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Regulation of Renal Blood Flow

Author: Sophia

what's covered

In this lesson, you will learn about the mechanisms that regulate blood flow through the kidney. Specifically, this lesson will cover:

1. Sympathetic Nerves
2. Autoregulation
- 2a. Arteriole Myogenic Mechanism
- 2b. Tubuloglomerular Feedback
3. Renin–Angiotensin–Aldosterone System

before you start

It is vital that the flow of blood through the kidney be at a suitable rate to allow for filtration. This rate determines how much solute is retained or discarded, how much water is retained or discarded, and ultimately, the osmolarity of blood and the blood pressure of the body. Therefore, mechanisms that regulate this blood flow are essential for the proper functioning of the human body.

1. Sympathetic Nerves

key concept

The kidneys are innervated (supplied with nerves) by the sympathetic neurons of the autonomic nervous system via the celiac plexus and splanchnic nerves. Reduction of sympathetic stimulation results in vasodilation and increased blood flow through the kidneys during resting conditions. When sympathetic stimulation increases, the arteriolar smooth muscle constricts (vasoconstriction), resulting in diminished glomerular flow, so less filtration occurs.

Under conditions of stress, sympathetic nervous activity increases, resulting in the direct vasoconstriction of afferent arterioles (the norepinephrine effect) as well as stimulation of the adrenal medulla. The adrenal medulla, in turn, produces a generalized vasoconstriction through the release of epinephrine. This includes vasoconstriction of the afferent arterioles, further reducing the volume of blood flowing through the kidneys. This process redirects blood to other organs with more immediate needs.

If blood pressure falls, the sympathetic nerves will also stimulate the release of renin. Additional renin increases the production of the powerful vasoconstrictor angiotensin II. Angiotensin II will also stimulate aldosterone production to augment blood volume through the retention of more Na⁺ and water. Only a 10 mm Hg pressure differential across the glomerulus is required for normal glomerular filtration rate (GFR), so very small changes in afferent arterial pressure significantly increase or decrease GFR.

The anatomy of the glomerulus and Bowman’s capsule (shown below) presents a unique physiological situation. The afferent arteriole flows into the glomerulus, which flows into the efferent arteriole. Both arterioles are resistance vessels whose diameters are influenced by sympathetic nerve activity and the activity of various drugs, which can target either the afferent arteriole or the efferent arteriole independently (see the figure below). As such, the drugs have different consequences on pressures in the afferent and affect arterioles, glomerular capsule pressure, glomerular filtration rate (GFR), and renal plasma flow (RPF)—see below.

Illustration highlights the Bowman’s Capsule along with the efferent and afferent arterioles from the nephron. — The Anatomy of the Glomerulus and Bowman’s Capsule

TBD — The effects of vasoconstrictions and vasodilations of the afferent and efferent arterioles on glomerular pressure, GFR, and RPF.
Abbreviations:
GFR - glomerular filtration rate
RPF - renal plasma flow
PGC - glomerular pressure
PAA - afferent arteriole pressure
PEA - efferent arteriole pressure
RAA - afferent arteriole resistance
REA - efferent arteriole resistance

The kidney’s afferent and efferent arterioles are unique in that they are two resistance vessels in series. Therefore, there can be different effects when one is constricted or dilated and the other is not, as shown above (this usually happens with certain drugs). For example:

When the afferent arteriole is constricted, glomerular pressure, GFR, and RPF are decreased.
When the efferent arteriole is constricted, glomerular pressure and GFR are increased, while RPF is decreased.
When the efferent arteriole is dilated, glomerular pressure and GFR are decreased, while RPF is increased.
When the afferent arteriole is dilated, glomerular pressure, GFR, and RPF are all increased.

2. Autoregulation

The kidneys are very effective at regulating the rate of blood flow over a wide range of blood pressures. Your blood pressure will decrease when you are relaxed or sleeping. It will increase when exercising. Yet, despite these changes, the filtration rate through the kidney will change very little. This is due to two internal autoregulatory mechanisms that operate without outside influence: the myogenic mechanism and the tubuloglomerular feedback mechanism.

2a. Arteriole Myogenic Mechanism

The myogenic mechanism regulating blood flow within the kidney depends upon a characteristic shared by most smooth muscle cells of the body. When you stretch a smooth muscle cell, it contracts; when you stop, it relaxes, restoring its resting length. This mechanism works in the afferent arteriole that supplies the glomerulus. When blood pressure increases, smooth muscle cells in the wall of the arteriole are stretched and respond by contracting to resist the pressure, resulting in little change in flow. When blood pressure drops, the same smooth muscle cells relax to lower resistance, allowing a continued even flow of blood.

2b. Tubuloglomerular Feedback

The tubuloglomerular feedback mechanism involves the JGA and a paracrine signaling mechanism utilizing ATP, adenosine, and nitric oxide (NO). This mechanism stimulates either contraction or relaxation of afferent arteriolar smooth muscle cells. Recall that the DCT is in intimate contact with the afferent and efferent arterioles of the glomerulus. Specialized macula densa cells in this segment of the tubule respond to changes in the fluid flow rate and Na⁺ concentration.

As GFR increases, there is less time for NaCl to be reabsorbed in the PCT, resulting in higher osmolarity in the filtrate. The increased fluid movement more strongly deflects single nonmotile cilia on macula densa cells. This increased osmolarity of the forming urine, and the greater flow rate within the DCT, activates macula densa cells to respond by releasing ATP and adenosine (a metabolite of ATP).

ATP and adenosine act locally as paracrine factors to stimulate the myogenic juxtaglomerular cells of the afferent arteriole to constrict, slowing blood flow and reducing GFR. Conversely, when GFR decreases, less Na⁺ is in the forming urine, and most will be reabsorbed before reaching the macula densa, which will result in decreased ATP and adenosine, allowing the afferent arteriole to dilate and increase GFR. NO has the opposite effect, relaxing the afferent arteriole at the same time ATP and adenosine are stimulating it to contract. Thus, NO fine-tunes the effects of adenosine and ATP on GFR.

Paracrine Mechanisms Controlling Glomerular Filtration Rate

Change in GFR	NaCl Absorption	Role of ATP and adenosine/Role of NO	Effect on GFR
Increased GFR	Tubular NaCl increases	ATP and adenosine increase, causing vasoconstriction	Vasoconstriction slows GFR
Decreased GFR	Tubular NaCl decreases	ATP and adenosine decrease, causing vasodilation	Vasodilation increases GFR
Increased GFR	Tubular NaCl increases	NO increases, causing vasodilation	Vasodilation increases GFR
Decreased GFR	Tubular NaCl decreases	NO decreases, causing vasoconstriction	Vasoconstriction decreases GFR

Term Pronunciation Table

Term	Pronunciation	Audio File
Myogenic	myo·gen·ic
Tubuloglomerular	tu·bu·lo·glo·mer·u·lar

terms to know

Myogenic Mechanism

The mechanism by which smooth muscle responds to stretch by contracting; an increase in blood pressure causes vasoconstriction and a decrease in blood pressure causes vasodilation so that blood flow downstream remains steady.

Tubuloglomerular Feedback

The feedback mechanism involving the JGA; macula densa cells monitor Na⁺ concentration in the terminal portion of the ascending loop of Henle and act to cause vasoconstriction or vasodilation of afferent and efferent arterioles to alter GFR.

3. Renin–Angiotensin–Aldosterone System

The renin–angiotensin–aldosterone system (RAAS), illustrated below, critically regulates blood pressure and blood volume over the long term. This system proceeds through several steps to produce angiotensin II, acting to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys directly control blood pressure and volume.

Renin acts on angiotensinogen, which is made in the liver, and converts it to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of antidiuretic hormone (ADH) from the hypothalamus. You may recall from a previous lesson that ADH promotes water retention in the kidneys by signaling the kidneys to reabsorb water. It acts directly on the nephrons and decreases the glomerular filtration rate.

did you know

Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).

Specialized cells in the wall of the atria produce and secrete the peptide hormone atrial natriuretic peptide (ANP). ANP signals the kidneys to reduce sodium reabsorption, thereby decreasing the amount of water reabsorbed from the urine filtrate and reducing blood volume. Other actions of ANP include the inhibition of renin secretion, which inhibits the RAAS and promotes vasodilation, and ADH secretion, which also affects kidney function. Therefore, ANP aids in decreasing blood pressure, blood volume, and blood sodium levels

The renin-angiotensin-aldosterone pathway involves four hormones: renin, which is made in the kidney, angiotensin, which is made in the liver, aldosterone, which is made in the adrenal glands, and A D H, which is made in the hypothalamus and secreted by the posterior pituitary. The adrenal glands are located on top of the kidneys, and the hypothalamus and pituitary are in the brain. The pathway begins when renin converts angiotensinogen into angiotensin I. An enzyme called A C E then converts angiotensin I into angiotensin I I. Angiotensin I I has several direct effects. These include arterial constriction, which increases blood pressure, decreasing the glomerular filtration rate, which results in water retention, and increasing thirst. Angiotensin I I also triggers the release of two other hormones, aldosterone and A D H. Aldosterone causes nephron distal tubules to reabsorb more sodium and water, which increases blood volume. A D H moderates the insertion of aquaporins into the nephridial collecting ducts. As a result, more water is reabsorbed by the blood. A D H also causes arteries to constrict. The hormone A N P is antagonistic to the angiotensin pathway. A N P decreases blood pressure and volume by increasing the glomerulus filtration rate, increasing reabsorption of sodium ions by the nephron, and by inhibiting the release of renin from the kidney and aldosterone from the adrenal gland. — The renin–angiotensin–aldosterone system increases blood pressure and volume. The hormone atrial natriuretic peptide (ANP) has antagonistic effects. (credit: modification of work by Mikael Häggström)

Term Pronunciation Table

Term	Pronunciation	Audio File
Renin–Angiotensin–Aldosterone	re·nin an·gio·ten·sin al·do·ste·rone
Antidiuretic	an·ti·di·uret·ic

term to know

Renin–Angiotensin–Aldosterone System (RAAS)

A system of various hormones, enzymes, proteins, and reactions that regulates blood volume and blood pressure over the long term.

summary

In this lesson, you learned about how blood flow is regulated through the kidney. You first examined how the sympathetic nerves can affect vasodilation and blood flow, and thus blood pressure. You then explored how autoregulation allows kidneys to effectively regulate blood flow rate over a range of blood pressures, specifically how this occurs by the arteriole myogenic mechanism and tubuloglomerular feedback. Finally, you learned about how the renin–angiotensin–aldosterone system regulates long-term blood volume and blood pressure.

Source: THIS TUTORIAL HAS BEEN ADAPTED FROM (1) "ANATOMY AND PHYSIOLOGY 2E" ACCESS FOR FREE AT OPENSTAX.ORG/DETAILS/BOOKS/ANATOMY-AND-PHYSIOLOGY-2E. (2) "BIOLOGY FOR AP COURSES" ACCESS FOR FREE AT OPENSTAX.ORG/DETAILS/BOOKS/BIOLOGY-AP-COURSES. LICENSING (1 & 2): CREATIVE COMMONS ATTRIBUTION 4.0 INTERNATIONAL

Terms to Know

Antidiuretic Hormone (ADH): A hormone that prevents the loss of water.
Myogenic Mechanism: The mechanism by which smooth muscle responds to stretch by contracting; an increase in blood pressure causes vasoconstriction and a decrease in blood pressure causes vasodilation so that blood flow downstream remains steady.
Renin–Angiotensin–Aldosterone System: A system of various hormones, enzymes, proteins, and reactions that regulates blood volume and blood pressure over the long term.
Tubuloglomerular Feedback: The feedback mechanism involving the JGA; macula densa cells monitor Na⁺ concentration in the terminal portion of the ascending loop of Henle and act to cause vasoconstriction or vasodilation of afferent and efferent arterioles to alter GFR.