Renal Physiology Overview

The rate at which blood is filtered by the glomeruli in the kidneys.

The kidney's ability to maintain a nearly constant GFR despite changes in blood pressure.

A type of renal autoregulation where smooth muscle in the afferent arterioles constricts when stretched (high blood pressure) and dilates when not stretched (low blood pressure).

A type of renal autoregulation that adjusts GFR in response to changes in sodium chloride concentration in the filtrate.

Neural and hormonal mechanisms that regulate GFR to maintain systemic blood pressure.

Urine formation involves three key processes: glomerular filtration, tubular reabsorption, and tubular secretion, all working together to regulate body fluid composition.

The first step in urine formation, where a protein-free filtrate is produced in the renal corpuscle of the nephron.

The process of selectively returning essential substances (like water and nutrients) from the filtrate back into the blood.

The process of selectively moving certain substances (like waste products) from the blood into the filtrate of the renal tubule.

The kidneys regulate water balance, electrolyte levels, acid-base balance, and remove wastes from the blood. They also produce hormones and activate vitamin D.

A transport pathway across the cells of the tubule epithelium.

A transport pathway through the spaces between the cells of the tubule epithelium.

The part of the nephron tubule where most reabsorption occurs.

A selectively permeable membrane that allows certain substances to pass through from blood to filtrate in the glomerulus.

In the nephron loop (loop of Henle), water reabsorption becomes independent of solute reabsorption. In the descending limb, water can leave but solutes cannot, while in the ascending limb, water cannot leave but solutes can.

The thin segment passively reabsorbs sodium, while the thick segment actively reabsorbs sodium using a Na+-K+-2Cl- symporter and a Na+-H+ antiporter. Some sodium also moves paracellularly.

Antidiuretic hormone (ADH) causes principal cells of collecting ducts to insert aquaporins in their apical membranes, increasing water reabsorption. Higher ADH levels lead to greater water reabsorption.

Aldosterone targets collecting ducts and the distal convoluted tubule, promoting sodium reabsorption. It increases the production of sodium and potassium channels and sodium-potassium ATPases, leading to increased water reabsorption.

ANP is released by cardiac atrial cells when blood volume or pressure is high. It reduces blood sodium levels, decreasing blood volume and pressure.

Antidiuretic hormone (ADH) causes principal cells of collecting ducts to insert aquaporins in their apical membranes, increasing water reabsorption. Higher ADH levels lead to greater water reabsorption.

Aldosterone targets collecting ducts and the distal convoluted tubule, promoting sodium reabsorption. It increases the production of sodium and potassium channels and sodium-potassium ATPases, leading to increased water reabsorption.

ANP is released by cardiac atrial cells when blood volume or pressure is high. It reduces blood sodium levels, decreasing blood volume and pressure.

The majority of tubular secretion happens in the proximal convoluted tubule (PCT).

Tubule cells can synthesize and secrete substances into the filtrate like bicarbonate ions (HCO3-) to help regulate blood pH.

Tubular secretion can eliminate drugs that are bound to plasma proteins, ensuring they're removed efficiently.

It regulates the amounts of H+ or HCO3- in urine. This allows the kidneys to maintain the proper blood pH balance.

Aldosterone is a hormone that increases sodium (Na+) reabsorption in the distal convoluted tubule and collecting ducts of the nephron. This increases water reabsorption as well, helping regulate blood volume and pressure.

The nephron loop (loop of Henle) is responsible for creating a concentration gradient in the medulla of the kidney. This gradient allows for the reabsorption of water from the collecting ducts, concentrating the urine.

The kidneys regulate blood pH by adjusting the reabsorption and secretion of hydrogen ions (H+), bicarbonate ions (HCO3-), and ammonium ions (NH4+). This helps maintain a stable pH level in the blood.

Most reabsorption of essential substances (like water, glucose, and amino acids) occurs in the proximal tubule of the nephron.

The two routes of tubular reabsorption are the transcellular route, where substances move across the cell membrane, and the paracellular route, where substances move between cells.

The paracellular route is most prominent in the proximal convoluted tubule (PCT) due to its 'leaky' tight junctions.

Sodium ions (Na+) are actively pumped out of the tubule cell across the basolateral membrane by the Na+-K+ ATPase pump. This movement utilizes energy and creates a concentration gradient for further reabsorption.

Sodium ions (Na+) move across the apical membrane through secondary active transport, utilizing the energy stored in the concentration gradient established by the primary active transport. This allows co-transport of other nutrients like glucose and amino acids.

Obligatory water reabsorption is always present in the proximal convoluted tubule (PCT), where water follows the osmotic gradient created by solute reabsorption. Facultative water reabsorption occurs in the collecting ducts only when antidiuretic hormone (ADH) is present, allowing for fine-tuning of water balance.

The maximum rate at which a substance can be reabsorbed by the renal tubules. This limit is determined by the number of carrier proteins available for transport. When carriers are saturated, excess substance is excreted in urine.

The PCT is the primary site of reabsorption in the nephron, responsible for reabsorbing most of the glucose, amino acids, 65% of sodium and water, and other ions. It also reabsorbs all uric acid and half the urea, which is later secreted back into the filtrate.

The process of selectively moving substances from blood into the filtrate within the renal tubules and collecting ducts.

Intrinsic controls (myogenic and tubuloglomerular feedback) maintain constant GFR when blood pressure is normal. Extrinsic controls (neural and hormonal) adjust GFR to maintain systemic blood pressure.

Macula densa cells in the nephron loop sense filtrate NaCl concentration. High NaCl leads to afferent arteriole constriction, lowering GFR and increasing reabsorption time.

A key mechanism for increasing blood pressure. Low BP triggers renin release, leading to angiotensin II production and aldosterone secretion, ultimately raising blood pressure.

The nephron loop (loop of Henle) has distinct water and solute reabsorption patterns. The descending limb allows water to leave but not solutes, while the ascending limb allows solutes to leave but not water.

The thick segment of the ascending limb actively reabsorbs sodium using two key transporters: Na+-K+-2Cl- symporter and Na+-H+ antiporter. Some sodium also moves paracellularly.

Antidiuretic hormone (ADH) increases water reabsorption by causing principal cells in collecting ducts to insert aquaporins in their apical membranes, allowing more water passage.

Aldosterone, a hormone, targets collecting ducts and distal tubules to increase sodium reabsorption. It promotes the synthesis of sodium and potassium channels and sodium-potassium ATPases.

Atrial natriuretic peptide (ANP), released by heart cells when blood volume or pressure is high, reduces blood sodium levels, decreasing blood volume and pressure.