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Adrenal Physiology

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imissyou419's version from 2017-04-01 20:16

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Question Answer
Where is the source of adrenal steroids? What is regulated by?adrenal cortex, pituitary ACTH
zona glomerulosaaldosterone
zona fasciculatacortisol
zona reticularissex steroids
Medulla is composed ofchromaffin cells
Where is the source of catecholaminesmedulla, secretions controlled by direct innervation; (your SNS also produce catecholamines)
Primarily E and NE (E Increase HR, BP, lipid breakdown, peripheral vasoconstriction, coronary dilation, bronchial dilation, muscle glycogen -> glucose; NE only increase HR, BP, lipid breakdown, peripheral vasoconstriction)
responds to ACUTE stress - fight or flight
Rate of release determined by frequency of APs at chromaffin cells (neuroendocrine cell)
cytochrome p450convert cholesterol into different steroid hormones, interconvert, found in membrane of mitochondria and ER, energy comes from ETC
ACTH regulate cortisol production in 4 ways:ACTH upregulate ACTH receptor (provide more ACTH binding to ACTH receptor)
Increase receptor for LDL/cholesterol (allow for more cholesterol to be brought into cell)
Increase activity CEH (liberate more cholesterol to make cortisol by taking esters of cholesterol)
Increase activity of StAR (mobilizes cholesterol and brings into mitochondria, lead to synthesis of bioactive cortisol)
StARrate limiting step in steroidogenesis (mobilizes cholesterol and brings it into mitochondria to be synthesized into cortisol by p450)
ACTH receptor is primary inzona reticularis and fasiculata
ACTH receptorGPCR coupled to cAMP
Cortisol mostly bound to75% in plasma bound to CBG (corticosteroid binding globulin or transcortin), 10% bound to Human Serum Albumin, 10% free
Where is cortisol metabolized in and excreted bymetabolized in liver to be water soluble, excreted by kidney (urine test for steroid abuse)
Cortisol release in pulsatilecircadian and ultradian, in stress information: coordinated increase in ACTH and cortisol
Cortisol actions (chronic stress)1. ↑ serum glucose and a.a. (↑ protein catabolism in muscle -> ↑ circulating a.a., ↑ a.a. uptake in liver -> ↑ gluconeogenesis and glycogenesis, ↓peripheral glucose uptake (muscle and adipose tissue) by impairing GLUT 4 activity,
2. ↑ catabolism (↑ lipid hydrolysis -> increase circulating fatty acids, bone and connective tissue catabolism -> osteopenia, thinning of skin and support structures); anti-inflammatory (inject cortisol locally for rheumatoid arthritis), suppress immune system
If you have a lot of 11beta-HSD-1convert cortisome to cortisol, cortisol response
If you have a lot of 11beta-HSD-2convert cortisol to cortisome by removing hydroxy from C11
Impairment of placental 11beta-HSD-2cannot convert cortisol to cortisome so baby exposed to high level of maternal cortisol and have IUGR (intrauterine growth restriction); impairment of 11beta-HSD-2 activity caused by black liquorice
Cushing's DiseaseHypercortisolism - fat deposition in face, back, central abdomen (paradox - more of a redistribution of fat), thinning of arms and legs (protein catabolism), loose skin with striae - thinning of skin and support structures, osteopenia/osteoporosis - bone and connective tissue catabolism, immune suppression
Aldosterone synthesis controlled by1. availability of precursors (indirect via ACTH stimulation of zona fasciculata to produce corticosterone; which is eventually converted to aldosterone) - in chronic stress, make higher levels of aldosterone, increase Na+ retention -> lead to hypertension,
2. ANG II from Ras,
3. In response to high K+
Aldosterone action1. increase ENac transcription (increase expression level of Na+ channels, Na+/K+ ATPase), 2. increase transcription of genes (structural/regulatory proteins) which activate current Na+ transporters (increase activity of Na+/K+ ATpase)
If there is more circulating cortisol than aldosterone, how do we prevent artifical increase in MR receptor function?High level of 11-beta-HSD-2 to inactivate cortisol into cortisone allowing MR to be stimulated when it is suppose to be aldosterone since it binds to MR with equal affinity
Apparent Mineralocorticoid Excess Syndrome (AME)caused by mutations/deficiencies in 11beta-HSD-2, increased 'alodsterone' like effect in kidney, leads to hypokalemia, high blood pressure
Catecholamine receptorsadrenergic receptors (several subtypes -> a1, a2, b1,b2,b3), regulate smooth muscle contractility (vascular tone, gastric tone)
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