Renal Autoregulation and Mechanisms

The kidney's ability to adjust blood flow and urine production.

Intrinsic mechanisms are internal processes within the kidney that manage blood flow and urine production. Examples include the myogenic mechanism and tubuloglomerular feedback.

The myogenic mechanism is the process of smooth muscle in the afferent arteriole (blood vessel leading to the glomerulus) contracting or relaxing in response to changes in blood pressure.

Higher blood pressure stretches the afferent arteriole, causing smooth muscle contraction, which narrows the vessel and reduces blood flow to the glomerulus, ultimately lowering the glomerular filtration rate (GFR).

Lower blood pressure causes relaxation of the afferent arteriole's smooth muscle, leading to dilation of the vessel, increasing blood flow and glomerular filtration rate (GFR).

The tubuloglomerular feedback (TGF) mechanism is another internal process used by the kidney to regulate filtration. It involves specialized cells in the juxtaglomerular apparatus (JGA), which sense changes in the concentration of sodium chloride (NaCl) in the tubule fluid.

If NaCl concentration in the tubule fluid is high, TGF triggers the production of vasoconstrictors, leading to constriction of the afferent arteriole, reducing blood flow and GFR.

If NaCl concentration is low, TGF triggers the production of vasodilators, causing dilation of the afferent arteriole, increasing blood flow and GFR.

When blood pressure increases, more blood flows to the afferent arteriole (AA). This stretches the AA's smooth muscle cells, causing them to vasoconstrict. This reduces glomerular blood flow (GBF) and glomerular filtration rate (GFR).

When blood pressure decreases, less blood flows to the afferent arteriole (AA). This relaxes the AA's smooth muscle cells, causing them to vasodilate. This increases glomerular blood flow (GBF) and glomerular filtration rate (GFR).

The tubuloglomerular feedback (TGF) mechanism regulates GFR by sensing sodium chloride (NaCl) levels in the distal convoluted tubule (DCT). When NaCl levels are high, the macula densa cells in the DCT signal the afferent arteriole to constrict, reducing GFR.

When blood pressure is high, the TGF mechanism responds by constricting the afferent arteriole. This reduces GFR back to normal levels.

When blood pressure is low, the TGF mechanism responds by dilating the afferent arteriole. This increases GFR back to normal levels.

Specialized sensory cells located in the distal convoluted tubule (DCT) of the nephron. They detect changes in sodium chloride (NaCl) concentration in the tubular fluid.

The macula densa cells release adenosine when they detect high NaCl levels in the DCT. Adenosine then vasoconstricts the afferent arteriole (AA) and inhibits the juxtaglomerular (JG) cells, leading to a decrease in glomerular filtration rate (GFR).

The macula densa cells release prostaglandin I2 (PGI2) and nitric oxide (NO) when they detect low NaCl levels in the DCT. These substances vasodilate the afferent arteriole (AA), increasing glomerular blood flow (GBF) and GFR, which in turn increases NaCl filtration.

These cells are located near the glomerulus and are responsible for producing renin, a hormone that ultimately increases blood pressure.

A hormone produced by the JG cells. It triggers a cascade of events leading to an increase in blood pressure.

Measure of the average pressure in the arteries during a cardiac cycle.

It refers to the kidney's ability to maintain a stable glomerular filtration rate (GFR) despite changes in blood pressure.

These cells, located in the juxtaglomerular apparatus (JGA), are sensitive to changes in blood pressure.

It is an enzyme released by the juxtoglomerular cells in response to low blood pressure.

Angiotensin II is a potent vasoconstrictor, meaning it constricts blood vessels, which increases systemic vascular resistance (SVR) and blood pressure.

Angiotensin II stimulates the release of aldosterone from the adrenal glands.

Angiotensin II acts on the collecting ducts of the kidneys, promoting water reabsorption.

Angiotensin II stimulates the release of antidiuretic hormone (ADH) from the posterior pituitary gland.

It is a hormone also known as antidiuretic hormone (ADH) or vasopressin.

ADH acts on the collecting ducts of the kidneys, increasing water reabsorption and leading to concentrated urine.

The myogenic mechanism is the intrinsic ability of the afferent arteriole's smooth muscle to contract or relax in response to blood pressure changes, helping to maintain a constant glomerular filtration rate (GFR).

When blood pressure increases, it stretches the afferent arteriole, causing its smooth muscle to contract, narrowing the vessel and reducing blood flow to the glomerulus, thereby decreasing GFR.

When blood pressure decreases, the afferent arteriole relaxes, widening the vessel and increasing blood flow to the glomerulus, thereby increasing GFR.

Tubuloglomerular feedback (TGF) is another intrinsic mechanism regulating GFR, involving specialized cells within the juxtaglomerular apparatus (JGA) that sense changes in the concentration of sodium chloride (NaCl) in the tubule fluid.

When NaCl concentration in the tubule fluid is high, TGF triggers the release of vasoconstrictors, leading to constriction of the afferent arteriole, reducing blood flow and GFR.

When NaCl concentration in the tubule fluid is low, TGF triggers the release of vasodilators, causing dilation of the afferent arteriole, increasing blood flow and GFR.

Atrial natriuretic peptide (ANP) is a hormone released from the heart in response to high blood pressure (BP) that helps lower BP by counteracting the effects of angiotensin II.

ANP blocks the release of aldosterone, preventing sodium and water reabsorption in the kidneys, which leads to increased urination and reduced blood volume, ultimately lowering BP.

ANP directly dilates blood vessels, reducing the overall resistance to blood flow (SVR), which lowers blood pressure.

ANP blocks the effects of angiotensin II, reducing vasoconstriction in the efferent arterioles and systemic vessels, which helps lower blood pressure.

Sympathetic nervous system activation is a key mechanism to increase blood pressure when it is low. It works by increasing heart rate and contractility, constricting blood vessels, and triggering the release of renin.

When blood pressure is low, baroreceptors in the body sense the change and send signals to the medulla oblongata in the brain.

The medulla oblongata receives signals from the baroreceptors and activates the sympathetic nervous system fibers in the thoracic region.

Norepinephrine and epinephrine are released from the sympathetic nerve fibers in the thoracic region, leading to increased heart rate (chronotropic effect) and increased contractility (inotropic effect).

Norepinephrine and epinephrine constrict afferent and efferent arterioles, reducing blood flow to the kidneys, ultimately decreasing glomerular filtration rate.

Norepinephrine and epinephrine constrict systemic vessels, increasing systemic vascular resistance (SVR) and thus increasing blood pressure.

Norepinephrine and epinephrine stimulate the β1 receptors on juxtaglomerular cells in the kidneys, leading to the release of renin, which in turn triggers the renin-angiotensin-aldosterone system, ultimately increasing blood pressure.

The sympathetic nervous system is responsible for the body's 'fight or flight' response, where it acts to increase blood pressure in times of stress or danger.

The sympathetic nervous system has opposite effects on the heart and vessels when blood pressure is high.

The sympathetic nervous system utilizes norepinephrine and epinephrine to mediate its effects on the body to restore normal blood pressure.