Cannabinoid CB1 and CB2 receptors antagonists AM251 and AM630 differentially modulate the chronotropic and inotropic effects of isoprenaline in isolated rat atria

2019 ◽  
Vol 71 (1) ◽  
pp. 82-89 ◽  
Author(s):  
Jolanta Weresa ◽  
Anna Pędzińska-Betiuk ◽  
Rafał Kossakowski ◽  
Barbara Malinowska
1982 ◽  
Vol 32 (2) ◽  
pp. 221-230 ◽  
Author(s):  
Atsuko HIRANO ◽  
Hisakuni HASHIMOTO ◽  
Mitsuyoshi NAKASHIMA

2002 ◽  
Vol 25 (2) ◽  
pp. 197-200 ◽  
Author(s):  
Yoko Kubota ◽  
Keizo Umegaki ◽  
Naoko Tanaka ◽  
Hideya Mizuno ◽  
Kazuki Nakamura ◽  
...  

2001 ◽  
Vol 169 (1) ◽  
pp. 177-183 ◽  
Author(s):  
K Terui ◽  
A Higashiyama ◽  
N Horiba ◽  
KI Furukawa ◽  
S Motomura ◽  
...  

Corticotropin-releasing factor (CRF) has a coronary vasodilator effect and a positive inotropic effect on the isolated rat heart. Recently, expression of CRF receptor type 2 (CRF-R2) has been demonstrated in the heart. In addition, urocortin (Ucn), a new member of the CRF family, has been reported to have much greater affinity for CRF-R2 than CRF. It is suggested that the cardiac effects of Ucn may be more potent than those of CRF. We compared the effect of Ucn with that of CRF on isolated rat heart. The effects of Ucn were then analyzed to determine whether these effects were mediated by CRF receptors and/or any other mediators under the following conditions: perfusion buffer containing (1) alpha-helical CRF 9-41, (2) indomethacin, (3) N(G)-nitro-l -arginine methylester and (4) propranolol. Ucn exhibited a greater effect with a longer duration of action than CRF. Indomethacin significantly attenuated the vasodilator effects of Ucn (P<0.05). CRF receptor antagonist diminished both coronary vasodilation and the positive inotropic effects of Ucn (P<0.05). These results suggest that the cardiac effects of Ucn may be mediated by a CRF receptor, and prostaglandins may be involved in the vasodilator effect.


2015 ◽  
Vol 93 (8) ◽  
pp. 721-726 ◽  
Author(s):  
Kajetan Juszczak ◽  
Piotr Maciukiewicz

The cannabinoid receptors CB1 and CB2 are localized in the urinary bladder and play a role in the regulation of its function. We investigated the pathomechanisms through which hyperosmolarity induces detrusor overactivity (DO). We compared urinary bladder activity in response to blockade of CB1 and CB2 receptors using AM281 and AM630, respectively, in normal rats and after hyperosmolar stimulation. Experiments were performed on 44 rats. DO was induced by intravesical instillation of hyperosmolar saline. Surgical procedures and cystometry were performed under urethane anaesthesia. The measurements represent the average of 5 bladder micturition cycles. We analysed basal, threshold, and micturition voiding pressure; intercontraction interval; compliance; functional bladder capacity; motility index; and detrusor overactivity index. The blockage of CB1 and CB2 receptors diminished the severity of hyperosmolar-induced DO. In comparison with naïve animals the increased frequency of voiding with no significant effect on intravesical voiding pressure profile was observed as a result of the blockage of CB1 and CB2 receptors. These results demonstrate that hyperosmolar-induced DO is mediated by CB1 and CB2 receptors. Therefore, the cannabinoid pathway could potentially be a target for the treatment of urinary bladder dysfunction.


1970 ◽  
Vol 27 (6) ◽  
pp. 867-873 ◽  
Author(s):  
ALBERT S. GRODNER ◽  
HANS-GUNTHER LAHRTZ ◽  
PETER E. POOL ◽  
EUGENE BRAUNWALD
Keyword(s):  

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