Cutaneous Circulation;
Is controlled by sympathetic adrenergic nervs by releasing Nor Epi acting on Alpha receptors....Beta 2 receptors dont exict physiologically......BUT Pharmacologically Beta2 receptors presence can be demonostrated by High Dose of Agonist to the receptors......
My question is if Beta 2 receptors are not present physiologically then how can one demonstrate their presence pharmacologically?
Can anyone PLEASE explain.....
Gracis
cutaneous nerves are NOT INNERVATED by adrenergic nerves but they do have B2 receptors... therefore:
a direct B2 agonist can cause vasodilation
and also remember (and this has come up in a few usmle q's) that indirect agonists eg cocaine, ephedrine, tyramine, amphetamine have NO effect on cutaneous B2 because they are not innervated
Thankyou hopingfor99,
Can you explain to me little bit more in detail or tell me where I can get more info cos I am getting more confused on this.
How can symp adrenergic control if it is not innervated? can you please explain to me a little bit basic......please
thanks
take a different example:
did u know that Ach causes vasodilation????
well i'm also gonna tell u that vessels have no parasymp innervation! so they have receptors but no innervation... this means that when there is a general parasympathetic outflow from the brain to all the body, vessels will NOT be effected by the parasymp because they are not innervated.. but if u give a muscarinic agonist eg bethanechol, it will DIRECTLY effect the receptors and cause vasodilation...
when it comes to sympathetic: the alpha receptors are innervated and so ARE affected by general sympathetic output but the beta receptors are not innervated...
any more q's and i'll be willin to answe
Thanks a ton Buddy that was a very good explanation cleared my doubt....
So correct me if I am wrong here......
on the arteriols there are Alpha and Beta2 receptors....Alpha are innerveted Where as Beta 2 are not innerveted but have Receptors....right....so when you give a high dose of Agonist they act directly on the receptors on the arteriols and do their action.......since alpha is controled by invertion it does not act by the agonist even though it has receptors...am I right....
Gracis
all correct except for ure last statement:
"since alpha is controled by invertion it does not act by the agonist even though it has receptors"
now alpha is innervated which means: an impulse travels across the nerve ---> reaches the end opening voltage gated Ca channels ---> which cause release of neurotransmitter (norepinephrine) into the synaptic space which acts on the alpha receptor to cause vasoconstriction... But since there are alpha receptors why wouldn't an exogenous agonist act on them!!!
so basically when it comes to alpha: both nerve stimulation and exogenous agonist (in the form of a drug) will work.... i hope its clear
So you mean that when a aganist is given it can act on Alpha as well as on Beta2 is this what I am getting.....right
I meant Agonist not Against
EXACTLY... take epinephrine as an example, it is agonistic at both alpha 1 and beta 2 (as well as beta 1)... now at low doses it acts on beta2 and causes vasodilation and hypotension, but at higher doses it prefers alpha1 and thus causes vasoconstriction and hypertension....
good I got it all for now......Thankyou very much hopingfor99
Good Luck for your exams