Effects of κ-opioid receptor agonists on stimulated phosphoinositide hydrolysis in rat kidney

Excitatory amino acid release in the locus coeruleus during naloxone-precipitated morphine withdrawal in adjuvant arthritic rats

“…Such an increase in Glu and Asp levels within the LC was consistent with the electrophysiological results that naloxoneprecipitated withdrawal stimulates Glu and Asp releases from excitatory amino acids (EAAs)-containing nerve terminals within the LC [6,25,26]. The hyperactivity of LC neurons seen after opioid antagonist-induced withdrawal is believed to be mediated by an excitatory amino acid pathway from the nucleus paragigantocellularis to the LC [1,2,10,27].…”

Opioids and renal function

“…20 Moreover, 1 opioid receptor stimulation might affect phosphoinositide metabolism in rat renal cortex by modulating the subcellular effects of renal ␣ 1 -adrenoceptor activation. 108 Kappa opioid agonists, although promising, should be better known before introducing them in the context of hepatorenal syndrome.…”

Opioid Mechanisms Controlling Renal Function

“…With regard to second messenger systems, studies by Mosaddeghi and colleagues (1995) have shown that, in rat renal cortex, kappa opioid receptors utilize signal transduction mechanisms involving phosphoinositide metabolism. An interaction of kappa opioid receptors and d-adrenoceptors was suggested to occur at the subcellular level because different kappa agonists (EKC, U-50488H) produced concentration-dependent decreases in noradrenaline (but not carbachol) stimulated phosphoinositide hydrolysis which were blocked by the selective kappa opioid antagonist, nor-binaltorphimine (Mosaddeghi et al 1995). Thus, while the kidneys have been shown to contain both opioid peptides and receptors (Hughes et al 1977;Simantov et al 1978;Neidle et al 1979;Quirion et al 1983;Slizgi & Ludens 1985), the physiological significance of opioid systems within the kidneys is not entirely clear.…”