Common variation in the adiponectin gene has an effect on systolic blood pressure

Avery, Peter; Patel, Sheila K.; Ibrahim, Ibrahim; Walker, Mark S.; Keavney, Bernard

doi:10.1038/jhh.2010.122

Cited by 12 publications

(9 citation statements)

References 25 publications

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“…Some of the effects of the liberated ADHF are L‐NMMA sensitive, a possible indication of adipocyte NO‐synthase activation also involving an AMPK‐dependent pathway (Figure ). The PVAT‐dependent, BK Ca ‐mediated hyperpolarizing effects of adiponectin on vascular myocytes may have a variety of long‐term consequences in vivo , and form the basis of the complex role of adiponectin in cardiovascular disease, including the effects of this adipokine on systolic blood pressure (Avery et al ., ).…”

Section: Discussionmentioning

confidence: 97%

Stimulated release of a hyperpolarizing factor (ADHF) from mesenteric artery perivascular adipose tissue: involvement of myocyte BK_Ca channels and adiponectin

Weston

Egner

Dong

et al. 2013

British J Pharmacology

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BACKGROUND AND PURPOSEPerivascular adipose tissue (PVAT) releases adipocyte-derived hyperpolarizing factors (ADHFs) that may partly act by opening myocyte K + channels. The present study in rat and mouse mesenteric arteries aimed to identify the myocyte K + channel activated by PVAT and to determine whether adiponectin contributed to the hyperpolarizing effects of PVAT. EXPERIMENTAL APPROACHMyocyte membrane potential was recorded from de-endothelialized, non-contracted rat and mouse mesenteric arteries in the presence and absence of PVAT. KEY RESULTSThe b3-adrenoceptor agonist, CL-316,243 (10 mM), generated PVAT-dependent, iberiotoxin-sensitive myocyte hyperpolarizations resulting from BKCa channel opening and which were partially blocked by L-NMMA (100 mM). Adiponectin (5 mg·mL -1 ) also produced iberiotoxin-sensitive hyperpolarizations in PVAT-denuded arterioles. Activation of myocyte AMP-activated protein kinase (AMPK) using 5 mM A-769662 also induced BKCa-mediated hyperpolarizations. Dorsomorphin abolished hyperpolarizations to CL-316,243, adiponectin and A-769662. In vessels from Adipo -/-mice, hyperpolarizations to CL-316,243 were absent whereas those to A-769662 and adiponectin were normal. In rat vessels, adipocyte-dependent hyperpolarizations were blocked by glibenclamide and clotrimazole but those to NS1619 (33 mM) were unaltered. CONCLUSIONS AND IMPLICATIONSUnder basal, non-contracted conditions, b3-adrenoceptor stimulation of PVAT releases an ADHF, which is probably adiponectin. This activates AMPK to open myocyte BKCa channels indirectly and additionally liberates NO, which also contributes to the observed PVAT-dependent myocyte hyperpolarizations. Clotrimazole and glibenclamide each reversed hyperpolarizations to adiponectin and A-769662, suggesting the involvement of myocyte TRPM4 channels in the ADHF-induced myocyte electrical changes mediated via the opening of BKCa channels. AbbreviationsA-769662, 4-hydroxy-3-(2′-hydroxybiphenyl-4-yl)-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carbonitrile; ADHF, adipocyte-derived hyperpolarizing factor; AMPK, AMP-activated kinase; BKCa, large-conductance Ca 2+

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Section: Discussionmentioning

confidence: 97%

Stimulated release of a hyperpolarizing factor (ADHF) from mesenteric artery perivascular adipose tissue: involvement of myocyte BK_Ca channels and adiponectin

Weston

Egner

Dong

et al. 2013

British J Pharmacology

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“…Avery et al [67] 255 families, 1425 individuals Cross-sectional study The C11377G SNP was found to have an independent effect on systolic blood pressure and waist/hip ratio. Hoefle et al [68] 402 men undergoing coronary angiography…”

Section: Discussionmentioning

confidence: 96%

The role of adiponectin in human vascular physiology

Vaiopoulos¹,

Marinou²,

Christodoulides

et al. 2012

International Journal of Cardiology

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“…We could report a higher cardiovascular risk for the C/C carrier compared to the two other genotypes among the females, but not among the males, even if the gender difference should be interpreted with caution due to a small sample size. As there are variables that are associated with the rs266729 SNP, as systolic blood pressure reported by Avery et al we have adjusted for hypertension in our multivariate evaluations, and still could report the significant difference in cardiovascular risk of the three genotypes in females [ 35 ]. As there is an association between b-glucose and adiponectin, and between high density lipoprotein, adjustments have also been done with these covariates.…”

Section: Discussionmentioning

confidence: 99%

Gender difference in adiponectin associated with cardiovascular mortality

et al. 2015

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BackgroundIt is important to identify cardiovascular diseases in patients at high risk. To include genetics into routine cardiological patients has therefore been discussed recently.We wanted to evaluate the association between high-molecular weight adiponectin and cardiovascular risk, and secondly in the same population evaluate if specific genotype differences regarding risk could be observed, and thirdly if gender differences could be seen.MethodFour hundred seventy-six elderly participants recruited from a rural community were included. All participants underwent a clinical examination, echocardiography, and blood sampling and the single nucleotide polymorphism (SNP) (rs266729) of adiponectin was analysed. Follow-up time was 6.7 years.ResultsThose with high serum concentration of adiponectin had a more 2 fold increased cardiovascular risk, and it might be that females exhibits even higher risk where a more than 5 fold increased risk could be seen. The result could be demonstrated even in a multivariate model adjusting for well-known clinical risk factors. However, as the sample size was small the gender differences should be interpreted with caution. In the genotype evaluation the C/C carriers of the female group had a more than 9-fold increased risk of cardiovascular mortality, however the confidence interval was wide. Such genotype difference could not be found in the male group.ConclusionHigh level of adiponectin was associated with increased cardiovascular risk. Also a gender difference in the genotype evaluation could be seen where the C/C carriers obtained higher risk in the female group but not in the male group. Thus, in order to identify patients at risk early, genetic analyses may add to the armamentarium used in the clinical routine. However, information should be regarded as hypothesis generating as the sample size was small and should stimulate further research in individualized cardiovascular prevention and treatment.

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Common variation in the adiponectin gene has an effect on systolic blood pressure

Cited by 12 publications

References 25 publications

Stimulated release of a hyperpolarizing factor (ADHF) from mesenteric artery perivascular adipose tissue: involvement of myocyte BK_Ca channels and adiponectin

Stimulated release of a hyperpolarizing factor (ADHF) from mesenteric artery perivascular adipose tissue: involvement of myocyte BK_Ca channels and adiponectin

The role of adiponectin in human vascular physiology

Gender difference in adiponectin associated with cardiovascular mortality

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Common variation in the adiponectin gene has an effect on systolic blood pressure

Cited by 12 publications

References 25 publications

Stimulated release of a hyperpolarizing factor (ADHF) from mesenteric artery perivascular adipose tissue: involvement of myocyte BKCa channels and adiponectin

Stimulated release of a hyperpolarizing factor (ADHF) from mesenteric artery perivascular adipose tissue: involvement of myocyte BKCa channels and adiponectin

The role of adiponectin in human vascular physiology

Gender difference in adiponectin associated with cardiovascular mortality

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Product

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Stimulated release of a hyperpolarizing factor (ADHF) from mesenteric artery perivascular adipose tissue: involvement of myocyte BK_Ca channels and adiponectin

Stimulated release of a hyperpolarizing factor (ADHF) from mesenteric artery perivascular adipose tissue: involvement of myocyte BK_Ca channels and adiponectin