Effects on kidney filtration rate by agmatine requires activation of ryanodine channels for nitric oxide generation
Open Access
- 1 April 2008
- journal article
- Published by American Physiological Society in American Journal of Physiology-Renal Physiology
- Vol. 294 (4), F795-F800
- https://doi.org/10.1152/ajprenal.00392.2007
Abstract
Agmatine, decarboxylated arginine, is produced in the kidney and can increase nephron and kidney filtration rate via renal vasodilatation and increases in plasma flow. This increase in filtration rate after agmatine is prevented by administration of nitric oxide synthase (NOS) inhibitors. In endothelial cells, agmatine-stimulated nitrite production is accompanied by induction of cytosolic calcium. NOS activity requires calcium for activation; however, the source of this calcium remains unknown. Ryanodine receptor (RyR) calcium-activated calcium release channels are present in the kidney cortex, and we evaluated if RyR contributes to the agmatine response. Agmatine microperfused into Bowman's space reversibly increases nephron filtration rate (SNGFR) by ∼30%. cADP-ribose (cADPR) regulates RyR channel activity. Concurrent infusion of agmatine with the cADPR blocker 8-bromo-cADPR (2 μM) prevents the increase in filtration rate. Furthermore, direct activation of the RyR channel with ryanodine at agonist concentrations (5 μM) increases SNGFR, and, like agmatine, this increase is prevented by administration of N G-monomethyl-l-arginine, a nonselective NOS blocker. We demonstrate that agmatine does not elicit ADPR cyclase activity in vascular smooth muscle membranes and does not directly affect RyR calcium channel responses using sea urchin egg homogenates. These results imply interplay between endothelial cell cADPR/RyR/Ca2+/NO and the cADPR/RyR/Ca2+ pathways in vascular smooth muscle cells in arterioles in the regulation of kidney filtration rate. In conclusion, we show that agmatine-induced effects require activation of cADPR and RyR calcium release channels for NO generation, vasodilation, and increased filtration rate.This publication has 52 references indexed in Scilit:
- ADP-ribosyl cyclase and ryanodine receptor activity contribute to basal renal vasomotor tone and agonist-induced renal vasoconstriction in vivoAmerican Journal of Physiology-Renal Physiology, 2007
- Receptor-mediated activation of nitric oxide synthesis by arginine in endothelial cellsProceedings of the National Academy of Sciences of the United States of America, 2007
- Voltage-gated Ca2+ entry and ryanodine receptor Ca2+-induced Ca2+ release in preglomerular arteriolesAmerican Journal of Physiology-Renal Physiology, 2007
- Renin-angiotensin system affects endothelial morphology and permeability of renal afferent arterioleActa Physiologica Hungarica, 2007
- Essential role of Ca2+ release channels in angiotensin II-induced Ca2+ oscillations and mesangial cell contractionKidney International, 2006
- Cyclic ADP ribose-mediated Ca2+signaling in mediating endothelial nitric oxide production in bovine coronary arteriesAmerican Journal of Physiology-Heart and Circulatory Physiology, 2006
- Production of arginine by the kidney is impaired in a model of sepsis: early events following LPSAmerican Journal of Physiology-Regulatory, Integrative and Comparative Physiology, 2004
- Nitric Oxide, NOC-12, and S-Nitrosoglutathione Modulate the Skeletal Muscle Calcium Release Channel/Ryanodine Receptor by Different MechanismsPublished by Elsevier BV ,2003
- Histamine‐induced Ca2+ oscillations in a human endothelial cell line depend on transmembrane ion flux, ryanodine receptors and endoplasmic reticulum Ca2+‐ATPaseThe Journal of Physiology, 2000
- Ryanodine Receptor Expression in the Kidney and a Non-excitable Kidney Epithelial CellPublished by Elsevier BV ,1996