renal

Blood vessel carrying blood to the kidney.

Arteries carrying blood within the kidney.

Arteries arching over the kidney's nephrons.

Arteries connecting smaller branches.

Blood vessels leading into the glomerulus.

Network of capillaries where filtration begins.

Blood vessels carrying blood away from glomerulus.

Capillaries around renal tubules.

Blood vessel carrying filtered blood from kidney.

Cup-shaped structure surrounding the glomerulus.

First section of the renal tubule.

U-shaped part of the nephron.

Part of Loop of Henle, permeable to water.

Part of Loop of Henle, impermeable to water later.

Specialized cells sensing sodium levels.

Part of the nephron past the Loop of Henle.

Final segment of the nephron.

Process of filtering blood in the glomerulus.

Returning useful molecules to the blood.

Adding substances from the blood to the filtrate.

Removal of waste products from the body.

Hormone that regulates water reabsorption and thirst.

Increased urine output due to high blood pressure.

Increased sodium excretion in response to high blood pressure.

Hormonal pathway regulating blood pressure.

The glomerulus filters plasma and dissolved substances like electrolytes, glucose, hormones, and drugs. It doesn't filter large molecules like proteins or cells.

Glomerular filtrate is the fluid that's filtered from the blood in the glomerulus and enters Bowman's capsule, the start of the renal tubular system.

Reabsorption is the process of returning useful substances from the glomerular filtrate back into the bloodstream through the peritubular capillaries.

Glucose is transported through special carriers in the tubular cells, allowing it to move back into the bloodstream. In healthy individuals, all filtered glucose should be reabsorbed.

Diabetic patients have high blood sugar levels, which can overwhelm the glucose transporters in the tubules. This leads to some glucose not being reabsorbed and ending up in the urine.

Sodium, calcium, bicarbonate, potassium, and many other molecules are reabsorbed through specialized transporters in different parts of the tubules.

Hormones like aldosterone control the reabsorption of substances by influencing transporter activity. This allows us to fine-tune the amount of each substance reabsorbed.

Creatinine is a by-product of muscle metabolism. It is not reabsorbed; it is completely filtered and excreted, making it a marker of kidney function.

Secretion is the process of moving substances from the peritubular capillaries back into the tubular system, where they eventually get excreted.

Hydrogen ions (H+) can be secreted into the tubular system, increasing their concentration in the urine. This helps regulate blood pH.

Excretion is the removal of waste products from the tubular system into the collecting ducts, leading to urine formation and elimination.

Osmoreceptors in the brain sense the concentration of solutes in the blood (osmolarity). High osmolarity indicates dehydration, while low osmolarity suggests overhydration.

Antidiuretic hormone (ADH) is released from the posterior pituitary when plasma osmolarity is high. ADH increases water reabsorption in the distal tubule and collecting ducts, resulting in more concentrated urine.

Increased plasma osmolarity triggers thirst, as the body tries to restore its water balance.

Low plasma osmolarity inhibits ADH release, leading to less water reabsorption and the production of a large volume of dilute urine.

Pressure diuresis is the increase in urine output that occurs when blood pressure rises. This is a protective mechanism to reduce blood volume and lower pressure.

Pressure natriuresis is the increase in sodium excretion that occurs when blood pressure rises, also helping to reduce blood volume and lower pressure.

Renin is synthesized and stored in the juxtaglomerular cells (JG cells) located in the walls of the afferent arterioles.

Decreased arterial pressure in the afferent arterioles triggers the release of renin. This can be caused by a drop in systemic blood pressure or renal ischemia.

Renin converts angiotensinogen, a precursor protein made in the liver, into angiotensin I.

Angiotensin I is mainly converted to angiotensin II in the lung vasculature by the enzyme angiotensin-converting enzyme (ACE).

Angiotensin II is the most potent vasoconstrictor, followed by angiotensin I, and then renin, which has the least vasoactive effect.

The renin-angiotensin system increases blood pressure through vasoconstriction (rapid) and decreased salt and water excretion (slow).

Angiotensin II stimulates the adrenal glands to release aldosterone, which promotes salt and water reabsorption, further increasing blood pressure.

Increased salt intake leads to increased blood volume and pressure. This inhibits renin release, reducing sodium and water retention and lowering blood pressure.

High sodium intake increases extracellular fluid volume, especially in the vascular compartment, leading to higher venous pressure, increased venous return, and ultimately, higher blood pressure.

Diuretic drugs help lower blood pressure by promoting fluid excretion, reducing blood volume, and thus decreasing venous pressure and cardiac output.

Rapid mechanisms include vasoconstriction/dilation and changes in heart rate and contractility. Intermediate mechanisms include the renin-angiotensin system and fluid shifts. Long-term mechanisms include renal-body control (pressure diuresis/natriuresis) and aldosterone.

Increased blood pressure decreases sympathetic activity, promoting diuresis and natriuresis. Conversely, decreased blood pressure increases sympathetic activity, leading to vasoconstriction, increased heart rate, and reduced urine output.

The initial step of blood processing in the kidneys, where plasma and small dissolved molecules are filtered from the blood in the glomerulus.

The process of returning valuable substances (e.g., glucose, water, electrolytes) from the glomerular filtrate back into the bloodstream.

Adding substances from the blood into the glomerular filtrate, often to eliminate waste or regulate blood pH.

The Loop of Henle plays a crucial role in regulating the concentration of urine by creating a concentration gradient in the medulla, allowing for water reabsorption.

Specialized cells in the distal tubule that monitor sodium levels in the filtrate, influencing blood pressure regulation.

This specialized structure in the kidney controls blood pressure by releasing renin, initiating the renin-angiotensin-aldosterone system (RAAS).

A hormonal pathway that regulates blood pressure by increasing water and salt reabsorption, leading to vasoconstriction and increased blood volume.

Reabsorption is the process of returning useful substances from the glomerular filtrate back into the bloodstream through the peritubular capillaries.

Besides glucose, sodium, calcium, bicarbonate, potassium, and many other essential molecules are reabsorbed through specialized transporters in different parts of the tubules.

Aldosterone is a hormone that controls sodium reabsorption. When blood pressure or sodium levels are low, aldosterone is released, causing more sodium to be reabsorbed back into the blood.

The types and concentrations of transporters vary across different sections of the renal tubules, like the proximal and distal tubules.

Diabetes causes 'sweet urine' because high blood glucose levels overwhelm the glucose transporters in the tubules, resulting in excess glucose being excreted in the urine.

Decreased arterial pressure in the afferent arterioles triggers renin release. This can occur due to low systemic blood pressure or reduced blood flow to the kidneys (renal ischemia).

Renin, an enzyme produced in the kidneys, converts angiotensinogen (a protein made in the liver) into angiotensin I, the first step in the renin-angiotensin system.

Angiotensin I is converted to Angiotensin II mainly in the lung vasculature by the enzyme angiotensin-converting enzyme (ACE).

Ranked from least to most vasoactive: Renin, angiotensin I, and angiotensin II. Angiotensin II is the strongest vasoconstrictor.

The renin-angiotensin system regulates blood pressure by two main mechanisms: rapid vasoconstriction throughout the body, mainly in arteries and arterioles, and slower decreased excretion of salt and water by the kidneys.

Angiotensin II stimulates the adrenal glands to release aldosterone, which promotes salt and water reabsorption, further increasing blood pressure.

Increased salt intake leads to higher extracellular fluid volume, increased blood volume, higher blood pressure, and increased renal blood flow. This inhibits renin release, reducing sodium and water retention, and lowering blood pressure.

The renin-angiotensin system inhibits renin release when salt intake is high, thus reducing sodium and water retention and lowering blood pressure. This counteracts the increase in blood volume and pressure caused by salt intake.

Plasma osmolarity is the concentration of solutes in the blood. It reflects how much water is present relative to dissolved substances.

Osmoreceptors are specialized cells located in the hypothalamus of the brain that detect changes in plasma osmolarity.

Antidiuretic hormone (ADH) is a hormone released from the posterior pituitary gland. ADH increases water reabsorption in the kidneys, leading to concentrated urine and reduced water loss.

High plasma osmolarity triggers the release of ADH, leading to increased water reabsorption in the kidneys. This concentrates urine and reduces water loss. It also stimulates thirst.

Low plasma osmolarity inhibits ADH release, leading to less water reabsorption and production of dilute urine. It also inhibits thirst.

Pressure diuresis describes the increase in urine output that occurs when blood pressure rises. This helps to reduce blood volume and lower pressure.

Pressure natriuresis is the increased excretion of sodium that occurs when blood pressure rises. This aids in the reduction of blood volume, contributing to the lowering of pressure.

Renin is synthesized and stored in the juxtaglomerular cells (JG cells) located in the walls of the afferent arterioles of the kidneys.

A decrease in the production and release of renin, an enzyme crucial for regulating blood pressure. This leads to reduced activation of the renin-angiotensin-aldosterone system (RAAS).

A large increase in sodium intake causes a rapid rise in arterial blood pressure. This is because high sodium intake increases extracellular fluids, particularly in the vascular compartment, leading to higher venous pressure, increased cardiac output, and consequently, higher blood pressure.

Chronic high sodium intake, while initially causing a rise in blood pressure, eventually leads to minimal changes. This is because the body adapts and compensates over time, often leading to chronically elevated blood pressure.

Diuretics help lower blood pressure by increasing urine and sodium excretion. This reduces plasma volume, venous pressure, and consequently, cardiac output, ultimately lowering blood pressure.

A state of excessive fluid volume in the body, often due to high sodium levels. This can contribute to high blood pressure.

The amount of blood flowing back to the heart from the veins. It's influenced by factors like venous pressure and the pressure gradient between the veins and heart.

The amount of blood in the ventricle at the end of diastole (relaxation) before contraction. It's a determinant of stroke volume.

The amount of blood ejected from the ventricle during each contraction. It's a measure of the heart's pumping efficiency.

A rapid blood pressure control mechanism. Baroreceptors in the carotid arteries and aorta sense changes in blood pressure and send signals to the brain to adjust heart rate, contractility, and blood vessel diameter.

The sympathetic nervous system responds to high blood pressure by decreasing activity, causing dilation of blood vessels and a slower heart rate. When blood pressure is low, sympathetic activity increases, causing constriction of blood vessels and a faster heart rate.