Question

1. Assuming that you had an agonist and an antagonist for every autonomic transmitter receptor, how could you determine which receptor types exist in any autonomically controlled effector?
2. Using the method you defined in Question 1 and your knowledge of the Autonomic control of the function of the internal organs, predict the effects (increase, decrease, or no change) of the following autonomic agonists on heart rate (HR).
   AGONIST                              HR CHANGE

alpha-adrenergic      

beta-adrenergic                                                                                          

muscarinic  

nicotinic    

3. Using autonomic pharmacological agents, how could you determine which receptors in an organ are subjected to a tonic release of neurotransmitter? By releasing an antagonist to the specific organ you are looking at. 4. Using your answer to Question 3 and your knowledge of the autonomic control of heart rate (HR), predict the heart changes (Indicate: increase, decrease, or no change next to each receptor kind) the pharmacological agents listed in the table below would produce in a resting individual.
   ANTAGONIST              HR CHANGE

alpha-adrenergic  

beta-adrenergic

muscarinic  

nicotinic        

5. Predict the heart rate change that the agents would produce in a vigorously exercising individual.
   ANTAGONIST                HR CHANGE

alpha-adrenergic

beta-adrenergic  

muscarinic    

nicotinic   

Answer 1

THIS QUESTION COMPRISES 5 PARTs

ANSWER OF EACH PART IS AS BELOW

PART 1

BY USING ANTAGONIST AND AGONIST, and OBSERVING THE EFFECT WE CAN CONCLUDE THAT ANY EFFECTOR ORGAN HAS WHICH TYPE OF RECEPTOR.

Part-1 и Ч effector organ , we can check/indentify agoinst of any ANS receptor by blocking other receptor. e'yi It we have a receptor A, B and C and I antogonists are antu. A, untu-B and unta-c agonists are ago- A , ago-B and ago - c inta-D All ugonists] All agonists] an Antare Anta-A Antarte All ugunists] V anta-A Anta B anta- B A B C D A B C D D A B C organ organ organ only effect of only effect of receptor-C will only effect of B will be observed A will be observed observed because A4B are untugunised Now, we observed effect conclude that effector of A, B and C organ has receptor so we can A, B and C.

PART 2

There are two types of Autonomic nervous System u Sympathetic ANS 3) Parasympathetic ANS Ne fos memo rising purpose you can consider broadly > Sympatheti An's as Catabolic enhancey - Para sympathetic ANS as Anabolic enhancer Now, Part 2 Agonist Explaination HR change y 2 → De Creuse -adrenergic - As there is no d- receptor on heart so. no direct effect but by 2-adrenergic receptor there will be Vaso-constriction and rise in sp and hence there will be reflex bradycordia 3) 8-adrenergic - Increase By direct action of B on heart, It will increase HR by increasing Resting Membrane potencial and Calcium load in Heart Cells = 3) Muscarine → Deisease direct action on M₂ receptor on heart. It will decrease HR by decreasing RMP (Hyper pelorisation) and also decrease Calcium influxe and bradycardio - - u Nicotine OTO mild decrease (Aro change) As there is no direct action on Heart but nicotone activate Bothy type of ganglia so no action but It has also a mild Dominant Para Sympathetic tone.

PART 3

Part -2 Using autonomic pharmological agents, we can determine which receptors in an organs are subjected to a tonic release of neurotransmitter by blocking that specific receptor and observing the physiological action. (like M₂, B, etc) 7 7 7 7 7 71111111 It an organ (let suppose Heart) has many receptor now, I want to effect of epinephrin so, J I wo will block M2 & obserre effect Heart (M2 + B) M₂- antagonist increase Heart and Heart-rate epinephrin Heart (M2 + B4) No change in HR Be - antagonist epinephrin So here we can say that ging epinephrin acts on B2-adrenergic receptor if it will blocked by antagonist then there will be no effect

PART 4

Part 4 Antogonist HR change Explaination mild SU 2-adreneryic Increuses ОХ No changes → Que to blockade of d-receptor there will be no contraction of Smooth muscle cells and hence there will be veno-dialation resulting in fall in BP and hence there will be reflex tachycardia. 17111 2 ß-adrenergic Decreases (mild) or No change Due to blockade of ß receptor there will be direct action. Due to blockade of B2 receptor on blood vessels there will be constriction in vessel and hence reflex bradycardia. 3) Muscarinic INDONNNNNNNNNN - Increase Because in Yestiny phase para sympathetic action is dominant Due to blockade of Mi receptor. there will be direct action. It will block the perrasympathetic action (vagal action) on heart u Nicotinec - No change As there is no nicotinic receptor on heart or blood vessels so, there is no direct action as well as no refles action. - > In Resting phase para sympathetic system is dominant so there will be no change in HR by a-adrenergic & ß-adrenergic.

PART 5

- Part 5 During vigorously exercising ephose sympia thetic and will stimulates so. Antagonist HR change explaination L-adrenergic → Due to blockage of &- receptor on vessels these will be vaso-dialation and hence reflex tuchycardia Increases - - 3 B-adrenergic- » Decrease By Blocking By receptor of adrenaline (released during exercise) it will give direct action on heart. Auscarine No change during vigously exercise parasympathetic action will be diminished No-change y u) Nicotinic During vigoursly exercise parasympathetic action will be diminished. n 1)

I HOPE THIS WILL HELP YOU A LOT FOR BETTER UNDERSTANDING OF RECEPTOR ALSO.