Mean Arterial Pressure Control
2 mechanisms exist to monitor and regulate changes in MAP (mean arterial pressure):
- Baroreceptor reflex—more important for short-term control of blood pressure
- Arterial baroreceptors in the carotid sinus sense and respond to acute increases or decreases in arterial pressures
- Arterial baroreceptors in the aortic arch respond to acute increases, but not decreases in arterial pressure.
- RAA (renin angiotensin aldosterone) system—more important for long-term control of blood pressure.
For example, how would the body respond to an acute hypotensive episode? - Baroreceptor reflex responds within seconds:
Acute ↓ in MAP →↓ afferent signals sent from the carotid sinus baroreceptors via glossopharyngeal nerve (CN IX) to the brain stem medulla →↓ in parasympathetic activity via the efferent vagus nerve to the heart, with a simultaneous ↑ in sympathetic outflow from the nucleus of the solitary tract to the heart and vasculature →
- ↑ Heart rate (chronotropic effect)
- ↑Myocardial contractility (inotropic effect) ∴↑ stroke volume
- ↑ AV conduction velocity (dromotropic effect)
- ↑ TPR (total peripheral resistance)
∴compensatory↑ of mean arterial pressure toward normal
Recall: MAP = CO*TPR, and CO = HR * SV
CO=cardiac output, HR=heart rate, SV=stroke volume
- RAA (renin angiotensin aldosterone) system senses the the acute drop in blood pressure but takes minutes-hours-days to kick into gear:
↓ MAP →↓ renal blood flow is sensed by the juxtaglomerular apparatus →↑ renin →↑ angiotensin II →
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Angiotensin II is a potent vasoconstrictor that increases total peripheral resistance.
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Angiotensin II also stimulates release of aldosterone → stimulates renal sodium retention and subsequent renal fluid reabsorption to help maintain total blood volume in an attempt to preserve stroke volume, cardiac output, and mean arterial pressure.