mechanism of action of hormones

sume hormone ke yang dicancel??ke cancel yg m/s 7 tu je??sorii aritu terlmbt dtg ms briefing..trlpas point doc ckp psl tjuk ni..

if im not mistaken, ALL hormones...doctor xnk tau psl mechanism of actions, they mean, mechanism of action ni yg pegi kt receptor, forming HRE, mRNA synthesis, channels formation, blablabla...sbab itu lebih krg serupa je bg semua hormone, cumenye doctor ambil berat psl effects of the hormones terhadap metabolism bdn...
rsenye la....

oohh gtu ek...seb bek..bnyk sgt mechanism die dah laa beza2 jgk sume nye..thanks.

ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

m/s yg mne actually ni???

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

1. Under the effect of ADH, water is reabsorbed. Water reabsorption occurs along with Na+ reabsorption. In Na+ reabsorption, it is coupled with secretion of H+ and K+. So, clearly, water and Na+ reabsorption will antagonize K+ secretion, kan, through ADH effect. Consequently, ADH will stimulate K+ secretion to balance the effect, because if there's no K+ secretion, there will be no Na+ reabsorption, when there's no Na+ reabsorption, there will be no water reabsorption.

2. Jap, tgh fikir~

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

V1 receptors kan action dia vasoconstriction..jadi dia nk balance effect tu la..
logically, kalau vasoconstriction jadi flow cikit kan? tp dlm case ni dia nk GFR tu high..jadi untuk balance effect vasocontriction tu, dia dilate glomerular tu..

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

ok answer for question 2.
Firstly, xjumpe pun V3 receptors dlm buku kidney. M/s berapa? Ade ke atau ana yg xperasan.

2. V3 receptors, based on my finding through Internet just now, V3 receptors are located at anterior pituitary gland and it is associated with the action of vasopressin. But, kalau nak dikaitkan dgn kidney, vasopressin functions as increasing arterial blood pressure, consequently, renal blood pressure through constricting renal blood vessels, thus increasing renal perfusion pressure. Stimulation of V3 receptors in glomerular mesangium would induce a local production of dilator prostaglandin which would dilate the local renal blood vessels as to maintain renal perfusion pressure, and not too high, as to maintain the GFR. As a conclusion, local production of dilator PG is a feedback mechanism of stimulation of V3 receptors through vasopressin.

If there's something wrong, please correct me.

drpetemd wrote:

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

m/s yg mne actually ni???

buku endocrine m/s 35

afnan fakhrurazi wrote:

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

V1 receptors kan action dia vasoconstriction..jadi dia nk balance effect tu la..
logically, kalau vasoconstriction jadi flow cikit kan? tp dlm case ni dia nk GFR tu high..jadi untuk balance effect vasocontriction tu, dia dilate glomerular tu..

drpetemd wrote:

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

ok answer for question 2.
Firstly, xjumpe pun V3 receptors dlm buku kidney. M/s berapa? Ade ke atau ana yg xperasan.

2. V3 receptors, based on my finding through Internet just now, V3 receptors are located at anterior pituitary gland and it is associated with the action of vasopressin. But, kalau nak dikaitkan dgn kidney, vasopressin functions as increasing arterial blood pressure, consequently, renal blood pressure through constricting renal blood vessels, thus increasing renal perfusion pressure. Stimulation of V3 receptors in glomerular mesangium would induce a local production of dilator prostaglandin which would dilate the local renal blood vessels as to maintain renal perfusion pressure, and not too high, as to maintain the GFR. As a conclusion, local production of dilator PG is a feedback mechanism of stimulation of V3 receptors through vasopressin.

If there's something wrong, please correct me.

activation V1 R>vasoconstriction + activation V3 R>local production PG> VD = maintain renal perfusion
kan?

ayunishafaf wrote:

afnan fakhrurazi wrote:

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

V1 receptors kan action dia vasoconstriction..jadi dia nk balance effect tu la..
logically, kalau vasoconstriction jadi flow cikit kan? tp dlm case ni dia nk GFR tu high..jadi untuk balance effect vasocontriction tu, dia dilate glomerular tu..

drpetemd wrote:

ayunishafaf wrote:ap dye nk ckp sbnrnyer
m/s 35

renal effects on tubular system..
"in cortical collecting tubule, water reabsorption under ADh effect lead to increase urinary K conc., which will antagonize K secretion??. ADH stim K secretion to balance this effect? -knp kne secrete K utk balance effect reabsorption of water?.. dlm kidney pn x citer

"V3 receptors in gromerular mesengium induce a local production of dilator prostaglandin................................. maintain renal perfusion.."?
pe maksud nk maintain renal perfusion?

ok answer for question 2.
Firstly, xjumpe pun V3 receptors dlm buku kidney. M/s berapa? Ade ke atau ana yg xperasan.

2. V3 receptors, based on my finding through Internet just now, V3 receptors are located at anterior pituitary gland and it is associated with the action of vasopressin. But, kalau nak dikaitkan dgn kidney, vasopressin functions as increasing arterial blood pressure, consequently, renal blood pressure through constricting renal blood vessels, thus increasing renal perfusion pressure. Stimulation of V3 receptors in glomerular mesangium would induce a local production of dilator prostaglandin which would dilate the local renal blood vessels as to maintain renal perfusion pressure, and not too high, as to maintain the GFR. As a conclusion, local production of dilator PG is a feedback mechanism of stimulation of V3 receptors through vasopressin.

If there's something wrong, please correct me.

activation V1 R>vasoconstriction + activation V3 R>local production PG> VD = maintain renal perfusion
kan?

rse2nyer V1 and V3 receptors sme je functions die tp location of the receptor tu je yg laen. V1 - in the brain, liver, kidney and vessels. V3 - anterior pituitary gland.

drpetemd wrote:

ayunishafaf wrote:


activation V1 R>vasoconstriction + activation V3 R>local production PG> VD = maintain renal perfusion
kan?

rse2nyer V1 and V3 receptors sme je functions die tp location of the receptor tu je yg laen. V1 - in the brain, liver, kidney and vessels. V3 - anterior pituitary gland.

yg pasal V3 kat anterior pituitary tu aku xtau lah. sebab ak merujuk buku..tp bgus la kalau ada inisiatif menggunakan internet sebagai sumber..

- mybe conclusion yg ringkas dan padat perlu kita concludekan kat cini..
- so apa conclusion yg drpetemd bleh bg berdasarkan huraian yg terperinci itu ??
- satu lagi, apa mksudnya function V3 & V1 tu sama?? action @ final feedback ?

afnan fakhrurazi wrote:

drpetemd wrote:

ayunishafaf wrote:


activation V1 R>vasoconstriction + activation V3 R>local production PG> VD = maintain renal perfusion
kan?

rse2nyer V1 and V3 receptors sme je functions die tp location of the receptor tu je yg laen. V1 - in the brain, liver, kidney and vessels. V3 - anterior pituitary gland.

yg pasal V3 kat anterior pituitary tu aku xtau lah. sebab ak merujuk buku..tp bgus la kalau ada inisiatif menggunakan internet sebagai sumber..

- mybe conclusion yg ringkas dan padat perlu kita concludekan kat cini..
- so apa conclusion yg drpetemd bleh bg berdasarkan huraian yg terperinci itu ??
- satu lagi, apa mksudnya function V3 & V1 tu sama?? action @ final feedback ?

Conclusion ak based on soalan yg tlah ditanyakan oleh ayunishafaf:
1. K+ secretion in balancing water reabsorption is needed; to keep Na+ reabsorption to occur. Actually, this is important in concentrating urine in the CT.
2. V3 receptors for vasopressin action, would produce local dilator PG as feedback mechanism as vasopressin contrict the BV while PG dilate the BV.

V3 & V1 tu sama bcoz, both of them are the receptors for Vasopressin. So, dia punye hasil stimulation sme je la kot. Vasopressin acts on both receptors > vasoconstriction. Particularly in kidney, they do constrict the renal vessels > local dilator PG as feedback mechanism to dilate the vessels as to maintain renal perfusion pressure. Mcm tu kot.

dalam buku page 35, V3 ada present jugak di corticotrope. ADH akan stimulate V3 receptor di corticotrope (ant pituitary), then akan produce ACTH dalam stress.

rasanyalah, utk action ke atas V3 di kidney - dia akan buat dilator prostaglandin. Dilator PGE2 akan buat VD. Reaction ni namanya ADH-prostaglandin relation which act as local -ve feedback utk balance kan action VC of ADH, so kita bolehlah maintain kan renal perfusion.

apsal xde org layan poll aku?!?!?!

https://gen9mdforum.forumegypt.net/t39-official-spam-thread-physiology-with-poll
cmon la guys!support the cause.


haha.

pipit,
aku nk bg kau tugas compile FAQ in physiology ni boleh?
berdasarkan apa bnde2 yg ditanya budak2 nih dkt forum nih
nnt aku buat satu thread baru.
senang sikit kalau ada org nk rujuk.

the question is
Can You DO It???
tibe.

Hamz!! wrote:apsal xde org layan poll aku?!?!?!

https://gen9mdforum.forumegypt.net/t39-official-spam-thread-physiology-with-poll
cmon la guys!support the cause.

"sometimes there's a need to cut some loose"

haha.

pipit,
aku nk bg kau tugas compile FAQ in physiology ni boleh?
berdasarkan apa bnde2 yg ditanya budak2 nih dkt forum nih
nnt aku buat satu thread baru.
senang sikit kalau ada org nk rujuk.

the question is
Can You DO It???
tibe.

haha bak kata NIKE Just Do it!
tp aku xjamin lah, byk lg yg xcover nih...tgoklah cne, kalau aku dpt buat, alhamdulillah, kalau xdpt, mtk maaf byk2