Corpus ID: 16958323

Inhibition by brimonidine of forskolin-induced nitrite production in isolated pig ciliary processes.

  title={Inhibition by brimonidine of forskolin-induced nitrite production in isolated pig ciliary processes.},
  author={Rong Liu and Renyi Wu and Josef Flammer and Ivan O. Haefliger},
  journal={Investigative ophthalmology \& visual science},
  volume={43 8},
PURPOSE To investigate by which mechanism the ocular hypotensive drug brimonidine (selective alpha(2)-adrenoreceptor agonist) inhibits the production of nitrite induced by forskolin in isolated porcine ciliary processes. METHODS Nitrite (a nitric oxide metabolite) was measured by Griess reaction in the medium surrounding the ciliary processes, before and after exposure to different drugs. Tissues were exposed for 120 minutes to forskolin (0.1 microM; an adenylylcyclase activator) or 8-bromo… Expand
7 Citations
Reduction of nitrite production by endothelin-1 in isolated porcine ciliary processes.
The results suggest that endothelin-1, through an ETA receptor activation, can reduce both basal and forskolin-induced nitrite production in isolated porcine ciliary processes. Expand
Role of anions in nitric oxide-induced short-circuit current increase in isolated porcine ciliary processes.
No activates a guanylate cyclase-cGMP-protein kinase G pathway that appears to stimulate stroma-to-aqueous anionic transport, possibly Cl-, in porcine ciliary epithelium. Expand
Inhibition by brimonidine of forskolin-induced nitric oxide synthase expression in human ciliary bodies in vitro
In human ciliary body (where aqueous humor is produced), brimonidine inhibits the up-regulation of nNOS expression induced by forskolin, but not that of iNOS or of eNOS. Expand
The vital role for nitric oxide in intraocular pressure homeostasis
A model whereby NO controls a feedback signaling loop in the conventional outflow pathway that is sensitive to changes in IOP and its oscillations is presented, which reduces the resistance to aqueous humor drainage and lower IOP, which diminishes the biomechanical signaling on SC. Expand
The discovery of the Flammer syndrome: a historical and personal perspective
Clinical and basic research that led to the description of Flammer syndrome is described, which seemed to increase the risk for certain eye diseases, particularly in younger patients and also for certain drugs and increased retinal venous pressure. Expand
Recurrent serous macular detachment after topical ocular hypotensive medication
It is recommended that patients with VTS, those with a history of CSMD or having developed recurrent episodes ofCSMD requiring management with topical ocular hypotensive medications, be cautiously monitored for the possible occurrence or exacerbation of CS MD. Expand
Vitreal pathogenic role in optic pit foveolar retinoschisis and central serous chorioretinopathy
The notion that vitreal traction may contribute to the pathogenesis of serous detachments in central serous chorioretinopathy (CSC) is proposed. Expand


Isoproterenol, forskolin, and cAMP-induced nitric oxide production in pig ciliary processes.
In isolated porcine ciliary processes, drugs activating adenylylcyclase or mimicking cAMP increase the production of NO by a mechanism that appears to involve both a cAMP-dependent protein kinase and NOS. Expand
β-Adrenergic agonist-induced nitrite production in isolated pig ciliary processes
In isolated porcine ciliary processes, β-adrenergic receptor stimulation increases NO production. Expand
NO/cGMP pathway activation and membrane potential depolarization in pig ciliary epithelium.
Activation of the nitric oxide-guanylate cyclase-cGMP pathway modulates epithelial transmembrane potential in isolated porcine ciliary processes is investigated. Expand
Alpha-2 adrenoceptor mediated changes in aqueous dynamics: effect of pertussis toxin.
It was postulated that these UK-induced effects involve activation of a Gi protein linked to alpha 2 adrenoceptors, and the suppression of aqueous humor inflow induced by UK was also prevented by the PTX treatment. Expand
Alpha(2)-adrenergic-mediated tubular NO production inhibits thick ascending limb chloride absorption.
  • C. Plato, J. Garvin
  • Chemistry, Medicine
  • American journal of physiology. Renal physiology
  • 2001
The data suggest that alpha(2)-receptors act as physiological regulators of THAL NO synthesis, thus inhibiting chloride transport and participating in the natriuretic and diuretic effects of clonidine in vivo. Expand
Carbachol inhibits Na(+)-K(+)-ATPase activity in choroid plexus via stimulation of the NO/cGMP pathway.
The data suggest that cholinergic regulation of the Na(+)-K( +)-ATPase is mediated by NO and involves activation of guanylate cyclase and elevation of cGMP. Expand
Prejunctional alpha 2-adrenoceptors and adenylyl cyclase regulation in the rabbit iris-ciliary body.
Findings suggest that prejunctional alpha 2-adrenoceptors in the rabbit iris-ciliary body are negatively coupled to adenylyl cyclase, a mechanism that may contribute to autofeedback regulation of NE biosynthesis and release. Expand
Nitric oxide is a neurotransmitter in the chloride secretory response to serotonin in rat colon.
The ability of exogenous NO to induce a change in circuit current in the presence of tetrodotoxin suggests that NO is a final neurotransmitter in this neural-mucosal reflex and therefore acts directly on the enterocyte to induce secretion. Expand
NO Inhibits NaCl Absorption by Rat Thick Ascending Limb Through Activation of cGMP-Stimulated Phosphodiesterase
It is concluded that endogenous NO inhibits THAL NaCl transport by stimulating soluble guanylate cyclase and increasing cGMP, which activates protein kinase G (PKG) and cG MP-stimulated phosphodiesterase (PDE II), which, in turn, decreases cAMP levels. Expand
Role of Nitric Oxide in Salivary Secretion
Analysis of the distribution of NOS in the salivary gland revealed that it was not present in the acinar cells, but in neural terminals within the gland and also in the ductile system which contained neural (n) NOS, leading to an increase in intracellular free calcium that activates NOS leading to the generation of cGMP that opens ion channels to initiate the secretory process. Expand