
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respiratory stimulation, increased arousal, decreased appetite
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Effects of a cholinergic blockade in the Parasympathetic system
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Mad as a hatter (delerium), blind as a bat (mydriasis), dry as a bone (inability to sweat or salivate), red as a beat (sympathetic flush), hot as a pistol (unable to dilate vessels or sweat causes inability to lose heat)
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Potential side effects of Adrenergic agents (peripheral and central) and NT systems effected
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Behavioral: sedation, anxiety, depression, attention, appetite;
Autonomic CNS control: respiration, CV, thermoregulation, GI function; Systems effected: 5-HT, DA, NE, Epi |