P.P. De Deyn, R. Vanholder, R. D'Hooge

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Presentation transcript:

P.P. De Deyn, R. Vanholder, R. D'Hooge Nitric oxide in uremia: Effects of several potentially toxic guanidino compounds P.P. De Deyn, R. Vanholder, R. D'Hooge Kidney International Volume 63, Pages S25-S28 (May 2003) DOI: 10.1046/j.1523-1755.63.s84.9.x Copyright © 2003 International Society of Nephrology Terms and Conditions

Figure 1 Hypothetical model for the excitatory and neurotoxic action of uremic retention solutes on the central nervous system. The model focuses on reported effects on GABAA receptor (GABAA-R), NMDA-type glutamate receptor (NMDA-R), and voltage-gated Ca2+ channel (VGCC), but may include other neuroexcitatory effects of these solutes. The excitatory neurotransmitter L-glutamate is released from presynaptic terminals and binds to AMPA and NMDA receptors. GABAergic interneurons provide synaptic inhibition through activation of GABAA-R and chloride influx (resulting in inhibitory hyperpolarization of the membrane). In the presence of GSA or other excitatory uremic retention solutes, GABAA-Rs will be blocked and NMDA receptors (NMDA-Rs) activated, lifting the voltage dependent block from NMDA-Rs. Ca2+ influx through NMDA-R ionophores and VGCCs activates postsynaptic Ca2+-triggered events. These may include activation of nitric oxide synthase (NOS) and postsynaptic density-95 (PSD-95) protein, leading to nitric oxide (NO) synthesis and anterograde NO diffusion. Presynaptic effects of NO and activation of presynaptic VGCC could increase excitatory glutamate release. Kidney International 2003 63, S25-S28DOI: (10.1046/j.1523-1755.63.s84.9.x) Copyright © 2003 International Society of Nephrology Terms and Conditions