Renal System 4 Lecture 26 Flashcards
Fluid dynamics
Water: Water equilibrates rapidly between the intracellular fluid (ICF) and extracellular fluid (ECF), which decreases osmolarity. This is because water moves freely across cell membranes to balance concentrations on both sides.
Isotonic Solution: An isotonic solution has the same osmolarity as the plasma, so it remains in the ECF and doesn’t affect plasma osmolarity. These solutions are commonly used in clinical settings to maintain hydration without causing fluid shifts.
Hypertonic Solution: A hypertonic solution has a higher osmolarity than the intracellular environment, so it draws water out of cells. This results in an increase in the volume of the plasma and ECF, while decreasing the intracellular cell volume. This kind of solution is used to treat conditions like edema or hyponatremia (low sodium levels).
ADH release
ADH Production: The precursor to ADH is synthesized in the hypothalamus, particularly in the supraoptic and paraventricular nuclei, and stored in vesicles in the posterior lobe of the pituitary gland.
Osmoreceptors and Baroreceptors:
Osmoreceptors in areas like the OVLT (organum vasculosum of the lamina terminalis) and SFO (subfornical organ) sense changes in the body’s fluid balance.
They are sensitive to increases in sodium ion (Na⁺) concentration and osmolarity (the concentration of solutes in body fluids).
When these receptors detect an increase in osmolarity or Na⁺ concentration, they send signals to the hypothalamus.
ADH Release: In response to these signals, the hypothalamus triggers the release of ADH from the posterior pituitary gland into the bloodstream.
Function of ADH: Once released, ADH helps the kidneys conserve water by increasing water reabsorption in the collecting ducts, leading to more concentrated urine and maintaining body fluid balance.
Osmoreceptors
Stretch-Activated Cation Channels: Osmoreceptors have specialized channels that open when the cell membrane is stretched. These channels allow cations like sodium (Na⁺) to enter the cell.
Hypertonic Extracellular Fluid:
If the extracellular fluid becomes hypertonic (higher concentration of solutes outside the cell than inside), water is drawn out of the osmoreceptor cells.
As water leaves the cell, the cell shrinks in size.
Cell Shrinkage and Channel Activation:
When the osmoreceptor cells shrink, the tension on the cell membrane increases, causing the stretch-activated cation channels to open.
The opening of these channels allows sodium ions to flow into the cells.
Triggering Action Potentials:
The influx of sodium ions depolarizes the cell, triggering action potentials.
These action potentials are then sent to the brain to signal changes in osmolarity, prompting the release of antidiuretic hormone (ADH) to retain water and restore fluid balance.
Relationship between plasma osmolality (the concentration of solutes in the blood) and the release of antidiuretic hormone (ADH)
Plasma ADH (AVP) Increases with Osmolality:
As plasma osmolality increases, the release of ADH also increases. This is shown by the upward slope of the curves on the graph. ADH helps retain water in the kidneys, reducing urine volume to concentrate body fluids when osmolality is high.
a = Normal Threshold for ADH Release:
The point labeled “a” represents the normal threshold for ADH release. This is typically around the normal plasma osmolality level (close to 280–290 mOsm). At this point, ADH secretion begins to regulate water retention.
b = Threshold for Thirst Sensation:
The point labeled “b” indicates the threshold where the sensation of thirst occurs. This happens at a slightly higher plasma osmolality (around 290–300 mOsm), prompting the body to increase water intake to counter the increased osmolarity.
Volume Expansion and Contraction:
The green line represents volume contraction, which is when blood volume is reduced (e.g., dehydration). In this case, ADH is released at a lower osmolality (earlier) to retain as much water as possible.
The red line represents euvolemia (normal blood volume), which is the typical response to changes in osmolality.
The blue line represents volume expansion, which occurs when blood volume is increased. In this case, ADH release is delayed (occurs at a higher osmolality) because there is less need to retain water.
Normal Plasma Osmolality:
Normal plasma osmolality is around 290 mOsm. This is the set point for fluid balance under normal conditions.
Sensitivity of ADH Release:
The sensitivity of ADH release to changes in plasma osmolality is also affected by blood volume. When blood volume decreases (hypovolemia), ADH release is more sensitive, meaning it occurs earlier to help conserve water.
How antidiuretic hormone (ADH), also known as vasopressin, acts on the collecting duct and distal convoluted tubule of the kidney to regulate water reabsorption.
Action of ADH:
ADH targets the last part of the distal convoluted tubule and the collecting duct.
It binds to vasopressin receptors on the membrane of the collecting duct cells, initiating a signaling cascade inside the cell.
Aquaporin-2 Insertion:
Once ADH binds to its receptor, a second messenger system is activated, specifically involving cAMP (cyclic AMP).
This signaling pathway stimulates the insertion of aquaporin-2 (AQP2) channels into the apical membrane of the collecting duct cells.
Aquaporin-2 channels are water channels, allowing water to pass from the tubule (inside the kidney) into the cell.
Water Reabsorption:
With the aquaporin-2 channels now inserted into the membrane, water moves from the filtrate (inside the kidney tubule) into the collecting duct cell, following the osmotic gradient.
The filtrate usually has lower osmolarity (~300 mOsm), while the medullary interstitial fluid has a much higher osmolarity (up to 700 mOsm), which draws water out.
Basolateral Membrane Permeability:
The basolateral membrane (the side facing the bloodstream) is always relatively permeable to water, meaning that water can move out of the cell into the bloodstream by osmosis, once it’s inside the cell.
This mechanism allows the body to reabsorb water efficiently, reducing urine output and helping to concentrate the urine.
Osmotic Gradient:
The osmotic gradient between the collecting duct (300 mOsm) and the medullary interstitial fluid (up to 700 mOsm) is maintained by the countercurrent mechanism in the kidney, allowing for efficient water reabsorption.
Key Sections of the Nephron
Glomerulus & Bowman’s Capsule:
Osmolarity: 300 mOsm.
Initial filtration of blood happens here, and the filtrate moves through the nephron.
Proximal Convoluted Tubule:
Sodium (Na+) movement: Active reabsorption occurs here (yellow arrows).
Passive Water movement: Water follows sodium via osmosis (blue arrows).
Glucose: Reabsorption of glucose occurs here (purple arrows).
Descending Loop of Henle:
Passive Water movement: Water is reabsorbed passively due to the osmotic gradient (blue arrows).
No Sodium movement: This part is impermeable to sodium.
Ascending Loop of Henle:
Sodium movement: Active transport of sodium occurs (yellow arrows).
Water impermeable: No water movement in this segment (marked impermeable to water).
Distal Convoluted Tubule:
Osmolarity: 100 mOsm.
More controlled reabsorption of ions like sodium takes place.
Collecting Duct:
Aquaporin-2 via ADH: Water permeability is regulated by ADH (vasopressin). Aquaporin-2 channels allow water to be reabsorbed (gray arrows), especially as the tubule passes through the highly concentrated medulla (osmolarity can reach up to 1200 mOsm at the end).
Summary of Functions:
Sodium Reabsorption: Active in the proximal convoluted tubule and thick ascending loop.
Water Reabsorption: Passive in the proximal convoluted tubule and descending loop, and regulated by ADH in the collecting duct.
Glucose Reabsorption: Happens in the proximal convoluted tubule.
ADH and Aquaporin-2: ADH increases water permeability in the collecting duct, allowing more water to be reabsorbed based on the body’s needs, concentrating the urine.
Mechanism for forming concentrated urine
ADH’s Role:
ADH facilitates the reabsorption of water in the distal convoluted tubule (DCT) and the collecting duct.
ADH increases water permeability, leading to water retention.
The presence of ADH results in highly concentrated urine, with osmolarity reaching up to 1200 mOsm.
The Osmolarity Gradient:
The nephron operates with a gradient of increasing osmolarity from the cortex (300 mOsm) to the inner medulla (1200 mOsm).
This gradient is crucial for water reabsorption and the concentration of urine.
Water and Sodium Movement:
Descending Limb (Loop of Henle): Water is passively reabsorbed (blue arrows), increasing the osmolarity of the filtrate as it moves deeper into the medulla.
Ascending Limb (Loop of Henle): Sodium chloride (NaCl) is actively transported out of the filtrate (red arrows), decreasing the osmolarity of the filtrate.
Collecting Duct: In the presence of ADH, water is reabsorbed from the filtrate into the concentrated interstitial fluid of the medulla, further concentrating the urine.
Final Urine Concentration:
The interstitial fluid in the medulla reaches a concentration of 1200 mOsm, allowing for the production of highly concentrated urine when ADH is present.
The volume of the urine is small but very concentrated, conserving water in the body.
Physiological regulation of antidiuretic hormone (ADH) release
Stimuli for ADH Release:
Increased osmolarity or Na⁺ concentration in plasma: Osmoreceptors in the hypothalamus detect an increase in osmolarity (i.e., higher solute concentration in the blood).
Decreased plasma volume or blood pressure (BP): Baroreceptors located in the atria of the heart and large blood vessels detect a drop in blood volume or BP (usually by 10-15%).
Osmoreceptors and Baroreceptors:
Osmoreceptors in the hypothalamus stimulate ADH release in response to increased plasma osmolarity or sodium levels.
Baroreceptors stimulate ADH release when they detect a decrease in blood pressure or volume. Baroreceptor input can inhibit ADH release if the blood pressure is stable or high.
Posterior Pituitary:
The hypothalamus signals the posterior pituitary gland, which releases ADH into the bloodstream in response to these stimuli.
ADH Action on the Kidneys:
ADH targets the collecting ducts in the kidneys.
It increases the permeability of the collecting ducts to water, which results in increased water reabsorption from the filtrate back into the bloodstream.
Resulting Effects:
Increased water reabsorption leads to:
- Decreased urine volume (scant, concentrated urine).
- Increased plasma volume and decreased plasma osmolarity (i.e., blood becomes more diluted).
Negative Feedback Loop:
Once plasma volume and osmolarity return to normal, negative feedback mechanisms inhibit further ADH release, helping maintain fluid balance in the body.
ADH Release Based on Osmolarity and Volume
Volume Contraction (green line):
When the body is experiencing volume contraction (low blood volume), ADH is released at lower plasma osmolarity levels (~280 mOsm). This helps the body conserve water even when plasma osmolarity isn’t significantly increased.
Euvolemia (Normal Blood Volume) (red line):
When blood volume is normal, ADH release follows the typical relationship with plasma osmolarity, where ADH starts increasing around 290 mOsm.
Volume Expansion (blue line):
When the body has excess blood volume, ADH release is suppressed, and it occurs only when plasma osmolarity rises significantly above the normal range (>300 mOsm).
ADH’s Role in Water Balance
High Plasma Osmolarity (left side):
Stimulus: High plasma osmolarity (increased solutes, e.g., sodium) or low circulating volume stimulates the release of ADH.
Effects:
Increased ADH release leads to:
Increased thirst, prompting the intake of water.
Increased water reabsorption in the kidneys, which decreases urine output and retains water in the body.
Outcome: The combined effect of drinking water and conserving it restores normal plasma osmolarity and volume.
Low Plasma Osmolarity (right side):
Stimulus: Low plasma osmolarity (dilute plasma) or high circulating volume reduces the release of ADH.
Effects:
Decreased ADH release leads to:
Decreased thirst, reducing water intake.
Reduced water reabsorption in the kidneys, increasing urine output.
Outcome: This loss of water helps restore normal plasma osmolarity by removing excess water from the body.
Renin-Angiotensin-Aldosterone System (RAAS) and its functions
Hormone system that regulates blood pressure, fluid balance, and electrolyte levels.
Main functions:
Maintaining Sodium (Na⁺) Balance:
The RAAS is crucial for regulating the amount of sodium in the body. Sodium balance is vital for fluid balance, nerve function, and muscle contractions.
When sodium levels in the blood are low, RAAS helps increase sodium reabsorption in the kidneys to prevent excessive sodium loss in urine.
Blood Pressure Regulation:
The RAAS plays an important role in regulating blood pressure. When blood pressure drops, this system is activated to increase blood pressure by:
Promoting sodium and water reabsorption in the kidneys (increasing blood volume).
Causing vasoconstriction (narrowing of blood vessels), which raises blood pressure.
What are ACE inhibitors?
Mechanism of Action:
ACE inhibitors (such as Lisinopril, shown on the slide) block the action of the enzyme angiotensin-converting enzyme (ACE), which converts angiotensin I to angiotensin II.
Angiotensin II is a powerful vasoconstrictor and stimulates the release of aldosterone, leading to sodium and water retention. By inhibiting this conversion, ACE inhibitors reduce the levels of circulating angiotensin II.
Clinical Uses:
ACE inhibitors are used clinically to promote sodium (Na⁺) loss from the body, with water following due to osmosis. This helps reduce fluid overload and lowers blood pressure.
They are commonly prescribed for patients with conditions like hypertension, heart failure, and chronic kidney disease because they help manage blood pressure and fluid balance.
What is edema?
The image of swollen ankles and feet represents edema, which occurs due to fluid retention in the tissues. This is a common symptom in patients with heart failure or kidney issues.
Role of the renin-angiotensin-aldosterone system (RAAS) in regulating glomerular filtration and blood pressure
Macula densa cells: These cells in the distal convoluted tubule sense low sodium levels in the filtrate. This triggers the release of nitric oxide (vasodilating the afferent arteriole) and the enzyme renin from the juxtaglomerular cells.
Renin release: Triggered by low sodium, decreased perfusion pressure in the afferent arteriole, or increased sympathetic activity (e.g., due to low blood pressure). Renin converts angiotensinogen (produced by the liver) into angiotensin I.
Angiotensin-converting enzyme (ACE): This enzyme, mainly from the lungs, converts angiotensin I to angiotensin II, which is a potent vasoconstrictor and stimulates the release of aldosterone (leading to sodium retention).
Angiotensin II: While a vasoconstrictor, it specifically constricts the efferent arteriole, helping maintain the glomerular filtration rate (GFR) even when blood pressure is low. Though Tortora’s text suggests that angiotensin II reduces GFR, the constriction of the efferent arteriole actually helps maintain GFR, thanks to tubuloglomerular feedback mechanisms.
Tubuloglomerular feedback: This system helps regulate the balance between afferent and efferent arteriole tone, ensuring GFR remains relatively stable despite fluctuations in blood pressure. Nitric oxide relaxes the afferent arteriole while angiotensin II constricts the efferent arteriole, maintaining glomerular hydrostatic pressure and GFR.
How does juxtaglomerular apparatus (JGA) play a crucial role in regulating blood pressure?
Macula Densa Cells (a)
These specialized cells are located in the distal convoluted tubule (DCT) and are sensitive to sodium chloride (NaCl) levels in the filtrate.
When there is a decrease in NaCl content, the macula densa cells respond by releasing prostaglandins. This signals nearby juxtaglomerular cells to release renin, which activates the RAAS.
Juxtaglomerular Cells (b)
The juxtaglomerular cells are located in the afferent arteriole, which supplies blood to the glomerulus. These cells are also called granular cells because they contain renin.
When signaled (e.g., by prostaglandins or other factors), they release renin into the bloodstream, initiating the RAAS cascade, which helps regulate blood pressure.
Response to Decreased Pressure or
Sympathetic Activity (c)
When there is a decrease in blood pressure or an increase in sympathetic nervous system activity, the juxtaglomerular cells are stimulated to release renin. This occurs through direct pressure sensors in the afferent arteriole and increased signaling from the sympathetic nervous system.
Angiotensin II as a Vasoconstrictor:
Ang II is a potent vasoconstrictor, which means it narrows blood vessels. However, its effects are specific depending on the part of the renal vasculature it acts upon.
Vasoconstriction of the Efferent Arteriole:
When Ang II constricts the efferent arteriole (the vessel leaving the glomerulus), this helps maintain or increase glomerular filtration rate (GFR).
By constricting the efferent arteriole, the pressure in the glomerulus remains high, ensuring that filtration continues even when blood pressure is low or renal perfusion is reduced. This is crucial for maintaining GFR during times of low systemic blood pressure.
Tubuloglomerular Feedback:
Tubuloglomerular feedback refers to the regulation of GFR based on signals from the macula densa (which senses sodium chloride concentration in the distal tubule). If Ang II constricts the afferent arteriole (which supplies blood to the glomerulus), this feedback mechanism counteracts that effect to protect the GFR.
The image indicates that Ang II’s effects on the afferent arteriole are counteracted by the tubuloglomerular feedback, helping to balance the pressure and preserve filtration.
Combined effect of tubuloglomerular feedback and Angiotensin II on glomerular filtration rate (GFR)
Decreased Arterial Pressure:
A drop in arterial pressure leads to a decrease in glomerular hydrostatic pressure, which lowers GFR.
Tubuloglomerular Feedback Mechanism:
The macula densa cells in the distal tubule detect changes in the sodium chloride (NaCl) concentration in the filtrate.
If there’s a decrease in NaCl due to lower GFR, this signals the release of renin from the juxtaglomerular apparatus.
Renin activates the RAAS, leading to increased Angiotensin II levels.
Effects of Angiotensin II:
Angiotensin II causes vasoconstriction of the efferent arteriole. This action helps to increase glomerular pressure, which helps maintain or increase GFR despite the low arterial pressure.
At the same time, Angiotensin II slightly constricts the afferent arteriole, but tubuloglomerular feedback counteracts this, ensuring that blood can still flow into the glomerulus to maintain filtration.
Overall Effect:
The net effect of these combined actions is to restore GFR towards normal despite the decrease in arterial pressure.
Efferent arteriole constriction helps maintain glomerular pressure and filtration.
Afferent arteriole regulation via tubuloglomerular feedback ensures appropriate blood flow into the glomerulus.
Overview of how Angiotensin II (Ang II) increases sodium (Na⁺) reabsorption in the proximal tubule of the kidney
Action of Angiotensin II on Sodium Reabsorption:
Angiotensin II directly increases sodium reabsorption in the proximal tubule.
It does so by upregulating Na⁺/H⁺ exchangers (NHE) on the luminal (apical) membrane of tubular cells, as well as influencing the Na⁺/K⁺ ATPase pump on the basolateral membrane, which moves sodium into the interstitial fluid and back into the bloodstream.
Mechanism in Proximal Tubule:
Na⁺/H⁺ Exchanger (NHE): This transporter exchanges sodium (Na⁺) from the tubular lumen with hydrogen ions (H⁺), facilitating sodium reabsorption from the filtrate.
Na⁺/K⁺ ATPase: This pump moves sodium from the tubular cells into the renal interstitial fluid and the vasa recta (blood vessels), maintaining a low intracellular sodium concentration, allowing more sodium to be absorbed.
Angiotensin II acts via its AT₁ receptors, which stimulate these processes.
Net Effect:
The net effect of Angiotensin II action in the proximal tubule is an increase in sodium and water reabsorption. This process helps to increase blood volume and maintain blood pressure during conditions of low blood volume or low sodium.
Full process of the Renin-Angiotensin-Aldosterone System (RAAS)
Triggering Factors:
Dehydration, Na⁺ deficiency, or hemorrhage (Step 1) cause a decrease in blood volume (Step 2) and subsequently, a decrease in blood pressure (Step 3).
Renin Release:
The juxtaglomerular cells of the kidneys detect the drop in blood pressure and release renin (Step 4 and 5).
Angiotensinogen
Conversion:
Renin acts on angiotensinogen, a protein produced by the liver (Step 6), and converts it into angiotensin I (Step 7).
Angiotensin I to Angiotensin II:
As blood circulates through the lungs, the enzyme ACE (Angiotensin-Converting Enzyme) converts angiotensin I into angiotensin II (Step 9), the active form.
Effects of Angiotensin II:
Angiotensin II has multiple effects:
It stimulates the release of aldosterone from the adrenal cortex (Step 10 and 11).
It causes vasoconstriction of arterioles (Step 15), which increases blood pressure.
Aldosterone’s Role:
Aldosterone acts on the kidneys to increase Na⁺ and water reabsorption in the distal tubules and collecting ducts (Step 12), raising blood volume (Step 13).
Aldosterone also increases K⁺ excretion in the extracellular fluid (Step 16), maintaining electrolyte balance.
Restoration of Blood Pressure:
Together, the vasoconstriction and increased blood volume lead to increased blood pressure until it returns to normal (Step 14).
Key effects of Angiotensin II
What happens when you increase salt intake?
Trigger: Hypovolemic Shock
Trigger: Hypovolemic Shock
Hypovolemic shock occurs due to moderate or severe fluid loss (e.g., from hemorrhage, dehydration), leading to decreased blood volume and blood pressure.
Receptors:
Baroreceptors in the juxtaglomerular cells of the kidneys and the carotid sinus and aortic arch detect this decrease.
The kidneys respond by increasing renin secretion, while the baroreceptors send signals through the nervous system indicating a decrease in nerve impulses due to lower pressure.
Control Centers:
The RAAS is activated when the kidneys release renin. Renin leads to the formation of angiotensin II, which causes vasoconstriction and the release of aldosterone from the adrenal cortex.
The hypothalamus and posterior pituitary release ADH in response to the low blood volume and pressure.
The cardiovascular center in the medulla oblongata increases sympathetic stimulation, causing further release of hormones from the adrenal medulla and enhancing cardiovascular responses.
Effectors:
Adrenal Cortex:
Releases aldosterone, which promotes sodium and water reabsorption in the kidneys.
This increases blood volume and helps raise blood pressure.
Kidneys:
The kidneys conserve salt and water under the influence of aldosterone and ADH, which also contributes to increasing blood volume.
Blood Vessels:
Angiotensin II and the increased sympathetic stimulation cause vasoconstriction, which increases systemic vascular resistance. This helps restore blood pressure.
Heart:
The heart responds to sympathetic stimulation by increasing heart rate and contractility, which helps boost cardiac output and blood pressure.
Responses:
Increased blood volume: From kidney reabsorption of water and sodium.
Increased systemic vascular resistance: From vasoconstriction, helping to raise blood pressure.
Increased blood pressure: From the combined effects of increased blood volume, vascular resistance, and cardiac output.
Restoration of Homeostasis:
Once these responses are in effect, blood volume and blood pressure return to normal levels, restoring homeostasis.
Thirst mechanism for regulating water intake
Triggers for Thirst:
The primary stimulus for thirst is an increase in plasma osmolarity (due to dehydration or high sodium intake), detected by osmoreceptors in the hypothalamus.
A decrease in plasma volume can also contribute to triggering thirst, though this is considered a minor stimulus compared to plasma osmolarity.
Plasma Osmolarity Pathway:
When plasma osmolarity increases, there’s a reduction in saliva production, leading to dry mouth.
This activates the hypothalamic thirst center, which creates the sensation of thirst.
When a person drinks, water moistens the mouth, stretches the stomach and intestines, and is absorbed into the bloodstream, helping to reduce plasma osmolarity.
Plasma Volume Pathway:
A decrease in blood volume (often due to low fluid intake or fluid loss) triggers the Renin-Angiotensin System (RAAS).
This leads to increased production of Angiotensin II, which can also stimulate thirst as part of its role in fluid retention and blood pressure regulation.
Thirst vs. ADH:
Thirst is considered a more behavior-driven mechanism and tends to be less sensitive than Antidiuretic Hormone (ADH) in regulating water balance.
ADH responds more precisely to changes in plasma osmolarity and directly promotes water reabsorption in the kidneys.
Graph Representation:
The graph compares the thresholds for ADH release (green line) and the thirst sensation (red line) relative to plasma osmolarity.
Thirst typically occurs at higher osmolarity levels compared to ADH release, indicating that ADH is the body’s first line of defense against dehydration, with thirst serving as a backup mechanism to encourage water intake.
Role of Atrial Natriuretic Peptide (ANP) in regulating blood volume and blood pressure. ANP is a hormone produced by the heart, and it acts in opposition to the Renin-Angiotensin-Aldosterone System (RAAS) to lower blood pressure and blood volume.
Trigger for ANP Release:
ANP is released from the atria of the heart in response to increased stretching of the atrial walls, which occurs when there is increased blood volume or increased blood pressure.
Main Effects of ANP:
ANP reduces blood volume and blood pressure by targeting multiple systems:
Inhibits Renin Release: ANP decreases renin release from the juxtaglomerular (JG) apparatus in the kidneys, which reduces the production of Angiotensin II.
Inhibits ADH Release: ANP suppresses the release of Antidiuretic Hormone (ADH) from the hypothalamus and posterior pituitary, reducing water reabsorption by the kidneys.
Inhibits Aldosterone Release: ANP also decreases aldosterone secretion from the adrenal cortex, which further reduces sodium (Na⁺) and water reabsorption by the kidneys.
Effects on the Kidneys:
Inhibits Na⁺ and Water Reabsorption: By reducing aldosterone and ADH, ANP decreases the reabsorption of sodium and water in the collecting ducts of the kidneys, promoting their excretion.
Increases GFR (Glomerular Filtration Rate): ANP promotes vasodilation of the afferent arteriole, increasing the filtration rate in the kidneys, which further helps to reduce blood volume by excreting more fluid.
Overall Outcome:
Decreased Blood Volume: By increasing sodium and water excretion, ANP lowers blood volume.
Decreased Blood Pressure: Vasodilation and reduced blood volume lead to a drop in blood pressure.
Negative Feedback: As blood volume and pressure decrease, ANP levels drop, restoring homeostasis.
