Epinephrine and Norepinephrine
Epinephrine and norepinephrine are released during the flight/fight response, causing vasoconstriction of blood vessels in the kidney.
Describe hormonal control by epinephrine and norepinephrine of osmoregulatory functions
- Epinephrine, produced by the adrenal medulla, causes either smooth muscle relaxation in the airways or contraction of the smooth muscle in arterioles, which results in blood vessel constriction in the kidneys, decreasing or inhibiting blood flow to the nephrons.
- Norepinephrine, produced by the adrenal medulla, is a stress hormone that increases blood pressure, heart rate, and glucose from energy stores; in the kidneys, it will cause constriction of the smooth muscles, resulting in decreased or inhibited flow to the nephrons.
- Together, epinephrine and norepinephrine cause constriction of the blood vessels associated with the kidneys to inhibit flow to the nephrons.
- epinephrine: (adrenaline) an amino acid-derived hormone secreted by the adrenal gland in response to stress
- norepinephrine: a neurotransmitter found in the locus coeruleus which is synthesized from dopamine
- catecholamine: any of a class of aromatic amines derived from pyrocatechol that are hormones produced by the adrenal gland
- adrenergic: containing or releasing adrenaline
Epinephrine and Norepinephrine
As a hormone and neurotransmitter, epinephrine acts on nearly all body tissues. Its actions vary by tissue type and tissue expression of adrenergic receptors. For example, high levels of epinephrine cause smooth muscle relaxation in the airways, but cause contraction of the smooth muscle that lines most arterioles. Epinephrine acts by binding to a variety of adrenergic receptors. Epinephrine is a nonselective agonist of all adrenergic receptors, including the major subtypes α1, α2, β1, β2, and β3. Epinephrine’s binding to these receptors triggers a number of metabolic changes. Binding to α-adrenergic receptors inhibits insulin secretion by the pancreas, stimulates glycogenolysis (the breakdown of glycogen) in the liver and muscle, and stimulates glycolysis (the metabolic pathway that converts glucose into pyruvate) in muscle. β-Adrenergic receptor binding triggers glucagon secretion in the pancreas, increased adrenocorticotropic hormone (ACTH) secretion by the pituitary gland, and increased lipolysis by adipose tissue. Together, these effects lead to increased blood glucose and fatty acids, providing substrates for energy production within cells throughout the body.
Norepinephrine is a catecholamine with multiple roles. It is the hormone and neurotransmitter most responsible for vigilant concentration in contrast to its most-chemically-similar hormone, dopamine, which is most responsible for cognitive alertness. Areas of the body that produce or are affected by norepinephrine are described as noradrenergic. One of the most important functions of norepinephrine is its role as the neurotransmitter released from the sympathetic neurons to affect the heart. An increase in norepinephrine from the sympathetic nervous system increases the rate of contractions in the heart. Norepinephrine also underlies the fight-or-flight response, along with epinephrine, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood flow to skeletal muscle. When norepinephrine acts as a drug, it increases blood pressure by increasing vascular tone through α-adrenergic receptor activation. Norepinephrine is synthesized from dopamine by dopamine β-hydroxylase in the secretory granules of the medullary chromaffin cells and is released from the adrenal medulla into the blood as a hormone. It is also a neurotransmitter in the central nervous system and sympathetic nervous system, where it is released from noradrenergic neurons in the locus coeruleus. The actions of norepinephrine are carried out via the binding to adrenergic receptors.
Role of Epinephrine and Norepinephrine in Kidney Function
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 of the kidneys stops. These hormones go one step further and trigger the renin-angiotensin-aldosterone system, the hormone system that regulates blood pressure and water (fluid) imbalance.
Other Hormonal Controls for Osmoregulation
The renin-angiotensin-aldosterone system (RAAS) stabilizes blood pressure and volume via the kidneys, liver, and adrenal cortex.
Describe hormonal control by the renin-angiotensin-aldosterone system
- Renin, a hormone produced by the juxtaglomerular apparatus in the kidneys, converts angiotensinogen (which is made in the liver) to angiotensin I.
- Angiotensin I is then converted to angiotensin II by the angiotensin converting enzyme (ACE), increasing blood pressure by causing vasoconstriction of the blood vessels.
- Angiotensin II causes the release of aldosterone which is produced by the adrenal cortex; it functions to maintain both sodium and water levels (osmotic balance) in the blood.
- Angiotensin II also causes the release of antidiuretic hormone (ADH) which functions to conserve water in the body when volume is low; it does this by inserting aquaporins in the collecting duct of the nephron to promote water reabsorption.
- The atrial natriuretic peptide (ANP) is another hormone that is produced to function as a vasodilator and lower blood pressure by preventing sodium reabsorption.
- renin: a circulating enzyme released by mammalian kidneys that converts angiotensinogen to angiotensin-I that plays a role in maintaining blood pressure
- aquaporin: any of a class of proteins that form pores in the membrane of biological cells
- angiotensin: any of several polypeptides that narrow blood vessels and thus regulate arterial pressure
The renin-angiotensin-aldosterone system (RAAS) is a hormone system that regulates blood pressure and water (fluid) balance. This system proceeds through several steps to produce angiotensin II, which acts to stabilize blood pressure and volume. Renin is secreted by a part of the juxtaglomerular complex and produced by the granular cells of the afferent and efferent arterioles. Renin is a circulating enzyme that acts on angiotensinogen, which is made in the liver, converting it to angiotensin I. Defective renin production can cause a continued decrease in blood pressure and cardiac output. After renin facilitates the production of angiotensis I, angiotensin converting enzyme (ACE) then converts angiotensin I to angiotensin II. Angiotensin II raises blood pressure by constricting blood vessels and also triggers the release of the mineralocorticoid aldosterone from the adrenal cortex. This, 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, decreasing glomerular filtration rate. Thus, via the RAAS, the kidneys control blood pressure and volume directly. Medically, blood pressure can be controlled by drugs that inhibit ACE (called ACE inhibitors).
Mineralocorticoids are hormones synthesized by the adrenal cortex that affect osmotic balance. One type of mineralocorticoid, known as aldosterone, 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. As 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. Aldosterone also stimulates potassium secretion concurrently with sodium reabsorption. By contrast, absence of aldosterone means that no sodium is reabsorbed in the renal tubules; all of it is excreted in the urine. In addition, the daily dietary potassium load is not secreted; retention of potassium ions (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 constantly lose sodium in their urine; if the supply is not replenished, the consequences can be fatal.
Antidiuretic hormone or ADH (also called vasopressin) helps the body conserve water when body fluid volume, especially that of blood, is low. It is formed by the hypothalamus, but is stored and released from the posterior pituitary gland. It acts by inserting aquaporins in the collecting ducts, promoting reabsorption of water. ADH also acts as a vasoconstrictor (constricting blood vessels) and increases blood pressure during hemorrhaging.
Atrial Natriuretic Peptide Hormone
The atrial natriuretic peptide (ANP) hormone lowers blood pressure by acting as a vasodilator (dilating or widening blood vessels). 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; 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.