The Body's Control of Blood Pressure: Mechanisms and Hypertension

This essay provides a comprehensive overview of blood pressure control mechanisms, differentiating between short-term and long-term regulation. Short-term control is primarily mediated by the baroreceptor reflex, a negative feedback loop involving pressure-sensitive receptors in the aorta and carotid sinus that communicate with cardiovascular centers in the brainstem to adjust heart rate, stroke volume, and peripheral resistance. Long-term control is achieved through the renin-angiotensin-aldosterone system (RAAS), where decreased renal blood flow triggers renin secretion, leading to angiotensin II production (a potent vasoconstrictor) and aldosterone release (promoting salt and water retention). The essay also addresses hypertension, a major disorder of blood pressure regulation, and discusses pharmacological treatments aimed at reducing peripheral resistance or cardiac output, such as ACE inhibitors, aldosterone receptor blockers, diuretics, and beta-blockers. This resource is available for students looking for detailed explanations and study aids on Desklib.

RUNNING HEAD: BP CONTROL 1
CONTROL OF BLOOD PRESSURE
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Blood pressure control can be a short-term reaction or long-term control. Short-term
control is via the baroreceptor reflex while long-term control is via the renin-angiotensin and
aldosterone system of the kidneys (Moon, 2013).
The baroreceptor reflex is the principle negative feedback mechanism for blood pressure
control (Martini, Nath, & Bartholomew, 2015). It Is negative feedback loop since a stimulus will
trigger processes that lower itself (Sarikas, 2014). The baroreceptors are located in the arch of
the aorta and the carotid sinus and they detect minor changes in blood pressure as they are
pressure sensitive (Waugh & Grant, 2010). They have neural connections to the cardiovascular
centers in the pons and medulla of the brainstem. A rise in blood pressure, for example, is sensed
by these baroreceptors which increase firing input to the cardiovascular centers. The
cardiovascular center, in turn, mediates return to normal pressure by affecting the heart and
blood vessels in order to alter cardiac output and peripheral resistance (Waugh & Grant, 2010).
Other sensors include the chemoreceptors in the aortic and carotid bodies that detect
changes in blood PH, carbon dioxide content in relation to blood pressure status and sending
impulses to the cardiovascular centers to reduce or increase the blood pressure (Waugh & Grant,
2010).
The cardiovascular center increases parasympathetic nervous activity to the heart. This
has the effect of reducing the heart rate and effectively reducing the stroke volume. Both heart
rate and stroke volume affect the cardiac output since it is a product of both, hence reduction will
effectively reduce the cardiac output and subsequently the blood pressure. (Waugh & Grant,
2010).

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The cardiovascular center including the vasomotor center in the medulla also acts on the
blood vessels by reducing the sympathetic discharge to the vessels. The action of the sympathetic
nervous system on smooth muscles of the blood vessels is to cause vasoconstriction hence a
reduction in sympathetic tone causes vasodilation (Martini, Nath, & Bartholomew, 2015). This
reduces the peripheral resistance, the second factor in blood pressure control, which reduces the
blood pressure. The reverse occurs in the case of a fall in blood pressure.
The other mechanism is the renin-angiotensin-aldosterone system. Increase in blood
pressure causes a reduction in renal blood flow which is detected by the juxtaglomerular cells of
the kidney (Moon, 2013). They secrete renin, which enzymatically turns angiotensinogen to
angiotensin 1. Angiotensin 1 is then turned by angiotensin converting enzyme to angiotensin 2 a
potent vasoconstrictor that increases the peripheral resistance hence the blood pressure. It also
stimulates the adrenal cortex to produce aldosterone, a hormone whose principle action is salt
and water retention (Moon, 2013). This aims to increase blood volume, cardiac output, and blood
pressure.
Elevated blood pressure is termed hypertension and is the major disorder of blood
pressure regulation. Treatment of hypertension is aimed at reducing the peripheral resistance,
reducing cardiac output or treating the underlying conditions that cause secondary hypertension.
Reducing peripheral resistance can be done pharmacologically using drugs that cause
vasodilation including ACE inhibitors, aldosterone receptor blockers and angiotensin antagonists
(Moon, 2013). Drugs that lower the cardiac output include diuretics that lower blood volume,
alpha and beta blockers, and calcium channel blockers that lower sympathetic activity hence
heart rate (Moon, 2013).

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References
Martini, F.H., Nath, J.L., & Bartholomew, E.F. (2015). Fundamentals of Anatomy and
Physiology. Pentice hall: New Jersyey
Moon, J. (2013). Recent update of Renin-angiotensin-aldosterone system in the pathogenesis of
hypertension. Electrolyte Blood Press, 11(2), 41-45
Raven, B & Chapleau, M. (2014). Blood pressure regulation XI: overview and future research
directions. European Journal of Applied Physiology, 114(3), 579-586.
Sarikas, S. (2014). Visual Anatomy and Physiology Lab Manual (pig version). London: Pearson
Waugh, A., & Grant, A. (2010). Ross & Wilson Anatomy and Physiology in Health and Illness
E-Book. Elsevier Health Sciences.