Kappa Opioid Agonist-Induced Changes in IOP: Correlation with3H-NE Release and cAMP Accumulation

Moore, Tisha T; Potter, David E.

doi:10.1006/exer.2001.1022

Cited by 14 publications

(6 citation statements)

References 35 publications

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“…However, as yet, there is no direct evidence of opioid receptors in the trabecular meshwork. Functional data generated in our laboratory (Russell et al, 2000; Moore and Potter, 2001; Russell and Potter, 2002) and others (Leopold and Comroe, 1946; Drago et al, 1985) do indicate that all three subtypes may be present in those tissues, thereby, suggesting that morphine could activate the receptors to release NO. Since morphine-stimulated NO release was reduced by a NOS inhibitor and a sulfhydryl compound, it is possible that the response is mediated by the mu-3 receptor, which has consistently been shown to be a NO-releasing receptor (Nieto-Fernandez et al, 1999; Welters et al, 2000; Rialas et al, 2000; Yahyavi-Firouz-Abadi et al, 2007).…”

Section: Discussionmentioning

confidence: 57%

Morphine-induced nitric oxide production in isolated, iris-ciliary bodies

Dortch-Carnes

Randall

2009

Experimental Eye Research

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Considerable evidence suggests that the nitric oxide (NO)/cGMP signaling pathway plays an integral role in opioid receptor-mediated responses in the cardiovascular and immune systems. Previous studies in our laboratory and others have shown that nitric oxide (NO) plays a role in morphineinduced reduction of intraocular pressure (IOP) and pupil diameter (PD) in the New Zealand white (NZW) rabbit. The present study is designed to determine the effect of morphine on NO production in the isolated, iris-ciliary body (ICB), site of aqueous humor production, as this effect could be associated with morphine-stimulated changes in aqueous humor dynamics and iris function. ICBs obtained from normal NZW rabbits were utilized in these experiments. In some experiments, ICB samples were treated with morphine (1, 10 and 100 μM) for 1 hour and later examined for changes in NO levels using a NO detection kit. In other experiments, tissue samples were pretreated with naloxone (non-selective opioid receptor antagonist), L-NAME (non-selective NO synthase inhibitor) or GSH (sulfhydryl reagent) for 30 minutes, followed by treatment with morphine (10 μM). Morphine caused a concentration-dependent increase in the release of NO from ICBs. Levels of NO detected in the incubation medium of ICB samples increased from 1.49 ± 0.19 (control) to 8.81 ± 2.20 μM/ mg protein (morphine treated; 100 μM). Morphine-stimulated release of NO was significantly inhibited in tissues pretreated with 10 μM naloxone, L-NAME, or GSH. Results obtained from this study suggest that morphine stimulates NO release from the ICB through a mechanism that involves activation of NO-releasing opioid receptors. These results support the in vivo effects of morphine demonstrated in previous studies.

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Section: Discussionmentioning

confidence: 57%

Morphine-induced nitric oxide production in isolated, iris-ciliary bodies

Dortch-Carnes

Randall

2009

Experimental Eye Research

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“…Subsequently, it was also demonstrated that IOP was signi®cantly lower in patients addicted to either morphine or heroin (Drago et al, 1985). Data from this laboratory have shown that the delta opioid peptide, DPDPE (Wang and Potter, 1996) and the non-peptide kappa opioid agonists, bremazocine, spiradoline and ICI 204448 (Russell et al, 2000;Moore and Potter, 2001) reduce IOP in rabbits. The results from this current study demonstrate that the endogenous kappa opioid peptide, Dyn, also reduces IOP as well as aqueous¯ow rates in rabbits by acting on KOR.…”

Section: Discussionmentioning

confidence: 96%

“…Additional data from this laboratory have demonstrated that the delta and KOR agonists can reduce intraocular pressure (IOP) in rabbits and may do this, in part, by reducing aqueous humor¯ow rates (AFRs) (Wang and Potter, 1996;Russell et al, 2000;Moore and Potter, 2001). Recently, this laboratory has also demonstrated that kappa agonists can elevate ANP levels in aqueous humor (Russell et al, 2001b).…”

Section: Introductionmentioning

confidence: 90%

Dynorphin Modulates Ocular Hydrodynamics and Releases Atrial Natriuretic Peptide via Activation of κ-Opioid Receptors

Russell

Potter

2002

Experimental Eye Research

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“…Intraocular pressure is determined primarily by the interaction between production of aqueous humor in the ciliary body and its efflux mainly through the trabecular meshwork and Schlemm's canal [15]. Because previous studies in our laboratory have shown that kappaopioid agonists reduce intraocular pressure and aqueous humor formation in rabbits [4,5] as well as elevate levels of ANP in the aqueous humor [6], this study was designed to examine BRE-induced effects on one of the well known Ca 2+ signaling cascades (IP 3 /Ca 2+ ) that modulates activity of the ciliary epithelium, moreover, activation of this pathway could result in the release of neuroendocrine modulators, such as ANP.…”

Section: Discussionmentioning

confidence: 99%

“…Recent studies in our laboratory have shown that the kappa-opioid receptor agonists, bremazocine (BRE) and spiradoline, reduce intraocular pressure (IOP) in rabbits [4,5]. Moreover, BRE has been demonstrated to increase levels of atrial natriuretic peptide (ANP) in the aqueous humor of rabbits [6].…”

Section: Introductionmentioning

confidence: 99%

Effect of Bremazocine, a Kappa-Opioid Receptor Agonist, on Inositol Phosphate Formation in Isolated Iris-Ciliary Bodies

Dortch-Carnes

Potter²

2002

Pharmacology

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The goal of the current study was to examine the effect of the kappa-opioid agonist, bremazocine (BRE), on inositol phosphate (IP) formation in the rabbit iris-ciliary body (ICB). Concentrations of BRE (10^–7 to 10^–5M) augmented levels of IP. Incubation of ICBs with BRE (10^–6M) produced a time-dependent increase in IP levels that peaked at 60 s and declined to basal levels by 5 min. The increase in IP levels produced by BRE (10^–6M) was inhibited by the kappa-opioid receptor antagonist, nor-binaltorphimine (nor-BNI, 10^–7 to 10^–5M) and by activation of PKC with PDBu (10^–7M). These results demonstrate that kappa-opioid receptor activation by BRE in the rabbit ICB is linked to IP production. Thus, opioid agonist-induced increases in IP activity could play a role in BRE-induced increases in atrial natriuretic peptide release and alterations in aqueous humor dynamics.

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Kappa Opioid Agonist-Induced Changes in IOP: Correlation with3H-NE Release and cAMP Accumulation

Cited by 14 publications

References 35 publications

Morphine-induced nitric oxide production in isolated, iris-ciliary bodies

Morphine-induced nitric oxide production in isolated, iris-ciliary bodies

Dynorphin Modulates Ocular Hydrodynamics and Releases Atrial Natriuretic Peptide via Activation of κ-Opioid Receptors

Effect of Bremazocine, a Kappa-Opioid Receptor Agonist, on Inositol Phosphate Formation in Isolated Iris-Ciliary Bodies

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