hypothalamic-pituitary physiology -Bi Flashcards
Where are ADH and Oxytocin synthesized?
in the magnocellular neurons of the SON and PVN (synthesized as precursors)
ADH in SON and OT in PVN, mostly.
What is an endocrine cell?
a cell that secretes their chemical products (hormones) into the interstitial space from where they reach circulation
Hormone=chemical product released by endocrine cells that have biological action
What are precursors for AVP (arginine vasopressin) and OT divided into? Where does this take place?
AVP precursor (prepropresophysin) = AVP and neurophysin II
OT precursor (preprooxyphysin) = oxytocin and neurophysin I
in the secretory vesicles
How are AVP and OT released?
controlled by Ca2+ influx through voltage-gated Ca2+ channels upon cell depolarization causing exocytosis from the nerve endings in the posterior lobe
What stimulates oxytocin release? What is the rate of this firing/release?
stimulation of stretch receptors in the female reproductive tract and breast nipples causes an increase in high-frequency discharge of oxytocin release
firing rate is fast at rest and higher frequency when stimulated
What stimulates ADH release? What is the rate of this firing/release?
increase in plasma osmolality (most effective) and decrease in ECF volume
- OVLT (osmolality change >1%)–> decrease inhibition on magnocellular neurons (to cause an increase in ADH secretion)
- baroreceptor (BP change >10%)–> decreases firing of CN 9 and 10–> NTS
- renin–> angiotensin –> increase in aldosterone
AVP fires slowly at rest –> stimulation due to decrease ECF volume–> fast firing–> release of AVP continues for at least 20 min after stimulation
What type of receptor does oxytocin have an effect on? What does this cause?
GPCR-Gq/11
–> increase PLC –> inc. [Ca2+] –> stimulate uterine and mammary myoepithelial cell contraction and milk ejection
What is the only positive feedback mechanism seen in the endocrine system?
the positive feedback of uterine contraction –> stretching of female reproductive organs/cervical distention–> increase of OT release
What type of receptors does ADH have an effect on (3)? What second messenger systems are used and what does this lead to?
V2R (Gs coupled): increase PKA–> inc adenylate cyclase –> increase cAMP–> V2Rs–> insert AQP2 water channels into the luminal membrane of cells in the distal tubule and collecting duct –> increase water retention
V1aR (coupled to Gq/11)==> PLC–> increase [Ca2+]==> inc. contraction of smooth mm cells and liver==> vasoconstriction ==> inc. BP
V3R (Gq coupled)–> inc. PLC –> inc [Ca2+] –> increase ACTH, prolactin, endorphin secretion from ant pit
What regulates the oxytocin receptors?
- estrogen increases receptor expression
- progesterone inhibits receptor sensitivity
- fear, pain, noise, fever inhibit OT release
What regions of the brain have been shown to be important in loyalty? What hormone interacts with these regions?
NAcc and PFC
oxytocin
What is Diabetes Insipidus?
a deficiency in ADH leading to polyuria and polydipsia
What hypothalamic product inhibits prolactin??
Dopamine
What effect does ADH have on the kidney?
increase in AQP2 channels on the lumen side of the distal collecting duct in order to decrease water excretion and increase urine osmolality
(Gs coupled –> PKA–>adenylate cyclase –> cAMP)
If a person is hypovolemic but has a low osmolality, will they produce ADH?
Yes!
at low blood volume, volume is more important than osmolality
How does the GH receptor function? What type of receptor is this?
cytokine receptor
dimerization and phosphorylation are essential for the activation–> JAK2-STAT pathway to lead to nuclear gene transcription
What are the effects of GH? (on bones, protein, electrolytes, carbs, fats)
- promotes long bone growth (unfused epiphysis–> gigantism) or increases bone turnover (closed epiphysis –> acromegaly)
- increase protein synthesis and cell proliferation in skeletal mm
- increase Ca2+ absorption and decrease Na+ and K+ excretion
- increased hepatic glucose output
- increase lipolysis
What does GH increase the secretion of?
IGF-1
also increases tissue sensitivity to IGF-1
What does IGF-1 do? What can this do to insulin receptors?
IGF-1 can promote maximal growth
IGF-1 receptor is simular to insulin receptors and can increase glucose uptake into mm. (decrease blood glucose level)
When is GH released?
pulsatile bursts during slow wave sleep.
What stimulates GH synthesis? Inhibits GH synthesis?
GHRH stimulates GH synthesis by binding to Gs
Somatostatin inhibits GH synthesis by binding to Gi. also, suppresses GH release by hyper polarization of the membrane
What cells secrete prolactin? What type of receptors are used?
lactotrophs synthesize and secrete prolactin
class 1 cytokine –> dimerization and phosphorylation
How does prolactin affect GnRH?
prolactin inhibits the synthesis and release of GnRH
How does dopamine affect prolactin?
dopamine inhibits prolactin through binding to D2 (Gi) receptor
What 3 things inhibit prolactin secretion?
dopamine, somatostating and GABA
How does suckling affect prolactin release?
suckling increases prolactin release by reducing dopamine inhibition
How does TRH affect prolactin? What can happen in a thyroid deficient patient?
TRH stimulated prolactin secretion
in a thyroid deficient patient, you lose the feedback inhibition of T4 on TRH==> too much TRH –> can lead to too much prolactin release and milk production
How does TRH affect prolactin? What can happen in a thyroid deficient patient? **
TRH stimulated prolactin secretion
in a thyroid deficient patient, you lose the feedback inhibition of T4 on TRH==> too much TRH –> can lead to too much prolactin release and milk production
How can elevated GH affect insulin?
IGF-1 can act at insulin receptors leading to an insulin resistance
