Jump to content
 







Main menu
   


Navigation  



Main page
Contents
Current events
Random article
About Wikipedia
Contact us
Donate
 




Contribute  



Help
Learn to edit
Community portal
Recent changes
Upload file
 








Search  

































Create account

Log in
 









Create account
 Log in
 




Pages for logged out editors learn more  



Contributions
Talk
 



















Contents

   



(Top)
 


1 Adipose tissue metabolism  
1 comment  




2 relationship between alpha1 and beta2 receptors  





3 Blood vessels of erectile tissue  
1 comment  




4 Use of β2 agonists to stop labor  
1 comment  













Talk:Alpha-1 adrenergic receptor




Page contents not supported in other languages.  









Article
Talk
 

















Read
Edit
Add topic
View history
 








Tools
   


Actions  



Read
Edit
Add topic
View history
 




General  



What links here
Related changes
Upload file
Special pages
Permanent link
Page information
Get shortened URL
Download QR code
 




Print/export  



Download as PDF
Printable version
 
















Appearance
   

 






From Wikipedia, the free encyclopedia
 


Adipose tissue metabolism[edit]

The adipose tissue doesn't carry out the glycogenolysis or the gluconeogenesis. The former mainly occurs in the skeletal and heart muscle, and in the liver, and the latter mainly in the liver, and during long-term fast or acidosis also in the kidney. 81.60.184.141 (talk) 11:14, 18 January 2011 (UTC)[reply]

relationship between alpha1 and beta2 receptors[edit]

There are Low levels of epinephrine cause dilation of blood vessels in skeletal muscle, while high levels cause constriction. Blood vessels have both alpha and beta2 receptors, but there are more alpha than beta. Beta receptors have a greater affinity for epinephrine, however, and at low levels of epinephrine there is a beta2 effect of vasodilation. At high levels, the alpha receptor stimulation overrides the beta2 and there is a vasoconstriction.

Blood vessels of erectile tissue[edit]

I don't think this is that big of an effect (relatively speaking, the parasympathetics do more), and by mentioning it may be misleading. BrotherSulayman (talk) 05:24, 12 March 2012 (UTC)[reply]

Use of β2 agonists to stop labor[edit]

As most recently added (04:07, 13 April 2019‎) by Prakash Nadkarni:『Uterus (when pregnant): this is minor compared to the relaxing effects of the β2 receptor, agonists of which - notably albuterol/salbutamol - were formerly used to inhibit premature labor.』The comment on the addition is somewhat more detailed: "(... - added a note that the beta-2 relaxant effects dominate for pregnant uterus. Albuterol and ritodrine were extensively used to inhibit premature labor, though their use has now been supplanted by (better-tolerated) Calcium-channel antagonists like nifedipine.)"

How recent is this change, and where has it taken place? A family member was given either albuterol or salbutamol to halt labor before conversion to Cesarean section two years ago. Might calcium-channel blockers (especially nifedipine) be contraindicated in some cases of concurrent medications or (non-circulatory) disorders?

In any case, it might be helpful to concisely add some of the information in your revision comment to the article itself, and add sources for the change in treatment strategies. I've added a non-judgmental [citation needed] to motivate others to find sources. My own (admittedly quick) search for use of β2 agonists to inhibit labor found papers within the last year or two noting it as a usual method. — Preceding unsigned comment added by 2605:E000:23D2:9000:B478:7CC1:38B:68E5 (talk) 15:47, 11 June 2019 (UTC)[reply]


Retrieved from "https://en.wikipedia.org/w/index.php?title=Talk:Alpha-1_adrenergic_receptor&oldid=1198485102"

Categories: 
C-Class Molecular Biology articles
Unknown-importance Molecular Biology articles
C-Class MCB articles
Low-importance MCB articles
WikiProject Molecular and Cellular Biology articles
All WikiProject Molecular Biology pages
 



This page was last edited on 24 January 2024, at 06:55 (UTC).

Text is available under the Creative Commons Attribution-ShareAlike License 4.0; additional terms may apply. By using this site, you agree to the Terms of Use and Privacy Policy. Wikipedia® is a registered trademark of the Wikimedia Foundation, Inc., a non-profit organization.



Privacy policy

About Wikipedia

Disclaimers

Contact Wikipedia

Code of Conduct

Developers

Statistics

Cookie statement

Mobile view



Wikimedia Foundation
Powered by MediaWiki