Effects of clonidine, dihydralazine and splanchnic nerve stimulation on the release of neuropeptide Y, MET-enkephalin and catecholamines from dog adrenal medulla

Author(s):  
Christine Damase-Michel ◽  
Genevi�ve Tavernier ◽  
Pierre Giraud ◽  
Jean-Louis Montastruc ◽  
Paul Montastruc ◽  
...  
1991 ◽  
Vol 69 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Sylvain Foucart ◽  
Jacques de Champlain ◽  
Réginald Nadeau

In the present study, we have evaluated the effect of both facilitatory β2-adrenoceptor and angiotensin II receptor on the release of adrenal catecholamines induced by electrical stimulation of the splanchnic nerve in anaesthetized and vagotomized dog. In these experiments, individual or combined treatments with the β2-adrenoceptor antagonist ICI 118551 (0.3 mg/kg i.v.), the converting enzyme inhibitor captopril (2 mg/kg i.v.), or the angiotensin II receptor antagonist saralasin (2 μg∙kg−1∙min−1 i.v.) were found to significantly decrease the release of adrenal catecholamines during splanchnic nerve stimulation (5-V pulses of 2 ms duration for 3 min at 1 Hz) whatever the order of administration of the drugs. On the other hand, the infusion of angiotensin II (20 ng∙kg−1∙min−1) was shown to potentiate the release of adrenal catecholamines in response to electrical stimulation, and this effect was totally blocked by treatment with saralasin (4 μg kg−1∙min−1 i.v.). This facilitating angiotensin mechanism differed from β-adrenoceptor facilitating mechanism, since following β-blockade with ICI 118551, angiotensin II infusion still significantly potentiated the release of catecholamines during splanchnic nerve stimulation. These observations thus suggest that both facilitating β2-adrenoceptors and angiotensin II receptors can independently modulate the release of adrenal catecholamines.Key words: adrenal catecholamines, β2-adrenoceptors, angiotensin II receptors, adrenal medulla, facilitating sympathetic mechanisms, receptor interactions.


1990 ◽  
Vol 68 (3) ◽  
pp. 363-369 ◽  
Author(s):  
Richard Briand ◽  
Nobuharu Yamaguchi ◽  
Jacques Gagne ◽  
Tomohiko Kimura ◽  
Lisa Farley ◽  
...  

The release of neuropeptide Y like immunoreactivity (NPY-li) from the adrenal gland was studied in relation to the secretion of catecholamines (CA:NE, norepinephrine; E, epinephrine) during the left splanchnic nerve stimulation in thiopental–chloralose anesthetized dogs (n = 16). Plasma concentrations of NE, E, and NPY-li were determined in the left adrenal venous and aortic blood. Adrenal outputs of NPY-li, NE, and E were 2.4 ± 0.4, 1.4 ± 0.2, and 7.3 ± 1.7 ng/min, under basal conditions, respectively. These values increased significantly (p < 0.05; n = 8) in response to a continuous stepwise stimulation at frequencies of 1, 3, and 10 Hz given at 3-min intervals during 9 min, reaching a maximum output of 4.6 ± 0.9 (NPY-li), 240.2 ± 50.2 (NE), and 1412.5 ± 309.7 ng/min (E) at a frequency of 10 Hz. Burst electrical stimulation at 40 Hz for 1 s at 10-s intervals for a period of 10 min produced similar increases (p < 0.05) in the release of NPY-li (4.8 ± 1.0 ng/min, n = 8), NE (283.5 ± 144.3 ng/min, n = 8), and E (1133.5 ± 430.6 ng/min, n = 8). Adrenal NPY-li output was significantly correlated with adrenal NE output (r = 0.606; n = 24; p < 0.05) and adrenal E output (r = 0.640; n = 24; p < 0.05) in dogs receiving the burst stimulation. The present findings demonstrate that NPY-li is coreleased with NE and E from the adrenal gland in response to direct splanchnic nerve stepwise or burst stimulation at high frequencies in anesthetized dogs. It is thus possible that the adrenal medullary NPY-li contributes to the modulation of circulating NPY-li levels under various physiopathological conditions.Key words: adrenal medulla, burst stimulation, catecholamines, corelease, neuropeptide Y, splanchnic nerves.


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