64. Physiology - ADH, Water Excretion, Renin-Angiotensin

The release of antidiuretic hormone (ADH) from the neural lobe of the brain, which affects the permeability of the collecting duct to water.

A measure of solute concentration in a solution, specifically in body fluids.

Specialized areas of the brain outside of the blood-brain barrier that detect changes in osmolality and trigger ADH secretion.

Sensors in the carotid and aortic arch that detect changes in blood pressure.

Stretch receptors in the atria of the heart that detect changes in blood volume.

Approximately 285 ± 5 mosm/kg H2O, a crucial value in regulating ADH.

A 1% increase above normal plasma osmolality triggers a substantial increase in ADH release.

ADH release stimulated by changes in blood pressure or volume, rather than osmolality.

Significant blood loss, resulting in decreased blood volume and pressure.

ADH secretion increases substantially in response to the decreased blood pressure and volume.

Antidiuretic hormone, also known as vasopressin (AVP), is a peptide hormone produced in the hypothalamus. It's released into the bloodstream from the posterior pituitary gland and regulates water reabsorption in the kidneys.

The concentration of solutes dissolved in blood plasma. It reflects the water balance in the body. A higher osmolality indicates less water.

Increased plasma osmolality (dehydration, decreased water content) stimulates ADH release. Conversely, decreased plasma osmolality (increased water content) inhibits ADH release.

Baroreceptors in the arteries and atria detect blood pressure. Lower blood pressure or volume triggers the release of ADH. Higher blood pressure or volume inhibits ADH release.

Nerve endings in large arteries (aorta and carotid) that detect pressure.

Nerve endings in the atria (heart chambers) that detect pressure; specifically, low pressure.

ADH is released via neurosecretion; i.e. from nerve cells.

Increased plasma osmolality (osmoreceptors), decreased arterial pressure, decreased blood volume, and various hormones, neurotransmitters, and drugs.

Sensory neurons in the brain that detect changes in plasma osmolality.

A condition where the body loses more water than it takes in.

A condition where the body takes in more water than it loses.

Sensory receptors in the aortic arch and carotid sinus that detect changes in blood pressure.

Sensory receptors primarily in the atria that detect changes in blood volume.

Increases water reabsorption in the kidney's collecting ducts, which concentrates urine and conserves water.

Substances like hormones, neurotransmitters, and drugs stimulate or inhibit ADH release; these factors are not directly related to plasma osmolarity or blood volume changes.

A potentially fatal condition caused by excessive water intake, leading to brain edema.

High concentration of salt within the kidney's medulla, essential for water reabsorption.

ADH (antidiuretic hormone) binds to V2 receptors on collecting tubules, triggering cAMP production and AQP2 (aquaporin 2) insertion into the apical membrane, increasing water reabsorption.

Insertion of aquaporin-2 channels into the apical membrane of collecting duct cells, enabling water passage from the tubule to the bloodstream.

Increased water reabsorption leads to concentrated urine as water is drawn into the bloodstream in response to the osmotic gradient maintained by the kidney's tubules.

Decreased ADH levels cause AQP2 removal from the apical membrane and vesicle recycling, making the membrane impermeable to water and allowing for dilute urine.

Condition characterized by excessive urination due to lack of ADH secretion (central DI) or ADH receptor/AQP2 malfunction (nephrogenic DI).

Drinking large volumes of water quickly can lead to decreased urine osmolality.

Excessive water intake after a marathon can severely lower plasma osmolality.

The release of renin, an enzyme that starts the renin-angiotensin-aldosterone system (RAAS)

Blood pressure in a specific location, affecting Juxtaglomerular (JG) cell stretch and renin release.

Signals from the nervous system that influence renin release through beta receptors on JG cells.

Cells in the kidney that sense sodium chloride (salt) concentration in the tubule.

Sodium chloride concentration in the tubule, influencing renin secretion.

A system in the body that regulates blood pressure by controlling salt and water balance.

A hormone that constricts blood vessels, increases sodium reabsorption, and raises blood pressure.

A hormone that increases sodium reabsorption in the kidneys, thus promoting water retention and raising blood pressure.