Adrenal gland Flashcards
What acts on the adrenal gland
Renin-angiotensin system and autonomic nervous system
Medulla function
secretes catecholamines eg adrenaline (noradrenaline)
Acts on alpha and beta adrenergic receptors to incr HR and RR
Acute stress response
Cortex function
Releases aldosterone (mineralcorticoid): Na+ reabsorption (NA+ leads, H2O follows), incr BV as a result
Releases Glucocorticoids eg cortisol: via glucocorticoid receptors- regulate gene transcription, mobilize glucose into the blood
adrenal glands overall function
mediating response to acute and chronic stress
What is acting on glucocorticoids
Hypo (CRH) –> Pituitary (ACTH)
Medulla structure
modified sympathetic ganglion
Outer cortex 3 zones
ZG- mineralocorticoid- aldosterone
ZF- glucorticoid or corticosteroid- cortisol
ZR- androgen precursors
Mineralcorticoids effects
blood volume/sodium effects
Glucocorticoids effects
metabolic effects
Catecholamines effects
bodily symptoms
Regulation of secretion in the adrenal medulla
adrenal medulla is part of the sympathetic division of the autonomic nervous system
Considered as specialised group of postganglionic neurones
Secretion of hormones controlled by sympathetic preganglionic nerve fibres
Effects of medullary catecholamines
same as direct activation of symp nerves but:
- lasts longer
- effects generalised to all cells with alpha and/or beta receptors (GPCRs)
Major effect is on CO and cellular metabolism due to greater effect of adrenaline than NA at beta receptors
action of adrenaline vs noradrenaline
Noradrenaline has a more specific action working mainly on alpha receptors to increase and maintain blood pressure whereas epinephrine has more wide-ranging effects. Norepinephrine is continuously released into circulation at low levels while epinephrine is only released during times of stress.
Specific effects of catecholamines
- incr release of glucose from liver
- incr release of fatty acids from fat stores
- incr HR
- incr constriction of visceral BVs
- incr BP
- Incr metabolic rate in skeletal muscles
Precursor of aldosterone
Cholesterol
Corticosterone
Actions of aldosterone
Stimulates reabsorption of Na+/excretion of K+ in cortical collecting ducts
Decr ratio of Na+ to K+ in sweat and saliva
Increases reabsorption of Na+ in the colon and excretion of K+ in the faeces
Overall retain Na+ and lose K+
Net effect incr in plasma vol and hence cardiovascular pressure
How does incr aldosterones increase NA+ reabsoprtion in the cortical collecting ducts
Increased synthesis of Na+ channels which move Na+ from tubular lumen into ccd cells (ATPase pump moves Na+ into ISF)
Renin-Angiotensin system
—-vanders
see kidney/CV lectures
BP drop- renin produced from kidney, travels in blood to the liver.
Angiotensinogen is produced by the liver, and is then broken up by renin, an enzyme produced in the kidney, to form angiotensin I.
This travels to the lungs, where the angiotensin converting enzyme converts Angiotensin I to to II
Angiotensin II acts on the adrenal cortex to produce aldosterone, leading to more Na+ reabsorption , incr BV etc which incr BP
Incr BP feeds back -vely to reduce renin secretion
Aldosterone anatgonist
Spironolactone: potassium-sparing diuretic hyperaldosteronism (Conn’s disease)
ACE inhibitors
Captopril, enalapril
Anti-hypertensive
Cardiac failure
ATII antagonist
Losartan
Similar to ACE inhibitors, used in hypertension
Common structure in all steroids
tetraplanar ring
Glucorticoids precursor
cholesterol
How are most glucorticoids transported
Bound to binding proteins
Regulation of glucorticoid secretion
Hypo, in response to stress releases CRH which acts on pituitary gland to produce ACTH, which acts on adrenal glands to produce cortisol, circulates and acts on tissues
Negative feedback - cortisol switches off pituitary production of ACTH and hypo production of CRH
CRH
corticotrophin releasing hormone
ACTH
adreno cortico Trophic hormone
Fluctuations in cortisol are caused by
fluctuations in ACTH secretion from the pituitary gland
Leads to circadian rhythm
Metabolic actions of glucorticoids
Stimulate gluconeogenesis in the liver- incr plasma glucose
Incr proteolysis in the muscle- creates AA’s which act as substrates for generation of glucose in the liver
Lipolysis of fat- incr glycerol production - alternative substrate for glucose so incr plasma glucose. Incr FFA production acts as fuel source for muscle and liver
Addison’s disease- cortisol deficiency
cellular metabolism: hypoglycaemaia, weight loss
CV: vasodilation, hypotension, reduced BV, anaemia and lymphocytosis
CNS: fatigue and anorexia
Salt balance: reduced Na, incr K (mineralcortocoid loss)
Inflammatory and immune system: tendency towards autoimmune disease
Corticosteroids
Cause rise in plasma glucose levels (release from liver and incr gluconeogenesis)
Causes incr in proteolysis, which can bring about muscle wasting skin thinning
Cause fat redistribution eg moon face (Cushings)
Cause incr breakdown of triglycerides, leading to rise in plasma Fatty acid levels
SUppress inflammation and immune responses
Cushing’s disease- cortisol excess
cellular metabolism: hyperglycaemia, fat redistribution, truncal obesity. Weak muscles, skin and bone and poor wound healing
CV: hypertension, incr BV, leukocytosis, erthyrocytosis
CNS: depression,euphoria
Salt balance: incr NA, decr K (more mineralocorticoid)
Inflammatory and immune response: decr inflam response, incr infection and decr fibrous tissue formation
