Effects of antihypertensive clonidine congeners on alpha-adrenergic receptors

1982 ◽  
Vol 60 (3) ◽  
pp. 342-344 ◽  
Author(s):  
Milt Titeler ◽  
Philip Seeman
Keyword(s):  
Frontal Cortex ◽  
Strong Correlation ◽  
Adrenergic Receptors ◽  
Alpha Adrenergic Receptors ◽  
Antihypertensive Action ◽  
Wb 4101

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.

Contraction of dog trachealis muscle in vivo: role of alpha-adrenergic receptors

1980 ◽  
Vol 48 (2) ◽  
pp. 329-336 ◽  
Author(s):  
W. H. Beinfield ◽  
J. Seifter
Keyword(s):  
Adrenergic Receptors ◽  
Beta Blockers ◽  
Systemic Arterial Pressure ◽  
Alpha Adrenergic Receptors ◽  
Bilateral Vagotomy ◽  
Cervical Trachea ◽  
Spontaneously Breathing ◽  
Trachealis Muscle

Contraction, relaxation, and longitudinal tension were recorded by isometric strain gauge arches attached to cervical tracheal muscle (CTM) in 60 spontaneously breathing dogs anesthetized with pentobarbital. Intravenous norepinephrine (NE) (3 X 10(-9), 6 X 10(-9), 1.2 X 10(-8), and 2.4 x 10(-8) mol/kg) increased spontaneous mechanical activities (SMA) and caused dose related contraction of CTM in all dogs even though there was no pretreatment with beta-blockers. These activities were first potentiated by propranolol and then prevented by phentolamine. NE briefly decreased SMA and induced CTM relaxation prior to the onset of contraction in one-third of dogs. Propranolol prevented this initial relaxation. CTM responses induced by NE were 1) not significantly altered by atropine, tripelennamine, bilateral vagotomy, curarization, and complete tracheal transection below transducer sites; 2) unrelated to passive constriction of cervical trachea associated with airway elongation; and 3) independent of reflexes initiated by elevations of systemic arterial pressure. The moles per kilogram doses of acetylcholine were found to exceed those of NE when their intravenous administration caused equal CTM contractions in the same dog. These findings are consistent with the existence of alpha-adrenergic receptors in CTM.

scholarly journals Distribution of alpha-adrenergic receptors in the rabbit nephron.

1984 ◽  
Vol 142 (3) ◽  
pp. 275-282 ◽  
Author(s):  
EIJI KUSANO ◽  
RYUICHI NAKAMURA ◽  
YASUSHI ASANO ◽  
MASASHI IMAI
Keyword(s):  
Adrenergic Receptors ◽  
Alpha Adrenergic Receptors
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