Abstract
1. Cardiac failure in humans and in animal models is associated with a marked desensitization of the catecholamine signalling pathway. 2. β1‐ and β2‐ and possibly β3‐adrenoceptors (β‐AR) are found in the hearts of humans and common laboratory animals such as rats and guinea‐pigs. In rats and guinea‐pigs chronic stimulation of cardiac β‐AR leads to a rapid loss of β2‐AR whereas heart failure in humans is associated with a loss of β1‐AR or β1‐AR and β2AR. 3. Desensitization is also associated with phosphorylation of β‐AR by β‐AR kinase β‐ARK) and uncoupling of receptors from the signalling pathway. β‐ARK but not β‐arrestin activity and mRNA are markedly increased in heart failure. 4. Chronic β‐AR stimulation and heart failure are associated with increases in Giα but little if any change in Gsα. 5. The roles of βm̀ subunits of G‐proteins, adenylate cyclase subtypes and cAMP dependent protein kinase A in heart failure are unclear at present.
| Original language | English |
|---|---|
| Pages (from-to) | 874-876 |
| Number of pages | 3 |
| Journal | Clinical and Experimental Pharmacology and Physiology |
| Volume | 22 |
| Issue number | 11 |
| DOIs | |
| Publication status | Published - 1 Jan 1995 |
| Externally published | Yes |
Keywords
- cardiac failure
- G‐proteins.
- β‐adrenoceptor kinase
- β‐adrenoceptors
- β‐arrestin
Cite this
}
Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, 1994 : SIGNALLING PATHWAYS IN CARDIAC FAILURE. / Summers, Roger J.; McMartin, Lynne R.; Kompa, Andrew; Gu, Xinhua; Molenaar, Peter.
In: Clinical and Experimental Pharmacology and Physiology, Vol. 22, No. 11, 01.01.1995, p. 874-876.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists, 1994
T2 - SIGNALLING PATHWAYS IN CARDIAC FAILURE
AU - Summers, Roger J.
AU - McMartin, Lynne R.
AU - Kompa, Andrew
AU - Gu, Xinhua
AU - Molenaar, Peter
PY - 1995/1/1
Y1 - 1995/1/1
N2 - 1. Cardiac failure in humans and in animal models is associated with a marked desensitization of the catecholamine signalling pathway. 2. β1‐ and β2‐ and possibly β3‐adrenoceptors (β‐AR) are found in the hearts of humans and common laboratory animals such as rats and guinea‐pigs. In rats and guinea‐pigs chronic stimulation of cardiac β‐AR leads to a rapid loss of β2‐AR whereas heart failure in humans is associated with a loss of β1‐AR or β1‐AR and β2AR. 3. Desensitization is also associated with phosphorylation of β‐AR by β‐AR kinase β‐ARK) and uncoupling of receptors from the signalling pathway. β‐ARK but not β‐arrestin activity and mRNA are markedly increased in heart failure. 4. Chronic β‐AR stimulation and heart failure are associated with increases in Giα but little if any change in Gsα. 5. The roles of βm̀ subunits of G‐proteins, adenylate cyclase subtypes and cAMP dependent protein kinase A in heart failure are unclear at present.
AB - 1. Cardiac failure in humans and in animal models is associated with a marked desensitization of the catecholamine signalling pathway. 2. β1‐ and β2‐ and possibly β3‐adrenoceptors (β‐AR) are found in the hearts of humans and common laboratory animals such as rats and guinea‐pigs. In rats and guinea‐pigs chronic stimulation of cardiac β‐AR leads to a rapid loss of β2‐AR whereas heart failure in humans is associated with a loss of β1‐AR or β1‐AR and β2AR. 3. Desensitization is also associated with phosphorylation of β‐AR by β‐AR kinase β‐ARK) and uncoupling of receptors from the signalling pathway. β‐ARK but not β‐arrestin activity and mRNA are markedly increased in heart failure. 4. Chronic β‐AR stimulation and heart failure are associated with increases in Giα but little if any change in Gsα. 5. The roles of βm̀ subunits of G‐proteins, adenylate cyclase subtypes and cAMP dependent protein kinase A in heart failure are unclear at present.
KW - cardiac failure
KW - G‐proteins.
KW - β‐adrenoceptor kinase
KW - β‐adrenoceptors
KW - β‐arrestin
UR - http://www.scopus.com/inward/record.url?scp=0028838529&partnerID=8YFLogxK
U2 - 10.1111/j.1440-1681.1995.tb01954.x
DO - 10.1111/j.1440-1681.1995.tb01954.x
M3 - Article
VL - 22
SP - 874
EP - 876
JO - Clinical and Experimental Pharmacology and Physiology
JF - Clinical and Experimental Pharmacology and Physiology
SN - 0305-1870
IS - 11
ER -