Unformatted text preview:

The Adrenal Glands- Located above kidneys- Adrenal medulla (inside) is innervated by sympathetic nervous system- Adrenal cortex (outside) is composed of three structural layers, each of which forms secretes a different hormoneo Zona Glomerulosa: mineralcotricoids (ex: aldosterone)o Zona fasciculate: glucocorticoids (ex: cortisol)o Zona reticularis: androgens (sex hormones)Women under a long term stress lose their hair because they produce a lot of androgens, which can cause male-pattern baldness.Hormones of the adrenal cortex are steroid hormones and all are produced from cholesterol. There are many intermediates, so enzyme mutations can prevent conversion from a precursor. This will lead to an abundance of the other cortex hormones. Mostly regulated by negative feedback. There is no set point because levels fluctuatethroughout the day; determined by higher brain centers. Adrenal medulla- Produces opioid peptides enkephalinso “natural pain killers”o inhibit the nociceptor (pain) pathway- Produces catecholamines: epinephrine and norepinephrine- Sympathetic nervous system releases acetylcholine, which innervates chromaffin cells to secret epi and norepi- Actions are identical to the neurotransmitters but these travel through the bloodstream- Help deal with short-term stress:o Increase heart rate, blood pressure & blood glucoseo Bronchodilationo Decrease blood flow & function of GI tracto Increase blood flow to skeletal muscleEpi and norepi bind adrenergic receptors with relative affinitieso Norepi: α1 and α2o Epi: β2o Equal for β1 and β3α 1 Gq -> PLC -> IP3 -> Ca2+ -> binds calmodulin- Smooth muscle contraction- GI vasoconstriction & sphincter contraction- Radial muscle contraction leads to pupil dilation, can see more in peripheral vision.α 2 Gi -> adenylyl cyclase -> decr cAMP- Inhibits insulin secretion to increase blood glucose- Inhibits digestive secretions- Fat cell lipolysis for ATP (energy)β 1 Gs -> activate adenylyl cyclase -> incr cAMP- increases myocardial activity, stroke volume, blood pressure- increase SA firing rate to increase heart rate- fat call lipolysis- renin release by kidneysβ 2 Gs -> activate adenylyl cyclase -> incr cAMP- bronchodilation- smooth muscle relaxation (bladder wall, to hold more urine)- liver gluconeogenesis and glycogenolysis to increase blood glucoseβ 3 Gs -> activate adenylyl cyclase -> incr cAMP- mostly located on fat cells- enhances lipolysisEpi action on SA nodeSA node contains autorhythmic cells, but can also be controlled by the autonomicand endocrine systemsepi binds β1Increase open funny channels (IF) and Ca channels openIncrease rate of spontaneous depolarizationat threshold, contraction occurs, thus heart rate increasesBeta blockers act as antagonists to decrease heart rate, allowing it to fill with more blood. This causes the heart to stretch and produce more forceful contractions. Beta blockers have side effects because β receptors are located throughout the body.Hypersecretion can lead to- paroxysmal HTN- blurred vision, tinnitus, diaphoresis, palpitations- stroke, aneurysm, arrhythmias -> MI- can be caused by pheochromocytoma, which may ultimately need surgical removal to correctHypersecretion generally is asymptomatic because it is compensated for by the sympathetic nervous system and corticosteroids. Adrenal cortex - Aldosterone- Cortisol- Androgens: Aldosterone- Increases osmolarity when needed by increasing sodium reabsorption- Blood pressure is the driving force for glomerular filtrationo Renin is produced by juxtaglomerular cells when blood pressure/Na concentration is low, converts angiotensinogen into angiotensin I, which is converted to angiotensin II by ACE (angiotensin converting enzyme)o Angiotensin II causes vasoconstriction and stimulates aldosterone releaseo People with HTN take ACE inhibitors to prevent this- Production stimulated by:o Angiotensin IIo Renin (indirectly)- Production inhibited by o atrial natriuretic peptide (ANP) o osmolarity or [Na] increases- Bound to cortisol-binding globulin (CBG) or albumin in circulation, then enters tubule cells of kidney- Activates cystolic mineralocorticoid receptorAldosterone binds receptorTranslocation into nucleusHomodimerizationBind to glucocorticoid response elements (GRE) in promotersIncrease gene transcription to stimulate Na/K pump and channel synthesisThis receptor binds aldosterone and cortisol with equal affinity.- Cortisol concentration is thousands-fold higher than aldosterone- Target cells for aldosterone express 11-beta-hydroxysteroid dehydrogenase 2 (HSD2), which converts cortisol to cortisone- Cortisone has a very weak affinity for mineralocorticoid receptor- Licorice contains glycyrrhetinic acids, which inhibit 11βHSD2- With excess licorice consumption, cortisol is not converted to cortisone and therefore, acts on the MR (called “aspseudohyperaldosteronism”)- Because [cortisol] is so high and it mimics the effect of aldosterone, this can cause hypertension and hypokalemiaAldosterone stimulates- opening of sodium and potassium channels on the apical membrane- synthesis of new Na and K channels on apical membrane- synthesis and insertion of Na/K pumps on basolateral membrane- Together, increases [Na] in blood. Water follows salt, thus, BP increasesAldosterone is both an antagonist and additive to ADH, based on stimulus. - If BP and blood volume are low, ADH and aldosterone are secreted together- If osmolarity is abnormal, they act in opposition to each othero ADH – increases water reabsorption so BP increases but osmolarity decreaseso Aldosterone – increases Na reabsorption, so osmolarity increases. Then water follows so BP increases. ANP is released from the atrium in response to wall stretching, which occurs when BP is too high. ANP increases sodium excretion to decrease blood pressure. Hyperaldosteronism aka Conn’s syndrome or aldosteronism symptoms include:- Hypernatremia & hypervolemia- Hypokalemia- Hypertension Primary is often caused by adrenal cortical adenoma. Secondary is due to activity of renin-angiotensin system. May also be due to defect in the enzyme 17α-hydroxylase, which allows synthesis of other adrenal cortex hormones. In the absence of those hormones, the concentration of aldosterone increases. Hypoaldosteronism symptoms include:- Hyponatremia & hypovolemia- Hyperkalemia- HypotensionMay be caused by primary adrenal insufficiency but more likely due to a person taking ACE


View Full Document

UMD BSCI 447 - The Adrenal Glands

Download The Adrenal Glands
Our administrator received your request to download this document. We will send you the file to your email shortly.
Loading Unlocking...
Login

Join to view The Adrenal Glands and access 3M+ class-specific study document.

or
We will never post anything without your permission.
Don't have an account?
Sign Up

Join to view The Adrenal Glands 2 2 and access 3M+ class-specific study document.

or

By creating an account you agree to our Privacy Policy and Terms Of Use

Already a member?