long term blood pressure control
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Consistent and Long-Term Control of Blood Pressure is
Determined by The Renin-Angiotensin System
LEARNIN !B"ECTI#E
• Describe the long-term renal regulation of blood pressure
$E% P!INTS
o When blood volume is low renin, excreted by the &idneys, stimulates production of angiotensin I
which is converted into angiotensin II, which has many effects, including increase in blood 'ressure due to its vasoconstrictive properties.
o The cells that excrete renin are called (u)taglomerular *ells. When blood volume is low
juxtaglomerular cells in the idneys secrete renin directly into circulation. Plasma renin then carries out theconversion of angiotensinogen released by the li+er to angiotensin I.
o Aldosterone secretion from the adrenal *orte) is induced by angiotensin II and causes the tubules of
the idneys to increase the reabsor'tion of sodium and water into the blood, thereby increasing blood volume and blood pressure.
TER,S
• (u)taglomerular *ells
The juxtaglomerular cells !"# cells, or granular cells$ are cells in the idney that synthesi%e, store, and
secrete the en%yme renin.
• aldosterone
& mineralocorticoid hormone, secreted by the adrenal cortex, that regulates the balance of sodium and
potassium in the body.
• adrenal *orte)
The outer portion of the adrenal glands that produces hormones essential to homeostasis.
There are many physical factors that influence arterial pressure. 'ach of these may in turn be influenced by
physiological factors such as diet, exercise, disease, drugs or alcohol, stress, obesity, and so-forth.
(ome physical factors are) Rate of pumping. In the *ir*ulatory system, this rate is
called heart rate, the rate at which blood !the fluid$ is pumped by the heart. The volume of blood o. from
the heart is called the *ardia* out'ut which is the heart rate !the rate of contraction$ multiplied by the stroe volume !the amount of blood pumped out from the heart with each contraction$. The higher the heart rate, the
higher themean arterial 'ressure, assuming no reduction in stroe volume or central venous return *olume of fluid or blood volume is the amount of blood that is present in the body. The more blood present in
the body, the higher the rate of blood return to the heart and the resulting cardiac output. There is some
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relationship between dietary salt intae and increased blood volume, potentially resulting in higher arterial
pressure, although this varies with the individual and is highly dependent on autonomi* ner+ous
system response and the renin-angiotensin system. Resistance. In the circulatory system, this is theresistance of the blood vessels. The higher the resistance, the higher the arterial pressure upstream from the
resistance to blood flow. +esistance is related to vessel radius !the larger the radius, the lower the resistance$ vessel length !the longer the vessel, the higher the resistance$, blood viscosity, as well as the smoothness of the
blood vessel walls. (moothness is reduced by the buildup of fatty deposits on the arterial walls. (ubstancescalled vasoconstrictors can reduce the si%e of blood vessels, thereby increasing blood pressure. *asodilators
!such as nitroglycerin$ increase the si%e of blood vessels, thereby decreasing arterial pressure. +esistance, and
its relation to volumetric flow rate !$ and pressure difference between the two ends of a vessel are described
by oiseuilles /aw.
*iscosity is the thicness of the fluid. If the blood gets thicer, the result is an increase in arterial
pressure. 0ertain medical conditions can change the viscosity of the blood. 1or instance, anemia !low red
blood *ell concentration$, reduces viscosity, whereas increased red blood cell concentration increases
viscosity. It had been thought that aspirin and related 2blood thinner2 drugs decreased the viscosity of blood but instead studies found that they act by reducing the tendency of the blood to *lot. In practice, eachindividuals autonomic nervous system responds to and regulates all these interacting factors so that, although
the above issues are important, the actual arterial pressure response of a given individual varies widely because
of both split-second and slow-moving responses of the nervous system and end organs. These responses are
very effective in changing the variables and resulting blood pressure from moment to moment.
The renin3angiotensin system !+&($ or the renin3angiotensin3aldosterone system !+&&($ is
a hormone system that regulates blood pressure and water !fluid$ balance. When blood volume is low,
juxtaglomerular cells in the idneys secrete renin directly into circulation. lasma renin then carries out theconversion of angiotensinogen released by the liver to angiotensin I. &ngiotensin I is subse4uently converted to
angiotensin II by the en3yme angiotensin converting en%yme found in the lungs. &ngiotensin II is a potent
vaso-active 'e'tide that causes blood vessels to constrict, resulting in increased blood pressure. &ngiotensinII also stimulates the secretion of the hormone aldosterone from the adrenal cortex. &ldosterone causes the
tubules of the idneys to increase the reabsorption of sodium and water into the blood. This increases the
volume of fluid in the body, which also increases blood pressure. If the renin3angiotensin3aldosterone system
is too active, blood pressure will be too high. There are many drugs that interrupt different steps in this system
to lower blood pressure. These drugs are one of the main ways to control high blood pressure !hypertension$,
heart failure, &idney failure, and harmful effects of diabetes.
It is believed that angiotensin I may have some minor activity, but angiotensin II is the major bio-active
product. &ngiotensin II has a variety of effects on the body) throughout the body, it is a potent vasoconstrictor
of arterioles.
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Source: Boundless. “Long-Term Renal Regulation.”Boundless Anatomy and Physiology. Boundless, 21 Jul. 2015.
Retrieved 21 Apr. 2016 from https://www.boundless.com/physiology/textbooks/boundless-anatomy-and-physiology-
textbook/cardiovascular-system-blood-vessels-19/control-of-blood-pressure-184/long-term-renal-regulation-914-3348/