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Control of heart rate in mammals

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There are just 2 scenarios involved here. Either the heart rate must be increased or decreased.

 

1. The heart rate must go up because the blood pressure is low, there’s a shortage of oxygen, an excess of CO2 or the pH is too low – some of these go together e.g. O2, CO2 and pH interaction during exercise, stress, etc.

 

The hormone that increases heart rate is noradrenaline. This can be released by the brain’s medulla via the sympathetic neurons when aortic and carotid baroreceptors which sense low blood pressure or chemoreceptors which sense excess or a lack of certain chemicals send signals via sensory neurons. The aorta is the principal vessel carrying oxygenated blood from the heart to the rest of the body, while the carotid arteries carry it on to the brain via the neck.

 

Noradrenaline then binds to the heart’s sino-atrial node which results in increased contractions.

 

2. The heart rate must go down because the blood pressure is high, there’s excess O2, low CO2 or the pH is too high

 

The sensing process is identical – baroreceptors and chemoreceptors do their jobs. The only difference? Of course, the released product must be different – the medulla orders acetylcholine instead of noradrenaline, and this signal follows the parasympathetic pathway.

 

Acetylcholine makes the SA node slow contractions.

 

 

The autonomic nervous system is hence central to the increase of heart rate as part of the sympathetic stress or flight/fight response. Upon perception of any stimulus that causes this response, the system directs the release of adrenaline to increase heart rate, alongside other outcomes such as increased blood pressure, inhibition of digestion, etc.

 

 

 

 

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