Mechanisms of the Antihypertensive Action of Captopril

Author(s):  
Johannes F. E. Mann
Life Sciences ◽  
1968 ◽  
Vol 7 (7) ◽  
pp. 381-387 ◽  
Author(s):  
Arnold J. Wohl ◽  
Lorraine M. Hausler ◽  
Franklin E. Roth

1997 ◽  
Vol 73 ◽  
pp. 161
Author(s):  
Yasushi Ohizumi ◽  
Yoichi Nakamura ◽  
Azusa Yoshida ◽  
Kimihiro Matsunaga ◽  
Kenichiro Nakao

2010 ◽  
Vol 33 (9) ◽  
pp. 1411-1418 ◽  
Author(s):  
Jung-Jin Lee ◽  
Chang-Yong Shin ◽  
Hong-Joon Park ◽  
Wei-Yun Zhang ◽  
Yohan Kim ◽  
...  

1982 ◽  
Vol 60 (3) ◽  
pp. 342-344 ◽  
Author(s):  
Milt Titeler ◽  
Philip Seeman

Evidence in the literature suggests that the antihypertensive effects of clonidine stem from its action on alpha-2 adrenergic receptors. In order to examine this possibility we tested the effects of 13 congeners of clonidine on the binding of [3H]WB-4101 and [3H]clonidine to calf frontal cortex homogenates; [3H]WB-4101 served as a label for alpha-1 receptors while [3H]clonidine served to label alpha-2 adrenergic receptors. All the substituted imidazolines were two to three orders more potent in inhibiting the binding of [3H]clonidine than they were against [3H]WB-4101. There was a strong correlation between the antihypertensive doses of these congeners and their concentrations required to inhibit the binding of [3H]clonidine. The results are compatible with the concept that the antihypertensive action of clonidine is more likely due to interactions with alpha-2 adrenergic receptors than with alpha-1 receptors.


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