Tweet
This was written by a good and knowledgable bro:
A basic description of how they work. ie. non scientific: In my own words
I have spent a lot of time over the last 9 months or so trying to understand how GRF / GHRP works in the human body. Given that I do not have any formal schooling in micro-biology I have to turn events into everyday type activities so that I can visualize / understand them.
Many seem confused about why there is a synergistic process that occurs when GRF and GHRP are used together and what role somatostatin plays in the whole GH release picture. Below I will summarize how I visualize the process. It is very simplistic and ignores many of the details of what is going on but it works well in my simple mind and allows me to remember how this stuff actually works.
For this process I picture the pituitary gland as being a hopper with a drain valve located at the bottom. This hopper is filled with marbles that represent GH.
There is a person (somatostatin) sitting at the drain valve. He is in charge of opening and closing this valve. As we age, he has more influence on keeping the valve closed. The hopper is full of GH but Somatostatin will not let anyone open the valve to any great extent. GRF (GHRH endogenously) wants to open the valve but cant. If Somatostatin goes on a break (a period of GH peak) and leaves the valve unattended the GRF can crack open the valve some, say 10%. If somatostatin is present (period of GH trhough) GRF can trick somatostatin into opening the valve fractionally, say 2%. We get some release but the trough is still a trough albeit a little bit higher.
GHRP is like a big brother to GRF. When working alone GHRP can force somatostatin to go on break and open the drain valve to say 80%. We get a good dump of GH whether we are in a trough period OR a peak period.
Now, if we introduce GRF and GHRP TOGETHER, GHRP sends somatostatin away on break so that GHRP and GRF can work together on opening the drain valve. Together they get it to open 120% (I use 120 to demonstrate synergy) and we get a complete dump of the GH hopper.
CJC 1295 is a peptide that tricks somatostatin to leaving the valve cracked causing GH bleed. GH bleed is not the ideal situation because GH receptors in body tissue do not have time to clear.
Keep in mind GRF and GHRP, on a micro level, actually work via different pathways but the above is a good illustration of what functionally is occurring.
Part 2. A more scientific description: Again in my own words:
what can I say, typing this shitt out helps me remember / understand wtf is going on.....
Also think of things this way.
There are 3 components, well lets say 4 if you count somatotrophs which are GH releasing cells.
Somatotropin inhibits GH release and is responsible in large part to GH pulsation (when its activity is low it allows a pulse)
GHRH (or GRF exogenously) initiates the GH pulse (but will not sustain it in the presence of high somatostatin activity)
Ghrelin (or GHRP exogenously) modulates the GH pulse
GRF and GHRP cause GH release via 2 different pathways, this is why their actions are synergistic.
GHRP acts directly on somatotrophs to cause a GH release and potentiate the effects of GRF. Also, GHRP is essentially an antagonist of somatostatin..... that is why by itself it can initiate a sizable GH release.
GRF causes cAMP production in somatotrophs, GHRP has no effect on cAMP.
When the 2 are combined GHRH's effects on cAMP production are amplified.
GHRH stimulates GH release through protein kinase A pathway, GHRP through protein kinase C..
So why is there a synergy between GRF and GHRP? GHRP is a GHS (growth hormone secretagogues) and has the ability to bind Growth Hormone Secretagogues receptors (GHS-R) thereby effecting GH release. It affects GH release in a couple of ways. First it induces GHRH to be released from the hypothalamus, once released this GHRH makes its way to the pituitary gland where it binds with Growth Hormone Releasing Receptors (GHRH-R). Once bound signals for GH release. GHS (GHRP) also makes its way to the pituitary gland where it can also bind with GHS-R and signal its own GH release. GHRH and GHRP signal GH release through completely different pathways. This is why the effects are synergistic.
Finally, GHS (GHRP) influence GH release by reducing the release of somatostatin from the hypothalamus and by reducing somatostatin inhibiting action once it binds to receptors in the pituitary. GHRH (GRF) does not have this influence over the actions of somatostatin.
So, GHS (GHRP) turns up the the signal to release GHRH, turns down the signal to release somatostatin, tells GH releasing cells in the pituitary gland to release GH while also telling them to ignore the message from somatostatin to stop releasing GH....
Hope this helps. I understand it better after I have to type out what I think I know...... If anyone notes errors here please post up!!
A basic description of how they work. ie. non scientific: In my own words
I have spent a lot of time over the last 9 months or so trying to understand how GRF / GHRP works in the human body. Given that I do not have any formal schooling in micro-biology I have to turn events into everyday type activities so that I can visualize / understand them.
Many seem confused about why there is a synergistic process that occurs when GRF and GHRP are used together and what role somatostatin plays in the whole GH release picture. Below I will summarize how I visualize the process. It is very simplistic and ignores many of the details of what is going on but it works well in my simple mind and allows me to remember how this stuff actually works.
For this process I picture the pituitary gland as being a hopper with a drain valve located at the bottom. This hopper is filled with marbles that represent GH.
There is a person (somatostatin) sitting at the drain valve. He is in charge of opening and closing this valve. As we age, he has more influence on keeping the valve closed. The hopper is full of GH but Somatostatin will not let anyone open the valve to any great extent. GRF (GHRH endogenously) wants to open the valve but cant. If Somatostatin goes on a break (a period of GH peak) and leaves the valve unattended the GRF can crack open the valve some, say 10%. If somatostatin is present (period of GH trhough) GRF can trick somatostatin into opening the valve fractionally, say 2%. We get some release but the trough is still a trough albeit a little bit higher.
GHRP is like a big brother to GRF. When working alone GHRP can force somatostatin to go on break and open the drain valve to say 80%. We get a good dump of GH whether we are in a trough period OR a peak period.
Now, if we introduce GRF and GHRP TOGETHER, GHRP sends somatostatin away on break so that GHRP and GRF can work together on opening the drain valve. Together they get it to open 120% (I use 120 to demonstrate synergy) and we get a complete dump of the GH hopper.
CJC 1295 is a peptide that tricks somatostatin to leaving the valve cracked causing GH bleed. GH bleed is not the ideal situation because GH receptors in body tissue do not have time to clear.
Keep in mind GRF and GHRP, on a micro level, actually work via different pathways but the above is a good illustration of what functionally is occurring.
Part 2. A more scientific description: Again in my own words:
what can I say, typing this shitt out helps me remember / understand wtf is going on.....
Also think of things this way.
There are 3 components, well lets say 4 if you count somatotrophs which are GH releasing cells.
Somatotropin inhibits GH release and is responsible in large part to GH pulsation (when its activity is low it allows a pulse)
GHRH (or GRF exogenously) initiates the GH pulse (but will not sustain it in the presence of high somatostatin activity)
Ghrelin (or GHRP exogenously) modulates the GH pulse
GRF and GHRP cause GH release via 2 different pathways, this is why their actions are synergistic.
GHRP acts directly on somatotrophs to cause a GH release and potentiate the effects of GRF. Also, GHRP is essentially an antagonist of somatostatin..... that is why by itself it can initiate a sizable GH release.
GRF causes cAMP production in somatotrophs, GHRP has no effect on cAMP.
When the 2 are combined GHRH's effects on cAMP production are amplified.
GHRH stimulates GH release through protein kinase A pathway, GHRP through protein kinase C..
So why is there a synergy between GRF and GHRP? GHRP is a GHS (growth hormone secretagogues) and has the ability to bind Growth Hormone Secretagogues receptors (GHS-R) thereby effecting GH release. It affects GH release in a couple of ways. First it induces GHRH to be released from the hypothalamus, once released this GHRH makes its way to the pituitary gland where it binds with Growth Hormone Releasing Receptors (GHRH-R). Once bound signals for GH release. GHS (GHRP) also makes its way to the pituitary gland where it can also bind with GHS-R and signal its own GH release. GHRH and GHRP signal GH release through completely different pathways. This is why the effects are synergistic.
Finally, GHS (GHRP) influence GH release by reducing the release of somatostatin from the hypothalamus and by reducing somatostatin inhibiting action once it binds to receptors in the pituitary. GHRH (GRF) does not have this influence over the actions of somatostatin.
So, GHS (GHRP) turns up the the signal to release GHRH, turns down the signal to release somatostatin, tells GH releasing cells in the pituitary gland to release GH while also telling them to ignore the message from somatostatin to stop releasing GH....
Hope this helps. I understand it better after I have to type out what I think I know...... If anyone notes errors here please post up!!