Autonomic Nervous System III Flashcards
(38 cards)
Table 4 understand the location, cellular effects, agonists, antagonists of M1, 2, and 3.
pp. 78
What are the organ distribution of parasympathetic receptors?
M1: gastric parietal cells, CNS, ganglia
M2: cardiac, atria, conducting tissue
M3: S mm, exocrine glands, endothelial cell
M4: confined to certain region of CNS (still under investigation)
M5: under investigation
Draw Figure (Table) 19 twice and understand the relationship.
pp. 79
Why is the name G-protein?
Because it requires GTP to function.
What is the G-protein utilized when Beta-adrenergic receptors are activated?
Gs- because it stimulates the cyclase.
What is the G-protein utilized when alpha 2-adrenergic receptors and M2 cholinergic receptors are activated?
Gi- because it inhibits the cyclase.
What is the G-protein utilized when alpha 1-adrenergic and M1 and M3 cholinergic receptors are activated?
Gq-activate phospholipase C (PLC)-hydrolyzes PIP2 into IP3 and DAG.
- IP3 mobilize Ca from internal stores.
- DAG activates PKC
How are the receptors in the ANS are related to the nervous system in general?
1) The same receptors found in the ANS are also present within the somatic and CNS.
2) Principles for the mode of action of receptors within the ANS also apply to CNS.
Discuss the effects mediated by adrenergic receptors.
TABLE 5 pp 81
What type of alpha-adrenergic receptors are found in S mm?
Alpha 1-adrenergic receptors are mainly found in S mm although there are alpha 2 in vascular S mm.
How do alpha 1 and alpha 2 work?
Alpha 1 via IP3 and DAG= increase in intracellular Ca (IP3) and activation of PKC (DAG)
Alpha 2 via inhibition of adenylyl cyclase and decrease of cAMP.
Use the example of vascular smooth mm to show how sympathetic pathways work to cause different outcomes.
FIGURE 20
pp. 82
NOTE: that sympathetic nervous system releases ACh causing vasodilation of vascular bed via M3-receptors in endothelial cells. (pp 84).
Show how B2-adrenergic receptor activation by NE results in Bronchiolar Smooth mm relaxation.
FIGURE 21
pp. 83
NOTE: B-adrenergic receptor activation usually causes relaxation of S mm.
Describe the physiological effects of alpha 1-adrenergic receptor activation.
Ca released via IP3 pathway, Ca-CaM complex activate MLCK (dephosphorylate it)-MLCK phosphorylate myosin light chain (MLC)-activating it and resulting in contraction.
-Constriction of large arteries, veins, arterioles-> decreased vascular compliance->increased central venous pressure->increased peripheral resistance->increased systolic and diastolic arterial pressure-> activate baroreceptor reflexes->bradycardia (inhibition of respiration)
T/F The parasympathetic system innervate vascular S mm.
F. Not involved in vascular S mm. But the sympathetic system indirectly induces cholinergic stimulation of blood vessels via the endothelial cells tht line the blood vessel lumen=>vasodilation
READ pp 84 (cholinergic) REFER to Fig. 20. pp83.
What is the notable exception to the general rule that alpha 1-adrenergic receptors cause S mm contraction?
S mm of the GI tract which relaxes when alpha 1-adrenergic receptors are activated.
-Occurs via increase in K permeability which causes hyperpolarization (precise method not known).
How can B-stimulation treat asthma?
B-stimulation leads to dilation of the bronchial S mm important in treating asthma (Figure 21 pp 83).
In general, what does the PS innervate when it comes to S mm? What receptors are mostly present?
PS innervate S mm other than those of blood vessels via the M3-cholinergic receptor and this results in mm contraction.
How does M3 and M1 receptors cause peristalsis in the GI and bladder emptying?
M3 stimulation results in increase of Ca via IP3-> tone and amplitude of contraction increases, as well as peristalsis in the GI.
NOTE: M3 also enhances the secretory activity of GI but gastric acid secretion stimulated by M1-receptor activation
M1 stimulation is more important in the bladder. And via the same way with increase in Ca through IP3 cause bladder contraction and emptying.
How does sympathetic nervous system activation affect the heart?
B1-adrenergic receptor activation->induce a cascade->cAMP increase->stimulate PKA-> phosphorylation of Ca channels=open at lower voltage and stay open longer—-depolarization at the SA node—faster HR.
NOTE: Pacemaker channels are rather directly stimulated by cAMP to shift activation curve of If to more +ve=the inward current is greater for every membrane potential.
STUDY Figure 22 pp 88
What happens during exercise in terms of sympathetic stimulation?
-Sympathetic nervous system activation leads to
*phosphorylation of the If channel (within SA node)
*phosphorylation of Iks, L-type Ca channels in the ventricles
=Stronger and shorter AP
How does the parasympathetic system affect HR?
PS stimulation decreases HR via
*inhibit adenylyl cyclase-decrease in cAMP
*Open K channels-hyperpolarization
=decreased HR
How does the sympathetic nervous system affect the force of contraction of the cardiac myocytes?
B1-adrenergic receptor stimulation leads to PKA increase:
- phosphorylation of L-type Ca channel +ve inotropic effect in both atria and ventricles-due to CICR and direct activation of contraction
- Increased filling of SR with Ca due to increased intracellular Ca and increased pump activity (cAMP-dependent phsphorylation of phspholamban). This enhances fast relaxation.
- Phosphorylation of Troponin I-reduces affinity of troponin C for Ca, allowing for more rapid dissociation of Ca from troponin-enhanced rate of relaxation.
FIGURE 23 pp88
What is thought to cause the increased conduction velocity at the AV node due to sympathetic stimulation?
Greater opening of Ca channels.
