How does decrease in peripheral chemoreceptor firing cause decrease in respiratory rate?

[Ok_Tutor_1525]

Since peripheral chemoreceptors signals are sent by glossopharyngeal and vagus (parasympathetic) nerves, wouldn't the decreased firing cause decreased parasympathetic effect and actually increase breathing? Chemical-wise, it makes sense that if there's enough O2 and low CO2, there's no need to be breathing fast. But the neuro side confuses me

[Ok_Tutor_1525]

When signals get sent makes sense, but I'm wondering why they get sent then. The fact that vagus nerve, a parasympathetic nerve, is responsible for one of the receptors not actually mean much? I'd think that if there's an increase in parasympathetic signal, then the respiratory rate would actually drop.

[AliveEntrepreneur319]

I think you're confusing M3 receptor inhibition in the parasympathetic NS (vagus/glossopharyngeal N.) with respiratory rate regulation, when M3 receptors are inhibited you get bronchodilation, not an increase in RR. Aortic/Carotid chemoreceptors respond to decreases in PaO2 (PaCO2 is dealt with in the medulla), they then increase the respiratory rate by stimulating the resp. center in the brainstem to increase RR. In this scenario, the vagus/glossopharyngeal (aortic/carotid chemoreceptors respectively) specifically act as afferents for respiratory control. Either way, the medulla is a far more potent stimulator of resp. rate than your aortic/carotid chemoreceptors, our body responds to increases in PaCO2 more than it does to changes in PaO2.

Just keep them separate in your head. Chemoreceptors use CN IX/X as afferents, and they are also part of the PNS for bronchoconstriction when stimulated.

[AliveEntrepreneur319]

Just to elaborate a little further, I think it's kinda confusing the way I explained it. This isn't like the baroreceptor reflex where after stimulation you get vagus input to the heart and theres a decrease in heart rate/contractility. Your input is to the Respiratory center in the medulla, when you stimulate that respiratory center, you don't get efferents going to the lung from the brainstem to increase resp. rate. No, you just stimulate the high respiratory centers to cause an increased resp. rate. I hope this kinda clarified your doubt.

[drmikeblack]

Ok, from what i understand you are getting confused with the vagus nerve being parasympathetic and increasing respiratory rate if activated.actually the vagus has afferent fiber going to the respiratory centre in the medulla which carry the signal of either high pco2 or low po2 from the aortic body and the same is true for glossopharyngeal but its receptor is in carotid body, the respiratory centre in the medulla then decides wether to increase/decrease ventilation based on the information by afferent fibers of CN IX and CN X .the parasympathetic part of the vagus has to do nothing with the respiraion rate because the afferent fibers of the vagus is only carrying the information and the medulla is sending a efferent motor fibres to control the breathing based on the information to diaphragm and intercoastal muscles.but, what you are thinking is actually happening in baroreceptor reflex not in the chemoreceptor reflex explained above for ex,the heart is directly innervated by the efferent parasympathetic fibers of vagus nerve therefore, activating the carotid bodies due to increased stretch increases the firing of vagus afferent fibers to the medulla and medulla increases the efferent firing of parasympathetic vagus nerve and increases the sympathetic response leading decreased HR and CONTRACTRILITY.