Cholinergic and Adrenergic System

2019 ◽  
pp. 69-81
Author(s):  
Roland Seifert
Keyword(s):  
Adrenergic System

Alterations in the regional   adrenergic system in experimental left ventricular hypertrophy

1990 ◽  
Vol 24 (1) ◽  
pp. 65-71 ◽  
Author(s):  
P. M Scholz ◽  
M. E Upsher ◽  
D. Eliades ◽  
J. Kedem ◽  
H. R Weiss
Keyword(s):  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Adrenergic System

Influnce of the beta-adrenergic agonist clenbuterol on plasma catecholamines and lymphocyte beta-receptors

1986 ◽  
Vol 1 (3) ◽  
pp. 234-236
Author(s):  
B. Bondy ◽  
M. Ackenheil ◽  
G. Laakmann ◽  
H.T. Munz
Keyword(s):  
Specific Binding ◽  
Plasma Catecholamines ◽  
Adrenergic System ◽  
Plasma Norepinephrine ◽  
Adrenergic Agonists ◽  
Adrenergic Agonist ◽  
Beta Receptors ◽  
Β Receptor ◽  
Beta Adrenergic Agonist ◽  
The Brain

SummaryThe influence of subchronic application of the β-adrenergic agonist clenbuterol on plasma norepinephrine (NE), epinephrine (E) and β-receptors on lymphocytes was investigated in 8 male, healthy volunteers. Treatment with clenbuterol (0.04 mg/day) for 6 days induced significant reduction of β-receptor specific binding in 7 of the 8 subjects with a mean decrease of 40% (p < 0.01) with no changes in affinity. Concomitantly an increase in the plasma NE concentration was observed (mean 50%, p < 0.01), but no significant overall alteration of E concentration. Our results suggest that β-adrenergic agonists exercise a similar effect on the peripheral adrenergic system and on the adrenergic system in the brain.

scholarly journals Effects of captopril on the beta-adrenergic system in noninfarcted myocardium in the rat heart failure model

1991 ◽  
Vol 17 (2) ◽  
pp. A133 ◽  
Author(s):  
Karil Bellah ◽  
Thomas Raya ◽  
Sheldon Litwin ◽  
Steven Goldman ◽  
Joel Karliner
Keyword(s):  
Heart Failure ◽  
Rat Heart ◽  
Adrenergic System ◽  
Failure Model ◽  
Beta Adrenergic ◽  
Heart Failure Model

scholarly journals Modulation of cannabinoid signaling by amygdala α2-adrenergic system in fear conditioning

2016 ◽  
Vol 300 ◽  
pp. 114-122 ◽  
Author(s):  
Mohammad Nasehi ◽  
Majid Zamanparvar ◽  
Mohaddeseh Ebrahimi-Ghiri ◽  
Mohammad-Reza Zarrindast
Keyword(s):  
Fear Conditioning ◽  
Adrenergic System

Direct vasoconstrictor action of homologous angiotensin II on isolated arterial ring preparations in an elasmobranch fish

1998 ◽  
Vol 158 (3) ◽  
pp. 419-423 ◽  
Author(s):  
K Hamano ◽  
ML Tierney ◽  
K Ashida ◽  
Y Takei ◽  
N Hazon
Keyword(s):  
Angiotensin Ii ◽  
Adrenergic System ◽  
Ang Ii ◽  
Unusual Structure ◽  
Coeliac Artery ◽  
Ventral Aorta ◽  
Pre Treatment ◽  
Vascular Receptor ◽  
Dose Dependent ◽  
Branchial Artery

Arterial rings were prepared from the branchial artery, coeliac artery and ventral aorta of the Japanese dogfish Triakis scyllia and used to determine arterial contraction in a myograph. Noradrenaline caused a dose-dependent contraction (10(-9)-3 x 10(-6) M) that was completely inhibited by pre-treatment with 10(-7) M phentolamine. Homologous dogfish angiotensin II (ANG II) ([Asn1, Pro3, Ile5]-ANG II) also caused dose-dependent contraction (10(-9)-3 x 10(-6) M), but phentolamine had no effect on this response. Administration of dogfish angiotensin I (ANG-I) ([Asn1, Pro3, Ile5, Gln9]-ANG I) resulted in a contraction similar to that produced by ANG II and the effect could be blocked with 10(-7) M captopril. The mammalian ANG II receptor antagonists [Sar1, Ile8]-ANG II and [Sar1, Ala8]-ANG II caused dose-dependent contractions of coeliac artery rings, but were less potent than homologous ANG I and ANG II. These results show that the contractile effect of [Asn1, Pro3, Ile5]-ANG II is not mediated by the alpha-adrenergic system and contractions of arterial rings by noradrenaline and elasmobranch ANG II are mediated by separate vascular receptors. The elasmobranch ANG II vascular receptor may have co-evolved with the unusual structure of this peptide.

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