Unit 4 Flashcards
Study
What are the consequences of a typical North American diet high in NaCl on body osmolarity without water intake?
Consuming 9g NaCl per day without additional water leads to an increase in [Na+] in the extracellular fluid (ECF), resulting in hyperosmolarity and potential cell shrinkage. If the kidneys are not clearing any salt, 1.1 L extra water per day is needed to maintain normal [Na+] in ECF.
How does the body respond to increased salt ingestion?
Ingested NaCl without change in volume leads to increased osmolarity, causing vasopressin secretion, thirst, increased water intake, increased renal water reabsorption, increased ECF volume, and increased blood pressure. Cardiovascular reflexes then lower blood pressure, and the kidneys excrete salt and water to normalize osmolarity and blood pressure.
Describe the reabsorption and secretion process in the nephron.
The nephron filters 180 L/day with 100% volume at Bowman’s capsule. Proximal tubule reabsorbs ~70% fluid and solute. Loop of Henle receives 30% volume, with the ascending loop being hypo-osmotic relative to plasma. Distal tubule and collecting duct fine-tune water/salt balance under endocrine control.
What happens to cell volume when high NaCl intake is not offset by water?
Cells shrink due to hyperosmolarity of the extracellular fluid.
Explain how the body’s osmoregulation mechanisms respond to high NaCl intake without an increase in volume.
Upon high NaCl intake, osmoregulation begins with the secretion of vasopressin and the sensation of thirst, leading to increased water intake and retention. This results in an increase in extracellular fluid volume, which elevates blood pressure. Cardiovascular reflexes and kidney excretion then act to reduce blood pressure and return osmolarity to normal.
How much fluid is reabsorbed in the proximal tubule of the nephron?
Approximately 70% of the fluid is reabsorbed in the proximal tubule.
What role does the loop of Henle play in urine concentration?
The loop of Henle establishes a concentration gradient that allows for the regulation of urine concentration and volume.
What stimulates aldosterone secretion and what are the implications of this secretion on ion balance and blood pressure?
Aldosterone secretion is stimulated by increased plasma [K+] and decreased blood pressure. It activates the renin-angiotensin-aldosterone system (RAAS) to increase Na+ reabsorption and K+ secretion, which in turn helps to increase blood volume and pressure.
What cellular mechanisms does aldosterone activate in the adrenal cortex?
Aldosterone acts on intracellular receptors to induce gene expression for new pumps and channels, particularly increasing the number of epithelial sodium channels (ENaC) and Na+/K+ ATPase pumps.
What are the specific roles of aldosterone at the apical and basolateral membranes of principal cells?
At the apical membrane, aldosterone increases Na+ import and K+ export, while at the basolateral membrane, it enhances the activity of Na+/K+ ATPase pumps.
Explain the dual impact of aldosterone on sodium and potassium homeostasis.
Aldosterone facilitates sodium reabsorption and potassium secretion in the distal nephron, aiding in fluid balance and preventing hyperkalemia.
How do the actions of aldosterone contribute to blood pressure regulation?
By increasing Na+ reabsorption, aldosterone contributes to water retention, which increases extracellular fluid volume and blood pressure.
What physiological conditions prompt the adrenal cortex to release aldosterone?
The adrenal cortex releases aldosterone in response to high plasma potassium levels or low blood pressure, as part of the body’s effort to maintain electrolyte balance and blood pressure.
What is the result of aldosterone-induced Na+ reabsorption in the distal nephron?
Enhanced Na+ reabsorption in the distal nephron leads to an increase in blood volume and pressure, as water passively follows the reabsorbed sodium.
Describe the process of aldosterone-mediated gene expression and its outcome in the distal nephron.
Aldosterone stimulates gene expression for sodium channels and pumps in the distal nephron, resulting in increased sodium reabsorption and potassium secretion.
What percentage of body potassium is found in the extracellular fluid (ECF)?
Only a small proportion (2%) of the body’s potassium is in the ECF, with the majority inside cells.
Why is it important to maintain ECF potassium concentrations within a narrow range?
ECF potassium concentrations are crucial in determining the resting membrane potential and excitability of excitable cells.
What are the effects of hyperkalemia on cellular function?
Hyperkalemia reduces the concentration gradient across the cell membrane, causing cells to be depolarized, which can lead to cardiac arrhythmias.
What is the role of the renin-angiotensin system (RAS)?
The RAS regulates blood pressure and fluid balance, where renin converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by ACE, leading to aldosterone release.
What is the function of granular cells in the juxtaglomerular apparatus?
Granular cells secrete the enzyme renin, which is involved in salt and water balance regulation.
What condition can result from hypokalemia, and how does it affect cell function?
Hypokalemia can cause cells to become hyperpolarized, leading to muscle weakness.
Explain the pathophysiology of how hyperkalemia and hypokalemia can affect cardiac and muscle cell function.
Hyperkalemia causes cells to depolarize prematurely, increasing the risk of arrhythmias, while hypokalemia leads to hyperpolarization, which decreases excitability and can result in muscle weakness.
Describe the regulatory mechanisms that the juxtaglomerular apparatus uses to control renal blood flow and filtration rate.
The juxtaglomerular apparatus regulates GFR by using the macula densa cells to detect changes in sodium chloride concentration, signaling granular cells to release renin, and altering arteriole resistance to adjust renal blood flow.
What are the components of the juxtaglomerular apparatus and their functions?
The juxtaglomerular apparatus includes the macula densa, which senses sodium chloride levels in the distal tubule, and the granular cells (JG cells), which secrete renin in response to low blood pressure.
How does the Renin-Angiotensin System (RAS) respond to a drop in blood pressure?
RAS responds to a drop in BP by releasing renin, which leads to the production of angiotensin II, causing vasoconstriction, increased aldosterone release, and a rise in BP.
What stimulates the release of renin from the juxtaglomerular cells?
Renin release is stimulated by low blood pressure detected by the granular cells, decreased NaCl transport across the macula densa, and sympathetic nervous system activation.
How does angiotensin II correct a drop in blood pressure?
Angiotensin II corrects low BP by causing vasoconstriction, increasing sympathetic activity, promoting aldosterone and antidiuretic hormone release, and triggering thirst and salt appetite.
What role does the liver play in the Renin-Angiotensin System?
The liver continuously produces angiotensinogen, which is the inactive precursor in the RAS pathway that is converted to active peptides by renin and ACE.
What is the significance of the RAS in treating hypertension?
RAS is targeted in hypertension treatment using ACE inhibitors, angiotensin receptor blockers, and direct renin inhibitors to reduce angiotensin II levels and its effects.
Describe the feedback loop involving the juxtaglomerular apparatus in regulating glomerular filtration rate (GFR) and blood pressure.
The juxtaglomerular apparatus regulates GFR and BP through a feedback loop where the macula densa senses changes in NaCl, and granular cells adjust renin release, influencing systemic blood pressure and nephron filtration rate.
Discuss the pharmacological interventions that target the RAS and their potential benefits in managing hypertension.
Pharmacological interventions in RAS include ACE inhibitors and angiotensin receptor blockers, which decrease angiotensin II activity, and direct renin inhibitors, which block the initial step in the RAS, each with potential benefits like fewer side effects and effective BP management.
What is the importance of blocking angiotensin II in the treatment of hypertension?
Blocking angiotensin II reduces vasoconstriction and sodium retention, thereby lowering blood pressure. This can be achieved with ACE inhibitors, angiotensin receptor blockers, and direct renin inhibitors.
What hormone opposes the actions of vasopressin and aldosterone, and what does it promote?
Atrial Natriuretic Peptide (ANP) opposes the actions of vasopressin and aldosterone by promoting the loss of sodium and water, aiding in reducing blood volume and pressure.
Who discovered ANP and what are its effects on the kidneys?
ANP was discovered by researchers, including Adolfo de Bold, in 1981. It increases sodium and water excretion by the kidneys, dilates afferent arterioles, and reduces aldosterone and vasopressin release, leading to decreased blood pressure.
How do natriuretic peptides, like ANP, affect the cardiovascular system and blood pressure?
Natriuretic peptides reduce blood volume and pressure by increasing sodium and water excretion in the kidneys and opposing the RAS and sympathetic nervous system.
What triggers the release of ANP from myocardial cells?
ANP is released from specialized myocardial cells, primarily in the atria, when these cells are stretched more than normal, typically due to increased blood volume.
How does ANP contribute to the regulation of blood pressure?
ANP contributes to blood pressure regulation by reducing sodium reabsorption in the kidneys, dilating the afferent arterioles to increase GFR, and suppressing renin and aldosterone secretion.
Explain the physiological mechanisms by which ANP serves as an antagonist to the renin-angiotensin-aldosterone system (RAS).
ANP antagonizes RAS by dilating the afferent arteriole of the glomerulus, reducing renin release, inhibiting aldosterone secretion, decreasing sodium reabsorption, and suppressing the sympathetic nervous system, all of which lead to decreased blood pressure.
Discuss the impact of ANP on the homeostatic balance of blood pressure in the context of RAS activation and its implications for therapeutic strategies in hypertension.
ANP counteracts RAS activation by promoting vasodilation, natriuresis, and diuresis, which leads to a decrease in blood volume and pressure. Therapeutically, this understanding has led to the development of drugs that mimic or enhance the effects of ANP, providing alternative strategies for managing hypertension and heart failure.
Elaborate on the physiological interplay between ANP and the sympathetic nervous system in the regulation of renal function and blood pressure.
ANP modulates renal function and blood pressure by inhibiting the sympathetic nervous system, leading to a decrease in renin release, vasodilation of the afferent arteriole, increased glomerular filtration rate, and enhanced excretion of sodium and water. This process effectively reduces blood volume and systemic vascular resistance, which are critical factors in the pathophysiology of hypertension.
What body changes occur with the ingestion of hypertonic water?
Ingestion of hypertonic water increases extracellular fluid osmolarity, leading to water movement from intracellular to extracellular spaces, potentially causing cellular dehydration.
What is the effect of drinking large amounts of water without solute on the body?
It leads to a decrease in extracellular fluid osmolarity, resulting in hyponatremia and a potential shift of water into cells, causing cellular swelling.
How does the body compensate for sweat loss with plain water replacement?
Replacing sweat loss with plain water can dilute extracellular sodium, leading to hyponatremia and a decrease in osmolarity.
What is the physiological response to hemorrhage in terms of fluid volume and osmolarity?
Hemorrhage triggers a low volume response without changing osmolarity, prompting the body to conserve both water and sodium to maintain blood pressure.
How does dehydration from sweat loss or diarrhea affect the body?
Dehydration from sweat loss or diarrhea leads to a decrease in volume and an increase in osmolarity, causing the body to conserve water and increase thirst.
What are the similarities between the body’s response to hemorrhage and severe dehydration?
Both conditions trigger a low volume response, activating mechanisms to conserve water and maintain blood pressure, despite their differences in osmolarity changes.
Compare and contrast the homeostatic responses to hemorrhage versus severe dehydration and the implications for intracellular and extracellular fluid compartments.
Hemorrhage maintains osmolarity but reduces volume, leading to conservation of water and salt without cellular dehydration. Severe dehydration increases osmolarity and reduces volume, leading to water conservation and increased thirst, with a risk of cellular dehydration if not corrected.
How do the renin-angiotensin-aldosterone system and atrial natriuretic peptide (ANP) interact during disturbances in blood volume and osmolarity?
RAAS and ANP have opposing actions; RAAS conserves sodium and water to increase volume and blood pressure, while ANP promotes natriuresis and diuresis to decrease volume and blood pressure. During volume depletion, RAAS is activated, whereas ANP is suppressed; the opposite occurs during volume expansion.
What is the normal range for plasma pH and how does this compare to intracellular pH?
Normal plasma pH ranges from 7.38-7.42, and intracellular pH is similar, although fluids outside the body can have pH values outside this range.
How does an abnormal pH affect enzyme function and protein structure?
Hydrogen ion concentration affects the structure of proteins and consequently, enzyme function. Abnormal pH can denature enzymes and disrupt metabolic pathways.
What are the effects of acidosis and alkalosis on the nervous system?
Acidosis can make neurons less excitable, leading to CNS depression, while alkalosis can make them hyperexcitable, which can cause sensory changes, twitches, or even tetanus.
How are disturbances in pH often associated with potassium (K+) disturbances?
pH disturbances are frequently linked to K+ levels due to shared renal transport mechanisms, like the antiporter and H+/K+ ATPase.
What is the primary source of H+ in the body?
CO2 produced during aerobic respiration is the main source of acid in the body. The reaction CO2 + H2O ↔ H2CO3 ↔ HCO3- + H+ occurs in all cells but is especially rapid in cells with high levels of carbonic anhydrase.
What are the three components of pH homeostasis in the body?
Buffers are the first line of defense against pH changes, ventilation is a rapid second line of defense that corrects 75% of disturbances, and renal regulation is slower but highly effective, involving direct excretion or reabsorption of H+.
Explain the role of bicarbonate as a buffer in plasma and how it interacts with ventilation and renal function to maintain pH homeostasis.
Bicarbonate acts as a buffer in plasma, neutralizing excess H+ to form carbonic acid, which can be exhaled as CO2. Ventilation adjusts the removal of CO2 to control pH, and the kidneys regulate the reabsorption or excretion of bicarbonate to maintain acid-base balance.
Describe the physiological processes that occur when plasma pH moves out of the normal range and the body’s buffering capacity is overwhelmed.
When plasma pH deviates from the norm and buffers are overwhelmed, the respiratory system alters CO2 exhalation to correct pH quickly. If the cause is respiratory, only renal mechanisms can compensate. If metabolic, both respiratory adjustments and renal modifications work to correct pH by altering bicarbonate and H+ concentrations.
How do the renal tubules compensate for acidosis?
Renal tubules compensate for acidosis by increasing the movement of H+/NH4+ into the tubule and HCO3- into the interstitium, which involves various transporters and exchangers.
How does respiratory compensation for acidosis work?
In response to increased plasma H+ (decreased pH), chemoreceptors stimulate the respiratory centers to increase the rate and depth of breathing, reducing plasma CO2 and thus lowering H+ concentration.
What triggers respiratory compensation in response to acidosis?
Increased plasma H+ concentration (decreased pH) triggers respiratory compensation, where chemoreceptors stimulate the respiratory centers to increase breathing rate and depth, thus lowering plasma CO2 and H+.
How does the kidney excrete hydrogen ions during acidosis?
The kidney secretes H+ ions, which are buffered in the urine by NH3 (ammonia) and HPO4^2- (dihydrogen phosphate), while reabsorbing bicarbonate to help buffer H+ in the extracellular fluid.
Where in the nephron does bicarbonate reabsorption occur?
Bicarbonate reabsorption primarily occurs in the proximal tubule, with indirect methods used due to the lack of direct transporters for bicarbonate on the apical membrane.
What is the function of intercalated cells in the distal nephron?
Intercalated cells in the distal nephron fine-tune acid-base balance. Type A intercalated cells secrete H+ and reabsorb bicarbonate to deal with acidosis, while type B cells do the opposite to compensate for alkalosis.
Explain the negative feedback loop involved in respiratory compensation for acidosis.
In respiratory compensation for acidosis, increased H+ stimulates chemoreceptors, which signal the respiratory centers to increase ventilation, reducing CO2 (and thus H+ via the law of mass action), which in turn decreases the stimulus on chemoreceptors, completing the feedback loop.
Discuss the renal adjustments in the secretion and reabsorption of ions that occur during acidosis and their impact on systemic pH levels.
During acidosis, renal adjustments include increased secretion of H+ and NH4+, enhanced reabsorption of bicarbonate, and increased production of buffer substances in urine. These changes lead to increased acid excretion and bicarbonate conservation, helping to raise systemic pH back towards normal levels.
What is the role of the Na+/H+ exchanger in the reabsorption of filtered bicarbonate in the proximal tubule?
The Na+/H+ exchanger facilitates the secretion of H+ into the tubular lumen, which combines with filtered bicarbonate to form CO2 and water, aiding in the reabsorption of bicarbonate.
How do Type A intercalated cells in the collecting duct contribute to acid-base homeostasis during acidosis?
Type A intercalated cells secrete H+ into the tubular lumen, helping to reabsorb bicarbonate and potassium, thereby reducing acidosis.
