Parasympathetic stimulation and baroreceptors

[Lothric]

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Hey,

If carotid massage is performed the afferent baroreceptor firing is increased meaning more signals go to the solitary nucleus in the medulla via either the glossopharyngeal or vagus nerve (depending on receptor location). This will stimulate parasympathetic nerves from the vagus and according to FA 2017 step 1 this increases AV node refractory period which reduces heart rate.

Questions:

1. When they say "refractory period", do they refer to the normal 100 msec delay in conduction from AV node to bundle of His or do they refer to the effective refractory period which is the period that has to pass before a new action potential can occur? I'm hoping the answer is the former, because I've learnt that the AV node does not induce action potentials unless the SA node is dysfunctional.

2. When heart rate decreases, this is dependent not only on the parasympathetic nerves on the AV node but also on the SA node, right? These nerves tend to release acetylcholine and adenosine which decreases the depolarization rate occuring via funny currents under diastole. These two factors cause the decreased heart rate together, not singely. Or at least I'm hoping that's how it works...

 

[chromuffin]

I believe they are referring to ERP. The AV node "inducing" APs with SA node dysfunction is false under the assumption that you're saying the AV node doesn't have its own basal AP. The AV is always propagating signals from the SA to the bundle of His. It is just slower in order to allow for atrial contraction against a relaxed ventricle.

For question 2.. I don't know. I have assumed the vagus nerve always affects the SA node. Affecting the AV node without affecting the SA node would result in a lengthened PR interval.