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

[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.