Anandamide Decreases Glomerular Filtration Rate through Predominant Vasodilation of Efferent Arterioles in Rat Kidneys

Koura, Yukako; Ichihara, Atsuhiro; Tada, Yuko; Kaneshiro, Yuki; Okada, Hirokazu; Temm, Constance J.; Hayashi, Matsuhiko; Saruta, Takao

doi:10.1097/01.asn.0000130561.82631.bc

Cited by 53 publications

(61 citation statements)

References 13 publications

(9 reference statements)

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“…Supporting this notion, Ritter et al (24) recently reported that acute intramedullarily infused anandamide has a diuretic and natriuretic effect with little effect on mean arterial pressure. On the other hand, intravenous administration of anandamide induced vasodilation of the efferent arteriole with a resultant decrease in glomerular filtration rate but with no effect on Na excretion (15). Since the discrepancy of these results could be due to different methods of administration, we used an ex vivo technique by which the hemodynamic effects or changes in systemic regulators are absent.…”

Section: Discussionmentioning

confidence: 99%

“…In fact, direct "in vivo" studies addressing anandamide effects on Na reabsorption are at best inconclusive. For instance, studies by Koura et al (15) showed that anandamide decreases glomerular filtration rate through efferent arteriolar dilation (via CB1 and non-CB1 receptors) but it does not affect Na excretion rate (15). On the other hand, Ritter et al (24) have recently reported that renal intramedullary infusion of anandamide increases urinary Na and volume excretion (24).…”

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confidence: 99%

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Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors

Silva

Atchison

Juncos³

et al. 2013

American Journal of Physiology-Renal Physiology

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The energy required for active Na chloride reabsorption in the thick ascending limb (TAL) depends on oxygen consumption and oxidative phosphorylation (OXP). In other cells, Na transport is inhibited by the endogenous cannabinoid anandamide through the activation of the cannabinoid receptors (CB) type 1 and 2. However, it is unclear whether anandamide alters TAL transport and the mechanisms that could be involved. We hypothesized that anandamide inhibits TAL transport via activation of CB1 receptors and NO. For this, we measured oxygen consumption (QO 2 ) in TAL suspensions to monitor the anandamide effects on transport and OXP. Anandamide reduced QO 2 in a concentration-dependent manner. During Na-K-2Cl cotransport and Na/H exchange inhibition, anandamide did not inhibit TAL QO 2 . To test the role of the cannabinoid receptors, we used specific agonists and antagonists of CB1 and CB2 receptors. The CB1-selective agonist WIN55212-2 reduced QO 2 in a concentration-dependent manner. Also, the CB1 receptor antagonist rimonabant blocked the effect of anandamide on QO 2 . In contrast, the CB2-selective agonist JHW-133 had no effect on QO 2 , while the CB2 receptor antagonist AM-630 failed to block the anandamide effects on Q O 2 . To confirm these results, we measured CB1 and CB2 receptor expression and only CB1 expression was detected. Because CB1 receptors are strong nitric oxide synthase (NOS) stimulators and NO inhibits transport in TALs, we evaluated the role of NO. Anandamide stimulated NO production and the NOS inhibitor N G -nitro-L-arginine methyl ester blocked the anandamide effects on Q O 2 . We conclude that anandamide inhibits TAL Na transport-related Q O 2 via activation of CB1 receptor and NOS.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors

Silva

Atchison

Juncos³

et al. 2013

American Journal of Physiology-Renal Physiology

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“…In vitro, AEA (1 M) vasodilates via CB1 the juxtamedullary afferent arterioles; at 10 nM, it stimulates NO release from perfused renal arterial segments; and at 1 M, it exerts neuromodulatory effects by inhibiting KCl-stimulated norepinephrine release from sympathetic nerves on isolated renal arterial segments (203). Therefore, the ECS regulates renal hemodynamics, and AEA via CB1 increases renal blood flow but also decreases the glomerular filtration rate (445). AEA has diuretic effects not mediated by either CB1 or TRPV1 but rather by the neuronal reflex of the kidney (474).…”

Section: Kidneysmentioning

confidence: 99%

From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology

Ligresti¹,

Petrocellis²,

Marzo³

2016

Physiological Reviews

341

323

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Apart from having been used and misused for at least four millennia for, among others, recreational and medicinal purposes, the cannabis plant and its most peculiar chemical components, the plant cannabinoids (phytocannabinoids), have the merit to have led humanity to discover one of the most intriguing and pleiotropic endogenous signaling systems, the endocannabinoid system (ECS). This review article aims to describe and critically discuss, in the most comprehensive possible manner, the multifaceted aspects of 1) the pharmacology and potential impact on mammalian physiology of all major phytocannabinoids, and not only of the most famous one ⌬ 9 -tetrahydrocannabinol, and 2) the adaptive prohomeostatic physiological, or maladaptive pathological, roles of the ECS in mammalian cells, tissues, and organs. In doing so, we have respected the chronological order of the milestones of the millennial route from medicinal/recreational cannabis to the ECS and beyond, as it is now clear that some of the early steps in this long path, which were originally neglected, are becoming important again. The emerging picture is rather complex, but still supports the belief that more important discoveries on human physiology, and new therapies, might come in the future from new knowledge in this field.

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“…More specifically, AEA, via activation of CB 1 receptors present in both afferent and efferent arterioles, increases renal blood flow and decreases the glomerular filtration rate (GFR), effects that are completely blocked by the CB 1 receptor antagonists AM281 and AM251. These findings are independent of its effects on blood pressure and the sodium excretion rate [39]. Using a methylated analog of AEA, methanandamide, Li and Wang [62] showed that its intrarenal medullary infusion to anesthetized rats increases urine flow rate without changing sodium excretion and decreases mean arterial blood pressure, suggesting a regulation of body volume homeostasis and blood pressure by the renal eCB system.…”

Section: Ecbs and Renal Hemodynamics And Functionmentioning

confidence: 98%

“…Two years later, transcripts for the CB 1 receptor were identified in human kidney [32]. Several recent reports (Table 1) have documented the presence of functional CB 1 receptor in the entire kidney [15,[33][34][35][36][37][38][40][41][42], including different parts of the nephron such as afferent and efferent arterioles [39], glomeruli [33,38,40,42,43], tubules [15], the loop of Henle [44], and collecting ducts [15]. It is also expressed in various subtypes of kidney cells such as podocytes [33,41,43,45,46], proximal and distal tubular epithelial cells [15,34,37,38,40,41,[47][48][49], and mesangial cells [50,54].…”

Section: The Renal Ecb Systemmentioning

confidence: 99%

The emerging role of the endocannabinoid system in the pathogenesis and treatment of kidney diseases

Tam

2015

Journal of Basic and Clinical Physiology and Pharmacology

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Endocannabinoids (eCBs) are endogenous lipid ligands that bind to cannabinoid receptors that also mediate the effects of marijuana. The eCB system is comprised of eCBs, anandamide, and 2-arachidonoyl glycerol, their cannabinoid-1 and cannabinoid-2 receptors (CB 1 and CB 2 , respectively), and the enzymes involved in their biosynthesis and degradation. It is present in both the central nervous system and peripheral organs including the kidney. The current review focuses on the role of the eCB system in normal kidney function and various diseases, such as diabetes and obesity, that directly contributes to the development of renal pathologies. Normally, activation of the CB 1 receptor regulates renal vascular hemodynamics and stimulates the transport of ions and proteins in different nephron compartments. In various mouse and rat models of obesity and type 1 and 2 diabetes mellitus, eCBs generated in various renal cells activate CB 1 receptors and contribute to the development of oxidative stress, inflammation, and renal fibrosis. These effects can be chronically ameliorated by CB 1 receptor blockers. In contrast, activation of the renal CB 2 receptors reduces the deleterious effects of these chronic diseases. Because the therapeutic potential of globally acting CB 1 receptor antagonists in these conditions is limited due to their neuropsychiatric adverse effects, the recent development of peripherally restricted CB 1 receptor antagonists may represent a novel pharmacological approach in treating renal diseases.Keywords: CB 1 receptor; CB 2 receptor; diabetic nephropathy; endocannabinoids; obesity; renal function. The endocannabinoid systemThe recreational, psychoactive, and medicinal effects of marijuana, many of which have important therapeutic potentials, have been recognized for thousands of years [1]. Yet, it is only in the last several decades that our understanding of these effects had grown following some landmark discoveries in the field of cannabinoid research. To date, more than 60 plant-derived cannabinoid molecules have been identified in marijuana [2], among which only Δ 9 -tetrahydrocannabinol (THC) is responsible for its psychoactive properties [3]. This initial discovery has allowed the synthesis of structurally modified molecules that have been used to study structure-activity relationships and reveal tight structural and steric selectivity in the biological actions of cannabinoids. Indeed, it took more than two decades to identify the THC binding site in the brain [4], which was later cloned and named cannabinoid-1 (CB 1 ) receptor [5]. In addition to the brain-type CB 1 receptor, a second cannabinoid receptor was identified in lymphoid tissue and was named CB 2 [6]. Both CB 1 and CB 2 receptors, which share a low level (44%) of sequence homology [6], are G protein-coupled receptors that mainly signal via G i /G o proteins, even though they may also activate G s , G q/11 , and G protein-independent signaling pathways [7]. These receptors are expressed in the brain [8][9][10], liver [11,...

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Anandamide Decreases Glomerular Filtration Rate through Predominant Vasodilation of Efferent Arterioles in Rat Kidneys

Cited by 53 publications

References 13 publications

Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors

Anandamide inhibits transport-related oxygen consumption in the loop of Henle by activating CB1 receptors

From Phytocannabinoids to Cannabinoid Receptors and Endocannabinoids: Pleiotropic Physiological and Pathological Roles Through Complex Pharmacology

The emerging role of the endocannabinoid system in the pathogenesis and treatment of kidney diseases

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