Role of anandamide transporter in regulating calcitonin gene-related peptide production and blood pressure in hypertension

Dai, Li; Chen, Ben-Mei; Peng, Jun; Zhang, Yi-Shuai; Li, Xiaohui; Yuan, Qiong; Hu, Chang-Ping; Deng, Han-Wu; Li, Yuan‐Jian

doi:10.1097/hjh.0b013e328329bbd7

Cited by 28 publications

(14 citation statements)

References 38 publications

(53 reference statements)

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“…However, Lu et al [52] observed that the ADMA level in serum is increased more in aged (24 months) rats than in young animals (six months), but in their study no difference in mRNA expression for CGRP in ADMA-treated rats was noted. In contrast, CGRP production was decreased in spontaneously hypertensive (SHR) rats and this effect was accompanied by elevated plasma levels of ADMA [53]. In our present study, the supplementation of ADMA-treated rats with exogenous CGRP attenuated I/R-induced gastric lesions potentiated by ADMA and reversed in part, the accompanying decrease in GBF and plasma CGRP levels in rats with or without capsaicin denervation in the presence of ADMA.…”

Section: Resultsmentioning

confidence: 44%

Exogenous Asymmetric Dimethylarginine (ADMA) in Pathogenesis of Ischemia-Reperfusion-Induced Gastric Lesions: Interaction with Protective Nitric Oxide (NO) and Calcitonin Gene-Related Peptide (CGRP)

Magierowski

Jasnos

Śliwowski

et al. 2014

IJMS

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Asymmetric dimethylarginine (ADMA) is an endogenous nitric oxide (NO) synthesis inhibitor and pro-inflammatory factor. We investigated the role of ADMA in rat gastric mucosa compromised through 30 min of gastric ischemia (I) and 3 h of reperfusion (R). These I/R animals were pretreated with ADMA with or without the combination of l-arginine, calcitonin gene-related peptide (CGRP) or a small dose of capsaicin, all of which are known to afford protection against gastric lesions, or with a farnesoid X receptor (FXR) agonist, GW 4064, to increase the metabolism of ADMA. In the second series, ADMA was administered to capsaicin-denervated rats. The area of gastric damage was measured with planimetry, gastric blood flow (GBF) was determined by H2-gas clearance, and plasma ADMA and CGRP levels were determined using ELISA and RIA. ADMA significantly increased I/R-induced gastric injury while significantly decreasing GBF, the luminal NO content, and the plasma level of CGRP. This effect of ADMA was significantly attenuated by pretreatment with CGRP, l-arginine, capsaicin, or a PGE2 analogue. In GW4064 pretreated animals, the I/R injury was significantly reduced and this effect was abolished by co-treatment with ADMA. I/R damage potentiated by ADMA was exacerbated in capsaicin-denervated animals with a further reduction of CGRP. Plasma levels of IL-10 were significantly decreased while malonylodialdehyde (MDA) and plasma TNF-α contents were significantly increased by ADMA. In conclusion, ADMA aggravates I/R-induced gastric lesions due to a decrease of GBF, which is mediated by a fall in NO and CGRP release, and the enhancement of lipid peroxidation and its pro-inflammatory properties.

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Section: Resultsmentioning

confidence: 44%

Exogenous Asymmetric Dimethylarginine (ADMA) in Pathogenesis of Ischemia-Reperfusion-Induced Gastric Lesions: Interaction with Protective Nitric Oxide (NO) and Calcitonin Gene-Related Peptide (CGRP)

Magierowski

Jasnos

Śliwowski

et al. 2014

IJMS

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“…Since numerous endocannabinoid-like compounds were changed in hypertensive animals, future studies should clarify whether these compounds affect the cardiovascular system. As suggested previously [49], the enhanced levels of AEA, LEA, OEA and SEA (all of which are degraded by FAAH) in spite of higher FAAH activity might indicate that in the heart of the DOCA group endocannabinoid synthesis is favoured [61] and/or AEA transporter activity is decreased [62].…”

Section: Effect Of Hypertensionmentioning

confidence: 61%

Chronic Cannabidiol Administration Fails to Diminish Blood Pressure in Rats with Primary and Secondary Hypertension Despite Its Effects on Cardiac and Plasma Endocannabinoid System, Oxidative Stress and Lipid Metabolism

Remiszewski

Jarocka-Karpowicz

Biernacki

et al. 2020

IJMS

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We investigated the influence of cannabidiol (CBD) on blood pressure (BP) and heart rate (HR) in spontaneously (SHR) and deoxycorticosterone (DOCA-salt) hypertensive rats. Hypertension was connected with increases in cardiac and plasma markers of lipid peroxidation in both models, whereas cardiac endocannabinoid levels decreased in SHR and increased in DOCA-salt. CBD (10 mg/kg once a day for 2 weeks) did not modify BP and HR in hypertension but counteracted pro-oxidant effects. Moreover, it decreased cardiac or plasma levels of anandamide, 2-arachidonoylglycerol and oleoyl ethanolamide in DOCA-salt and inhibited the activity of fatty acid amide hydrolase (FAAH) in both models. In the respective normotensive control rats, CBD increased lipid peroxidation, free fatty acid levels and FAAH activity. In conclusion, chronic CBD administration does not possess antihypertensive activity in a model of primary and secondary (DOCA-salt) hypertension, despite its antioxidant effect. The latter may be direct rather than based on the endocannabinoid system. The unexpected CBD-related increase in lipid peroxidation in normotensive controls may lead to untoward effects; thus, caution should be kept if CBD is used therapeutically.

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“…The endocannabinoid system is suggested to buffer increases in BP in hypertension. In support of this, the plasma level of the best known endocannabinoid, anandamide (AEA), was higher in hypertensive patients (Engeli et al , ) and in spontaneously hypertensive rats (SHR; Li et al , ). Moreover, in acute experiments, (1) the CB receptor‐mediated hypotension elicited by AEA was stronger in anaesthetized SHR than in normotensive controls (Lake et al , ; Bátkai et al , ); (2) in conscious SHR, AEA decreased BP, but increased it in normotensive controls (Lake et al , ); and (3) the systemic acute blockade of fatty acid amide hydrolase (FAAH; the key enzyme responsible for AEA degradation) by URB597 (Bátkai et al , ) and AM3506 (Godlewski et al , ) has been shown to normalize BP in SHR.…”

Section: Introductionmentioning

confidence: 93%

Chronic inhibition of fatty acid amide hydrolase by URB597 produces differential effects on cardiac performance in normotensive and hypertensive rats

Pędzińska-Betiuk

Weresa

Toczek

et al. 2017

British J Pharmacology

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Role of anandamide transporter in regulating calcitonin gene-related peptide production and blood pressure in hypertension

Abstract: Decreased plasma CGRP level in patients with essential hypertension or SHRs is likely due to the reduced AEA transporter activity, and the increased ADMA level may account for the reduced AEA transporter activity.

Cited by 28 publications

References 38 publications

Exogenous Asymmetric Dimethylarginine (ADMA) in Pathogenesis of Ischemia-Reperfusion-Induced Gastric Lesions: Interaction with Protective Nitric Oxide (NO) and Calcitonin Gene-Related Peptide (CGRP)

Exogenous Asymmetric Dimethylarginine (ADMA) in Pathogenesis of Ischemia-Reperfusion-Induced Gastric Lesions: Interaction with Protective Nitric Oxide (NO) and Calcitonin Gene-Related Peptide (CGRP)

Chronic Cannabidiol Administration Fails to Diminish Blood Pressure in Rats with Primary and Secondary Hypertension Despite Its Effects on Cardiac and Plasma Endocannabinoid System, Oxidative Stress and Lipid Metabolism

Chronic inhibition of fatty acid amide hydrolase by URB597 produces differential effects on cardiac performance in normotensive and hypertensive rats

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