Vasomodulatory effect of novel peroxovanadate compounds on rat aorta: Role of rho kinase and nitric oxide/cGMP pathway

2011 ◽  
Vol 64 (3) ◽  
pp. 274-282 ◽  
Author(s):  
Vivek Khanna ◽  
Manish Jain ◽  
Manoj Kumar Barthwal ◽  
Diganta Kalita ◽  
Jeena Jyoti Boruah ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Rho Kinase ◽  
Rat Aorta ◽  
Cgmp Pathway

scholarly journals The Role of Endothelium-Derived Nitric Oxide in Relaxations to Levcromakalim in the Rat Aorta.

1999 ◽  
Vol 81 (4) ◽  
pp. 362-366 ◽  
Author(s):  
Hiroyuki Kinoshita ◽  
Shizue Iwahashi ◽  
Tetsuya Kakutani ◽  
Kazuhiro Mizumoto ◽  
Hiroshi Iranami ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Rat Aorta

Acute and chronic NOS inhibition enhances α2- adrenoreceptor-stimulated RhoA and Rho kinase in rat aorta

2002 ◽  
Vol 283 (4) ◽  
pp. H1361-H1369 ◽  
Author(s):  
Rebecca W. Carter ◽  
McKenzie Begaye ◽  
Nancy L. Kanagy
Keyword(s):  
Nitric Oxide ◽  
Drinking Water ◽  
Adrenergic Receptors ◽  
Membrane Fraction ◽  
Vascular Tone ◽  
Rho Kinase ◽  
Rat Aorta ◽  
No Synthase ◽  
Rhoa Activation

We demonstrated that arteries from rats made hypertensive with chronic nitric oxide (NO) synthase (NOS) inhibition ( N ω-nitro-l-arginine in drinking water, LHR) have enhanced contractile sensitivity to α2-adrenergic receptors (α2-AR) agonist UK-14304 compared with arteries from normotensive rats (NR). NO may regulate vascular tone in part through suppression of RhoA and Rho kinase (ROK). We hypothesized that enhanced RhoA and ROK activity augments α2-AR contraction in LHR aortic rings. Y-27632 eliminated UK-14304 contraction in LHR and NR aortic rings. The order of increasing sensitivity to Y-27632 was the following: endothelium-intact NR, LHR, and endothelium-denuded NR. UK-14304 stimulated RhoA translocation to the membrane fraction in LHR and denuded NR but not in intact NR aorta. Basally, more RhoA was present in the membrane fraction in denuded NR than in intact NR or LHR aorta. Relaxation to S-nitroso- N-acetyl-penicillamine and Y-27632 in denuded ionomycin-permeabilized rings was greater in NR than in LHR. Together these studies indicate α2-AR contraction depends on ROK activity more in NR than LHR aorta. Additionally, endogenous NO may regulate RhoA activation, whereas chronic NOS inhibition appears to cause RhoA desensitization.

scholarly journals The proconvulsant effect of sildenafil in mice: role of nitric oxide-cGMP pathway

2006 ◽  
Vol 147 (8) ◽  
pp. 935-943 ◽  
Author(s):  
Kiarash Riazi ◽  
Maryam Roshanpour ◽  
Neda Rafiei-Tabatabaei ◽  
Houman Homayoun ◽  
Farzad Ebrahimi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cgmp Pathway

Thromboxane prostanoid receptor activation impairs endothelial nitric oxide-dependent vasorelaxations: The role of Rho kinase

2009 ◽  
Vol 78 (4) ◽  
pp. 374-381 ◽  
Author(s):  
Cui Qing Liu ◽  
Fung Ping Leung ◽  
Siu Ling Wong ◽  
Wing Tak Wong ◽  
Chi Wai Lau ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Rho Kinase ◽  
Receptor Activation ◽  
Prostanoid Receptor ◽  
Endothelial Nitric Oxide

Role of ventral hippocampal nitric oxide/cGMP pathway in anxiety-related behaviors in rats submitted to the elevated T-maze

2010 ◽  
Vol 207 (1) ◽  
pp. 112-117 ◽  
Author(s):  
A.V. Calixto ◽  
F.S. Duarte ◽  
M. Duzzioni ◽  
L.P. Nascimento Häckl ◽  
M.S. Faria ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cgmp Pathway

scholarly journals The Role of Endothelium-Derived Nitric Oxide in Relaxations to Levcromakalim in the Rat Aorta

1999 ◽  
Vol 81 (4) ◽  
pp. 362-366
Author(s):  
Hiroyuki Kinoshita ◽  
Shizue Iwahashi ◽  
Tetsuya Kakutani ◽  
Kazuhiro Mizumoto ◽  
Hiroshi Iranami ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Rat Aorta

scholarly journals A Critical Role of the Nitric Oxide/cGMP Pathway in Corticostriatal Long-Term Depression

1999 ◽  
Vol 19 (7) ◽  
pp. 2489-2499 ◽  
Author(s):  
Paolo Calabresi ◽  
Paolo Gubellini ◽  
Diego Centonze ◽  
Giuseppe Sancesario ◽  
Maria Morello ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Critical Role ◽  
Long Term Depression ◽  
Cgmp Pathway

Alpha-2 Adrenoceptor Agonists Decrease Cyclic Guanosine 3',5'-Monophosphate in the Mouse Brain

1996 ◽  
Vol 85 (3) ◽  
pp. 544-550. ◽  
Author(s):  
Yvonne Vulliemoz ◽  
Hong Shen ◽  
Laszlo Virag
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Maximum Dose ◽  
Anticonvulsant Effect ◽  
Effector System ◽  
Cgmp Pathway ◽  
Adrenoceptor Agonists ◽  
The Central Nervous System ◽  
Oxide Synthase

Background In the central nervous system neurotransmitters, drugs or conditions that excite increase cyclic guanosine 3',5'-monophosphate (cGMP), an effect mediated by the neuromodulator nitric oxide, whereas those that sedate decrease cGMP. Volatile anesthetics were shown to decrease cerebellar cGMP, an effect that correlates with their anesthetic and anticonvulsant effect. Because alpha-2 adrenoceptor agonists have anesthetic properties, the role of the nitric oxide-cGMP pathway in the action of the alpha-2 adrenoceptor agonists clonidine and dexmedetomidine was investigated. Methods Groups of mice were given, intraperitoneally, one dose of either 30-600 micrograms/kg clonidine, or 3-300 micrograms/kg D-medetomidine (dexmedetomidine) or L-medetomidine. The alpha-2 adrenoceptor antagonists, 0.3-5 mg/kg yohimbine or 1 mg/kg atipamezole, 1 mg/kg of the alpha-1 antagonist prazosin, and 10-300 mg/kg of the nitric oxide synthase inhibitors, N omega-nitro-1-arginine methylester and N omega-nitro-1-arginine, were given 10-20 min before the agonist. The mice were killed by microwave radiation focused to the head. Cyclic GMP was measured by radioimmunoassay in deproteinized extracts from different brain areas. Results Clonidine and dexmedetomidine, at sedative doses, dose-dependently decreased cerebellar cGMP (ED50: 100 and 50 micrograms/kg for clonidine and dexmedetomidine, respectively). This effect was inhibited by yohimbine and atipamezole, but not by prazosin, confirming the alpha-2 nature of the response to the agonists. L-medetomidine, which has no sedative/hypnotic effect, did not decrease cGMP. Pretreatment of the mice with a maximum dose of 100 mg/kg of a nitric oxide synthase antagonist abolished the cGMP response to the agonists. Similar results were obtained in the cerebral cortex, hippocampus and caudate nucleus. Conclusions The results suggest that the nitric oxide-cGMP pathway is an effector system coupled to the alpha-2 adrenoceptor mediating sedation.

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