Explain the mechanisms wherebt acetylcholine and epineephine alter the heart rate?

and the respond of the heart to acetylcholine following application of atropine?

Explain the mechanisms wherebt acetylcholine and epineephine alter the heart rate?

Hi. I am unsure as to why you have no answers. I%26#039;ll see if I can help.

The heart rate and contractility is controlled by the sympathetic and parasympathetic nervous system (SNS and PSNS). The SNS releases norepinephrine at the presynaptic terminal, onto adrenoreceptors on the myocardia.

The PSNS releases acetylcholine onto cholinergic receptors on the myocardia.

So, when the SNS releases norepinephrine onto the myocardia, it binds to a serpentine (%26#039;7-pass%26#039;) receptor. This activates a G protein, which splits into alpha and beta-gamma sub units. The beta-gamma subunit then reacts with other proteins in the cell, and increases the intracellular cAMP (cyclic adensosine monophosphate) levels. cAMP concentration is directly linked with the tendancy for sodium channels to open. So, as cAMP levels increase, more sodium channels stay open.

The heart rate is controlled by the SA node in the heart. It slowly depolarises, to the threshold point. Once it reaches the threshold, it then fully depolarises and sends a wave of excitation down across the myocardia (heart) making it contract. The way it slowly depolarises is the inflow of sodium ions. So, if the SNS makes sodium ion channels open more, more sodium flows into the SA nodal cells, depolarising it quicker, so it reaches threshold level quicker, and so contractions are initiated quicker, and so heart rate has increased.

The other thing that increases intracellular cAMP levels do is to stimulate the myocardial sarcoplasmic reticulum to release more calcium ions during myocardial contraction. So, the plateau phase of the action potential is prolonged, and so the muscle continues to contract for longer, and so the contractions are harder - this therefore increases contractility.

So, the point about above is that the SNS increases cAMP levels, which increases heart rate and contractility.

The PSNS does the opposite. It prevents the production of cAMP, and so will stop all of the above happening. Sodium channels will have a tendancy to remain closed, and calcium will not be released in as much volume during contraction, and so heart rate and contractility are decreased.

Atropine is a PSNS antagonist (it works on M2 cholinergic receptors, if you care). It STOPS the PSNS doing what it does, it it stops the PSNS from stopping production of cAMP. This means cAMP IS produced, and so similar things will happen to the SNS working normally. So, cAMP is increased, and so heart rate and contractility is increased.

Hope that helps, email me any more questions - I like to help!

Ashley