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26 Cards in this Set

  • Front
  • Back
Parasympathetic control of the heart
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
Sympathetic control of the heart
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)
Baroreceptor reflex for low BP
Baroreceptors on aortic arch detect dec BP -> Nucleus of Solitary Tract -> inhibit PS and promote sympathetic activity = vasoconstriction and increased cardiac output
Main action of α1 receptor and compensatory effect
Main action is vasoconstriction (inc TPR)
Increasing TPR (and BP) causes compensatory dec in HR
Main action of α2 receptor and compensatory effect
Main action is through CNS control to decrease TPR - no compensatory response usually because it is CNS controlled
Main action of β1 receptor and compensatory effect
Main action is increasing cardiac muscle contractility that increase HR and SV = inc CO
no compensatory effect of the heart is possible
Main action of β2 receptor and compensatory effect
Main action is vasodilation (dec TPR)
Decreasing TPR (and BP) causes compensatory inc in HR
Where is the α1 receptor in the cardiovascular system, what is the biological action, and what preference for endogenous ligands?
Vascular smooth muscle, especially small arterioles in skin, mucous membranes and kidneys
Vasoconstriction increases MAP
NE >> Epi
Where is the β1 receptor in the cardiovascular system, what is the biological action, and what preference for endogenous ligands?
Cardiac tissue and myocardium
Increasing Cardiac output increases MAP
NE = Epi
Where is the β2 receptor in the cardiovascular system, what is the biological action, and what preference for endogenous ligands?
Coronary arteries and skeletal muscle arterioles
Vasodilation increases perfusion of cardiac and skeletal muscles
Epi >>> NE
Sympathetic control of urinary bladder
Tonic control of urine retention
α1 receptors contract internal sphincter, β2 receptors inhibit detrusor muscle, presynaptic α2 receptors inhibit PS influence
Parasympathetic control of urinary bladder
Ability to micturate with voluntary input
M2 receptors allow contraction of detrusor and relaxation of the internal sphincter by inhibiting sympathetic inputs
Sympathetic control of the eye
α1 receptors on pupillary dilator = mydriasis
β2 receptors on ciliary muscle = relax lens for far vision (minor role)
Dilated pupil
Parasympathetic control of the eye
M2 receptors inhibit dilator muscles = miosis
M3 receptors on ciliary muscle = fatten lens for close focus
Constricted pupil
*Dominant tonic input
How can two different drugs acting on separately on the sympathetic and parasympathetic systems both cause mydriasis?
α1 receptor agonist (symp)
Muscarinic antagonist (PS)
Which autonomic system has the greater control of ganglia in the ARTERIOLES and what would be the effect of a blockade of that ganglia?
Sympathetic
Blockade = vasodilation and dec BP
Which autonomic system has the greater control of ganglia in the VEINS and what would be the effect of a blockade of that ganglia?
Sympathetic
Blockade = vasodilation, dec venous return
Which autonomic system has the greater control of ganglia in the HEART and what would be the effect of a blockade of that ganglia?
Parasympathetic
Blockade = tachycardia
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?
Parasympathetic
Blockade = mydriasis
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?
Parasympathetic
Blockade = inability to accomadate and focus
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?
Parasympathetic
Blockade = constipation and urinary retention
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?
Sympathetic
Blockade = anhidrosis (inability to sweat)
Major peripheral actions of catecholamines/sympathomimetics (8)
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
Major CNS actions of catecholamines/sympathomimetics (3)
respiratory stimulation, increased arousal, decreased appetite
Effects of a cholinergic blockade in the Parasympathetic system
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)
Potential side effects of Adrenergic agents (peripheral and central) and NT systems effected
Behavioral: sedation, anxiety, depression, attention, appetite;
Autonomic CNS control: respiration, CV, thermoregulation, GI function;
Systems effected: 5-HT, DA, NE, Epi