Hormonal Control of Osmoregulatory Functions Quiz

PDF page 1423: osmotic balance, eliminate wastes, and maintain blood pressure. For AP , you do not need to memorize the list of hormones that control osmoregulatory functions or their specific function(s). However, information in this section applies to concepts previously explored. The kidneys synchronize with hormonal cues. As you recall from our study of the endocrine system, hormones are small messenger molecules that travel in the bloodstream to affect a target cell. Different regions of the nephron have specialized cells with receptors to respond to chemical messengers and hormones. Table 32.1 summarizes the hormones that control the osmoregulatory functions. For example, the flight/flight hormones epinephrine and norepinephrine, released by the adrenal medulla and nervous subsystem, respectively, halt kidney function temporarily when the body is under extreme stress and much of the body’s energy is used to combat imminent danger. Another example is the rennin-angiotensin-aldosterone system that increases blood pressure and volume primarily by constricting blood vessels. Another hormone, antidiuretic hormone (ADH) increases membrane permeability to water in the collecting ducts of the nephron by adding aquaporins, causing more water to be reabsorbed. You’ve experienced the effects of ADH when it’s hot outside and you’re running around the athletic field; since you’re losing water by sweating and breathing hard, ADH prevents you from losing more water in urine and risking dehydration.

PDF page 1424: Epinephrine and norepinephrine are released by the adrenal medulla and nervous system respectively. They are the flight/ fight hormones that are released when the body is under extreme stress. During stress, much of the body’s energy is used to combat imminent danger. Kidney function is halted temporarily by epinephrine and norepinephrine. These hormones function by acting directly on the smooth muscles of blood vessels to constrict them. Once the afferent arterioles are constricted, blood flow into the nephrons stops. These hormones go one step further and trigger the renin-angiotensinaldosterone system.

PDF page 1424: Hormone Where produced Function Epinephrine and Adrenal medulla Can decrease kidney function temporarily by vasoconstriction Norepinephrine Renin Kidney nephrons Increases blood pressure by acting on angiotensinogen Angiotensin II affects multiple processes and increases blood Angiotensin Liver pressure Aldosterone Adrenal cortex Prevents loss of sodium and water Hypothalamus (stored Anti-diuretic in the posterior Prevents water loss hormone pituitary) (vasopressin) Decreases blood pressure by acting as a vasodilator and Atrial natriuretic Heart atrium increasing glomerular filtration rate; decreases sodium peptide reabsorption in kidneys

PDF page 1424: Hormone Where produced Function Epinephrine and Adrenal medulla Can decrease kidney function temporarily by vasoconstriction Norepinephrine Renin Kidney nephrons Increases blood pressure by acting on angiotensinogen Angiotensin II affects multiple processes and increases blood Angiotensin Liver pressure Aldosterone Adrenal cortex Prevents loss of sodium and water Hypothalamus (stored Anti-diuretic in the posterior Prevents water loss hormone pituitary) (vasopressin) Decreases blood pressure by acting as a vasodilator and Atrial natriuretic Heart atrium increasing glomerular filtration rate; decreases sodium peptide reabsorption in kidneys

PDF page 1424: Hormone Where produced Function Epinephrine and Adrenal medulla Can decrease kidney function temporarily by vasoconstriction Norepinephrine Renin Kidney nephrons Increases blood pressure by acting on angiotensinogen Angiotensin II affects multiple processes and increases blood Angiotensin Liver pressure Aldosterone Adrenal cortex Prevents loss of sodium and water Hypothalamus (stored Anti-diuretic in the posterior Prevents water loss hormone pituitary) (vasopressin) Decreases blood pressure by acting as a vasodilator and Atrial natriuretic Heart atrium increasing glomerular filtration rate; decreases sodium peptide reabsorption in kidneys

PDF page 1425: The atrial natriuretic peptide (ANP) lowers blood pressure by acting as a vasodilator. It is released by cells in the atrium of the heart in response to high blood pressure and in patients with sleep apnea. ANP affects salt release, and because water passively follows salt to maintain osmotic balance, it also has a diuretic effect. ANP also prevents sodium reabsorption by the renal tubules, decreasing water reabsorption (thus acting as a diuretic) and lowering blood pressure. Its actions suppress the actions of aldosterone, ADH, and renin.

PDF page 1423: osmotic balance, eliminate wastes, and maintain blood pressure. For AP , you do not need to memorize the list of hormones that control osmoregulatory functions or their specific function(s). However, information in this section applies to concepts previously explored. The kidneys synchronize with hormonal cues. As you recall from our study of the endocrine system, hormones are small messenger molecules that travel in the bloodstream to affect a target cell. Different regions of the nephron have specialized cells with receptors to respond to chemical messengers and hormones. Table 32.1 summarizes the hormones that control the osmoregulatory functions. For example, the flight/flight hormones epinephrine and norepinephrine, released by the adrenal medulla and nervous subsystem, respectively, halt kidney function temporarily when the body is under extreme stress and much of the body’s energy is used to combat imminent danger. Another example is the rennin-angiotensin-aldosterone system that increases blood pressure and volume primarily by constricting blood vessels. Another hormone, antidiuretic hormone (ADH) increases membrane permeability to water in the collecting ducts of the nephron by adding aquaporins, causing more water to be reabsorbed. You’ve experienced the effects of ADH when it’s hot outside and you’re running around the athletic field; since you’re losing water by sweating and breathing hard, ADH prevents you from losing more water in urine and risking dehydration.

PDF page 1424: The renin-angiotensin-aldosterone system, illustrated in Figure 32.16 proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone (ADH) from the hypothalamus, leading to water retention in the kidneys. It acts directly on the nephrons and decreases glomerular filtration rate. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).

PDF page 1424: The renin-angiotensin-aldosterone system, illustrated in Figure 32.16 proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone (ADH) from the hypothalamus, leading to water retention in the kidneys. It acts directly on the nephrons and decreases glomerular filtration rate. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).

PDF page 1424: The renin-angiotensin-aldosterone system, illustrated in Figure 32.16 proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone (ADH) from the hypothalamus, leading to water retention in the kidneys. It acts directly on the nephrons and decreases glomerular filtration rate. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).

PDF page 1424: The renin-angiotensin-aldosterone system, illustrated in Figure 32.16 proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin (secreted by a part of the juxtaglomerular complex) is produced by the granular cells of the afferent and efferent arterioles. Thus, the kidneys control blood pressure and volume directly. Renin acts on angiotensinogen, which is made in the liver and converts it to angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels. It also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex, which in turn stimulates the renal tubules to reabsorb more sodium. Angiotensin II also triggers the release of anti-diuretic hormone (ADH) from the hypothalamus, leading to water retention in the kidneys. It acts directly on the nephrons and decreases glomerular filtration rate. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).

PDF page 1425: Mineralocorticoids are hormones synthesized by the adrenal cortex that affect osmotic balance. Aldosterone is a mineralocorticoid that regulates sodium levels in the blood. Almost all of the sodium in the blood is reclaimed by the renal tubules under the influence of aldosterone. Because sodium is always reabsorbed by active transport and water follows sodium to maintain osmotic balance, aldosterone manages not only sodium levels but also the water levels in body fluids. In contrast, the aldosterone also stimulates potassium secretion concurrently with sodium reabsorption. In contrast, absence of aldosterone means that no sodium gets reabsorbed in the renal tubules and all of it gets excreted in the urine. In addition,

PDF page 1425: the daily dietary potassium load is not secreted and the retention of K can cause a dangerous increase in plasma K concentration. Patients who have Addison's disease have a failing adrenal cortex and cannot produce aldosterone. They lose sodium in their urine constantly, and if the supply is not replenished, the consequences can be fatal.

PDF page 1425: As previously discussed, antidiuretic hormone or ADH (also called vasopressin), as the name suggests, helps the body conserve water when body fluid volume, especially that of blood, is low. It is formed by the hypothalamus and is stored and released from the posterior pituitary. It acts by inserting aquaporins in the collecting ducts and promotes reabsorption of water. ADH also acts as a vasoconstrictor and increases blood pressure during hemorrhaging.

PDF page 1425: The atrial natriuretic peptide (ANP) lowers blood pressure by acting as a vasodilator. It is released by cells in the atrium of the heart in response to high blood pressure and in patients with sleep apnea. ANP affects salt release, and because water passively follows salt to maintain osmotic balance, it also has a diuretic effect. ANP also prevents sodium reabsorption by the renal tubules, decreasing water reabsorption (thus acting as a diuretic) and lowering blood pressure. Its actions suppress the actions of aldosterone, ADH, and renin.