Exam 5 Review:  Chapter 16:  The Adrenal Glands

mineralocorticoids - The class of steroid hormones produced by the outermost layer of the adrenal cortex, whose release is stimulated by increased potassium levels in the plasma; the mineralocorticoids (aldosterone) target the kidney to transport sodium ions out of the urine and potassium ions into the urine (chloride ions and water passively follow the sodium ions back to the bloodstream).

aldosterone - The main steroid hormone produced by the outermost layer of the adrenal cortex, whose release is stimulated by increased potassium levels in the plasma; this mineralocorticoid  targets the kidney to actively transport sodium ions out of the urine and potassium ions into the urine (chloride ions and water passively follow the sodium ions back to the bloodstream); the net effects of this hormone are to increase blood pressure and blood volume and to adjust sodium and potassium levels in the blood.

aldosteronism - A disorder marked by excessive secretion of the steroid hormone aldosterone from the adrenal cortex, which can cause fluid and salt retention, edema, weakness, cardiac irregularities, and abnormally high blood pressure.

glucocorticoids - The class of steroid hormones produced by the middle layer of the adrenal cortex, whose release is stimulated by adenohypophyseal ACTH; examples include cortisol, cortisone, and hydrocortisone; the glucocorticoids are involved in carbohydrate, protein, and fat metabolism, and have anti-inflammatory properties; they are insulin antagonists contributing to increasing blood glucose levels and fat catabolism; they play a role in maintaining arterial blood pressure, alter the response of connective tissue to injury, reduce the number of circulating lymphocytes, and play a role in the functioning of the CNS.

cortisol - The main steroid hormone produced by the middle layer of the adrenal cortex, whose release is stimulated by adenohypophyseal ACTH; this steroid hormone  is involved in carbohydrate, protein, and fat metabolism, and has anti-inflammatory properties; it is an insulin antagonist contributing to increasing blood glucose levels and fat catabolism; it plays a role in maintaining arterial blood pressure, alters the response of connective tissue to injury, reduces the number of circulating lymphocytes, and plays a role in the functioning of the CNS.

protein catabolism - The metabolic breakdown of protein molecules into simpler ones, often resulting in a release of useful chemical energy.

gluconeogenesis - The formation of "new" glucose, especially by the liver, from noncarbohydrate sources, such as pyruvate, amino acids and the glycerol portion of fats; this process is stimulated by those hormones termed insulin antagonists, which includes glucagon, human growth hormone, and the glucocorticoids.

lipolysis - The hydrolysis of lipids which may lead to fat catabolism which will result in a release of useful chemical energy; this process is stimulated by those hormones termed insulin antagonists, which includes glucagon, human growth hormone, and the glucocorticoids.

sympathomimetic - Producing physiological effects resembling those caused by the activity or stimulation of the sympathetic nervous system. e.g., sympathomimetic hormones and drugs.

epinephrine = adrenalin - A catecholamine  neurohormone derived from the amino acid tyrosine in the same pathway which produces norepinephrine, from which epinephrine is derived; it is released by the adrenal medulla and interacts with all target cells which have adrenergic receptors to ready the body for increased skeletal muscular activity or fight-or-flight emergencies.

norepinephrine = noradrenaline - A catecholamine neurotransmitter and neurohormone derived from the amino acid tyrosine which is the neurotransmitter released by most sympathetic postganglionic neurons and by the adrenal medulla; it interacts with all target cells which have adrenergic receptors to ready the body for increased skeletal muscular activity or fight-or-flight emergencies.

atrial natriuretic peptide = ANP - The peptide hormone released from special endocrine cells in the walls of the upper chambers/atria of the heart in response to the stretching of the chamber walls due to increased blood volume or increased blood pressure; ANP is the antagonist to aldosterone and thus triggers salt (NaCl) and water excretion and potassium ion reabsorption at the kidney tubules.

renin-angiotensin system - A complex endocrine negative feedback control system which plays important role in regulating blood volume, arterial pressure, and cardiac and vascular function; in response to sympathetic stimulation, low blood pressure or low blood sodium levels, (1) the juxtaglomerular apparatus of the kidney will release the enzyme renin, (2) renin will catalyze the activation of an inactive precursor substance, angiotensinogen, which is made by the liver, into angiotensin I, (3) angiotensin I (which has some activity of its own) will be further activated by an enzyme found in the lungs, angiotensin-converting enzyme (ACE), into active angiotensin II, (4) angiotensin I & II stimulate these physiological responses:  (a) enlargement of the heart and blood vessels, (b) systemic vasoconstriction, (c) aldosterone release from the adrenal cortex, (d) activation of the hypothalamic thirst center, (e) ADH release from the posterior pituitary/neurohypophysis; processes (c, d, and e) cause retention of salt and water by the kidneys and as a result, increased blood volume; thus this system has a powerful hypertensive effect.

angiotensinogen - A peptide synthesized in the liver which is released into the bloodstream to be the substrate for the enzyme renin which converts it to angiotensin I, a moderately effective hyperensive control substance, but more importantly angiotensin I is, itself, the precursor to angiotensin II [See ACE]; these vasoactive peptide products can also stimulate aldosterone release from the adrenal cortex, ADH/vasopressin from the posterior pituitary, and stimulate the hypothalamic thirst center.

angiotensin I - The peptide product of the circulating enzyme renin which converts the inactive precursor angiotensinogen to angiotensin I, a moderately effective hypertensive regulatory substance, but more importantly, the precursor to angiotensin II.

angiotensin II - The peptide product of the lung enzyme angiotensin-converting enzyme (ACE) which converts the angiotensin I into angiotensin II, a highly effective hypertensive regulatory substance which targets the adrenal cortex for aldosterone release, the anterior pituitary for ADH/vasopressin release, the hypothalamic thirst center, and the smooth muscle in arterial walls for contraction.

Addison's disease - The primary disorder of hyposecretion of the adrenal cortex which causes lowered levels of both mineralocorticoids and glucocorticoids, and symptoms of weight loss, abnormal pigmentation, hypoglycemia, hyponatremia (decreased Na+), hyperkalemia (increased K+), and possibly dehydration and hypotension (decreased blood pressure).

Diagram:

Sketch and Label:

6. a negative feedback pathway for the regulation of:

       d.  Glucocorticoids

 

Cortisol and other glucocorticoids are secreted in response to adrenocorticotropic hormone (ACTH) from the anterior pituitary.  ACTH is itself secreted under control of the hypothalamic peptide, corticotropic-releasing hormone (CRH).  This is an example of nervous system control of the pituitary and trophic endocrine control of the adrenal cortex. Virtually any type of physical or mental stress results in elevation of cortisol concentrations in blood due to enhanced secretion of CRH in the hypothalamus. [This fact sometimes makes it very difficult to assess glucocorticoid levels. A distressed patient, e.g., on admission to the emergency room, observing the approach of a phlebotomist, and especially being restrained for blood sampling, may be stressed enough to artificially elevate cortisol levels several fold!] Remember that some glucocorticoid release occurs in the absence of significant stress, just as a part of overall control of metabolism. Cortisol secretion is suppressed by classical negative feedback loops.  When blood concentrations rise above a certain theshold, cortisol inhibits CRH secretion from the hypothalamus, which turns off ACTH secretion, which leads to a turning off of cortisol secretion from the adrenal cortex. The combination of positive and negative control on CRH secretion results in fluctuating secretion of cortisol.  Typically, the pulse amplitude and frequency are highest in the morning and lowest at night.  [This, too, impacts the accuracy of clinical laboratory testing of glucocorticoid levels.]