hypothalamic-pituitary physiology -Bi

Question 1

Where are ADH and Oxytocin synthesized?

Answer 1

in the magnocellular neurons of the SON and PVN (synthesized as precursors)

ADH in SON and OT in PVN, mostly.

Question 2

What is an endocrine cell?

Answer 2

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

Question 3

What are precursors for AVP (arginine vasopressin) and OT divided into? Where does this take place?

Answer 3

AVP precursor (prepropresophysin) = AVP and neurophysin II

OT precursor (preprooxyphysin) = oxytocin and neurophysin I

in the secretory vesicles

Question 4

How are AVP and OT released?

Answer 4

controlled by Ca2+ influx through voltage-gated Ca2+ channels upon cell depolarization causing exocytosis from the nerve endings in the posterior lobe

Question 5

What stimulates oxytocin release? What is the rate of this firing/release?

Answer 5

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

Question 6

What stimulates ADH release? What is the rate of this firing/release?

Answer 6

increase in plasma osmolality (most effective) and decrease in ECF volume

1. OVLT (osmolality change >1%)–> decrease inhibition on magnocellular neurons (to cause an increase in ADH secretion)
2. baroreceptor (BP change >10%)–> decreases firing of CN 9 and 10–> NTS
3. 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

Question 7

What type of receptor does oxytocin have an effect on? What does this cause?

Answer 7

GPCR-Gq/11

–> increase PLC –> inc. [Ca2+] –> stimulate uterine and mammary myoepithelial cell contraction and milk ejection

Question 8

What is the only positive feedback mechanism seen in the endocrine system?

Answer 8

the positive feedback of uterine contraction –> stretching of female reproductive organs/cervical distention–> increase of OT release

Question 9

What type of receptors does ADH have an effect on (3)? What second messenger systems are used and what does this lead to?

Answer 9

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

Question 10

What regulates the oxytocin receptors?

Answer 10

• estrogen increases receptor expression
• progesterone inhibits receptor sensitivity
• fear, pain, noise, fever inhibit OT release

Question 11

What regions of the brain have been shown to be important in loyalty? What hormone interacts with these regions?

Answer 11

NAcc and PFC

oxytocin

Question 12

What is Diabetes Insipidus?

Answer 12

a deficiency in ADH leading to polyuria and polydipsia

Question 13

What hypothalamic product inhibits prolactin??

Answer 13

Dopamine

Question 14

What effect does ADH have on the kidney?

Answer 14

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)

Question 15

If a person is hypovolemic but has a low osmolality, will they produce ADH?

Answer 15

Yes!

at low blood volume, volume is more important than osmolality

Question 16

How does the GH receptor function? What type of receptor is this?

Answer 16

cytokine receptor

dimerization and phosphorylation are essential for the activation–> JAK2-STAT pathway to lead to nuclear gene transcription

Question 17

What are the effects of GH? (on bones, protein, electrolytes, carbs, fats)

Answer 17

1. promotes long bone growth (unfused epiphysis–> gigantism) or increases bone turnover (closed epiphysis –> acromegaly)
2. increase protein synthesis and cell proliferation in skeletal mm
3. increase Ca2+ absorption and decrease Na+ and K+ excretion
4. increased hepatic glucose output
5. increase lipolysis

Question 18

What does GH increase the secretion of?

Answer 18

IGF-1

also increases tissue sensitivity to IGF-1

Question 19

What does IGF-1 do? What can this do to insulin receptors?

Answer 19

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)

Question 20

When is GH released?

Answer 20

pulsatile bursts during slow wave sleep.

Question 21

What stimulates GH synthesis? Inhibits GH synthesis?

Answer 21

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

Question 22

What cells secrete prolactin? What type of receptors are used?

Answer 22

lactotrophs synthesize and secrete prolactin

class 1 cytokine –> dimerization and phosphorylation

Question 23

How does prolactin affect GnRH?

Answer 23

prolactin inhibits the synthesis and release of GnRH

Question 24

How does dopamine affect prolactin?

Answer 24

dopamine inhibits prolactin through binding to D2 (Gi) receptor

Question 25

What 3 things inhibit prolactin secretion?

Answer 25

dopamine, somatostating and GABA

Question 26

How does suckling affect prolactin release?

Answer 26

suckling increases prolactin release by reducing dopamine inhibition

Question 27

How does TRH affect prolactin? What can happen in a thyroid deficient patient?

Answer 27

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

Question 28

How does TRH affect prolactin? What can happen in a thyroid deficient patient? **

Answer 28

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

Question 29

How can elevated GH affect insulin?

Answer 29

IGF-1 can act at insulin receptors leading to an insulin resistance