Autonomic Pharm II Flashcards
Effects of M2 receptor stimulation?
decreased neuronal activity to SA node and decreased atrial contractility (little to no effect on ventricles)
Effects of M3 and M5 receptor stimulation?
vasodilation of vasculature by Nitric Oxide production
Mechanism of M2 receptor activation?
Gi signaling, inhibition of adenylate cyclase–> decrease cAMP–> hyper-polarization of membrane by opening on inward potassium channels
Mechanism of M3 receptor activation?
couples through Gq–> increase IP3 and DAG levels–> increase in PKC and Calcium levels–>excitatory
Where in the heart does parasympathetic activity act?
SA and AV nodes
Does vasculature receive parasympathetic innervation?
No, but it will respond to exogenous muscarinic agonists/antagonists
Effect of IV acetylcholine on the vasculature?
vasodilation via NO synthesis
Effect of IV acetylcholine on damaged vasculature?
activation of M3 receptors–> smooth muscle contraction and vasoconstriction
Main effect of Atropine on the heart?
To increase heart rate, it is a competitive antagonist of muscarinic Ach receptors (acting mainly in the SA node)
Atropine at low doses?
Inhibits presynaptic M1 receptors–> Increase in PS activity (Ach release)–> slight slowing of heart rate
Atropine at higher doses?
Blockade of PS inhibitory effects on the SA node leading to progressive tachycardia
Effect of Atropine on the vasculature?
Minimal given that most vascular beds lack significant cholinergic innervation
What is Atropine Flush?
High doses of Atropine can dilate cutaneous blood vessels in a local area causing flushing of the skin
Atropine indications?
Abolish temporary over-activity of the Vagal tone of the heart; facilitates AV node conduction (useful in patients with inferior or posterior wall MIs)
Effect of Beta-2 receptor activation?
vasodilation in skeletal muscle vasculature and dilation of bronchial smooth muscle
Effect of Beta-1 receptor activation?
Increased heart rate and cardiac contractility; Renin release from JGA in the nephrons
How direct-acting drugs work?
stimulate the postsynaptic receptors
How indirect-acting drugs work?
stimulate the presynaptic terminal to cause release of Epi or Norepi
What is Tachyphylaxis?
Reduction in effect seen with chronic therapy
What are MAOIs and how do they work?
Monoamine oxidase Inhibitors, prevent the breakdown of neurotransmitter (indirect)
How does Tyramine and Amphetamine work?
cause the release of preformed transmitter from storage in the pre-synaptic vesicles (indirect)
How does Reserpine work?
depletes Norepi from presynaptic sympathetic neurons