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  • 1
    Online Resource
    Online Resource
    Ethanol: striking the cardiovascular system by harming the gut microbiota
    American Physiological Society ; 2021
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 321, No. 2 ( 2021-08-01), p. H275-H291
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 321, No. 2 ( 2021-08-01), p. H275-H291
    Abstract: Ethanol consumption represents a significant public health problem, and excessive ethanol intake is a risk factor for cardiovascular disease (CVD), one of the leading causes of death and disability worldwide. The mechanisms underlying the effects of ethanol on the cardiovascular system are complex and not fully comprehended. The gut microbiota and their metabolites are indispensable symbionts essential for health and homeostasis and therefore, have emerged as potential contributors to ethanol-induced cardiovascular system dysfunction. By mechanisms that are not completely understood, the gut microbiota modulates the immune system and activates several signaling pathways that stimulate inflammatory responses, which in turn, contribute to the development and progression of CVD. This review summarizes preclinical and clinical evidence on the effects of ethanol in the gut microbiota and discusses the mechanisms by which ethanol-induced gut dysbiosis leads to the activation of the immune system and cardiovascular dysfunction. The cross talk between ethanol consumption and the gut microbiota and its implications are detailed. In summary, an imbalance in the symbiotic relationship between the host and the commensal microbiota in a holobiont, as seen with ethanol consumption, may contribute to CVD. Therefore, manipulating the gut microbiota, by using antibiotics, probiotics, prebiotics, and fecal microbiota transplantation might prove a valuable opportunity to prevent/mitigate the deleterious effects of ethanol and improve cardiovascular health and risk prevention.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00225.2021
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2021
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Reply to Boedtkjer and Aalkjaer
    American Physiological Society ; 2022
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 322, No. 4 ( 2022-04-01), p. H687-H688
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 322, No. 4 ( 2022-04-01), p. H687-H688
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00117.2022
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2022
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Toll-like receptors and damage-associated molecular patterns: novel links between inflammation and hypertension
    American Physiological Society ; 2014
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 306, No. 2 ( 2014-01-15), p. H184-H196
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 306, No. 2 ( 2014-01-15), p. H184-H196
    Abstract: Low-grade systemic inflammation is a common manifestation of hypertension; however, the exact mechanisms that initiate this pathophysiological response, thereby contributing to further increases in blood pressure, are not well understood. Aberrant vascular inflammation and reactivity via activation of the innate immune system may be the first step in the pathogenesis of hypertension. One of the functions of the innate immune system is to recognize and respond to danger. Danger signals can arise from not only pathogenic stimuli but also endogenous molecules released following cell injury and/or death [damage-associated molecular patterns (DAMPs)]. In the short-term, activation of the innate immune system is beneficial in the vasculature by providing cytoprotective mechanisms and facilitating tissue repair following injury or infection. However, sustained or excessive immune system activation, such as in autoimmune diseases, may be deleterious and can lead to maladaptive, irreversible chan ges to vascular structure and function. An initial source of DAMPs that enter the circulation to activate the innate immune system could arise from modest elevations in peripheral vascular resistance. These stimuli could subsequently lead to ischemic- or pressure-induced events aggravating further cell injury and/or death, providing more DAMPs for innate immune system activation. This review will address and critically evaluate the current literature on the role of the innate immune system in hypertension pathogenesis. The role of Toll-like receptor activation on somatic cells of the vasculature in response to the release of DAMPs and the consequences of this activation on inflammation, vasoreactivity, and vascular remodeling will be specifically discussed.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00328.2013
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2014
    detail.hit.zdb_id: 1477308-9
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  • 4
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    Online Resource
    Endothelial Dysfunction and Phenylephrine-Induced Hypocontractility Occurs in Mesenteric Resistance Arteries Prior to the Onset of Alzheimer's Disease in Mice
    American Physiological Society ; 2023
    In:  Physiology Vol. 38, No. S1 ( 2023-05)
    Details
    In: Physiology, American Physiological Society, Vol. 38, No. S1 ( 2023-05)
    Abstract: Alzheimer’s Disease (AD) is the most common form of dementia and a major cause of disability and death among the older population. In addition, Cardiovascular dieseases (CVDs) and their risk factors are associated with an increased risk of the progression of AD and cognitive impairment. Despite this, studying the combination of these diseases constitutes a clinical challenge, and investigations to understand the mechanistic pathways for the cause-effect and/or shared pathology between them remains an active area of research. One form of AD, familial AD, is linked with an early onset AD (EOAD) pathology ( 〈 65years) that manifests through pathogenic mutations in the genes encoding the amyloid precursor protein (APP) and the g-secretase complex enzymes presenilin (PSEN)1 and PSEN2 which result in the increased production of central amyloid β (Aβ) peptides. There is increasing evidence that amyloid deposition in peripheral vessels has powerful structural effects in CVDs which, in turn, increase the risk of cognitive decline later in life. With this premise, we hypothesized that vascular dysfunction would be observed in the resistance arteries prior to the development of EOAD regardless of sex. To test the hypothesis, mesenteric resistance arteries (MRA) were isolated from male and female early onset AD mice (B6.CApptm1Dbo Tg(APPswe, PSEN1dE9)85Dbo/Mmjax) prior to (9 weeks of age) and after the onset of AD (28 weeks of age). Vascular function was evaluated using wire myography and concentration-effect curves to acetylcholine, phenylephrine and to U46619, a thromboxane A2 analog, were performed. Data were analyzed using non-linear regression analysis and maximum response (Rmax) analyzed by Student t test (p 〈 0.05*). Arteries from 9-week-old AD mice showed impaired acetylcholine-induced relaxation and phenylephrine-induced hypocontractility for males [Rmax: control 11.72±0.9 vs. AD 7.70±0.8*, n=3-4]. Females presented a similar tendency of phenylephrine-induced hypocontractility. However, a “catch-up phenomenon” was observed and resulted in phenylephrine-induced hypercontractility in arteries from 28-weeks-old AD mice Males [Rmax: control 9.34±1.3 vs. AD 14.5±0.4*, n=3-5] and Females [Rmax: control 10.4± 2.8 vs. AD 13.8±1.5mN, n=3-4]. The same hypercontractility profile was observed in the arteries isolated from 28-weeks-old AD mice for U46619 agonist in both males [Rmax: control 12.4±1.5 vs. AD 15.6± 0.6*mN, n=3-5] and the females [Rmax: control 9.3± 1.7 vs. AD 14.3±1.9mN, n=3-4]. Overall, our data suggest that vascular dysfunction, which may lead to disrupted blood flow, nutrients and oxygen delivery to the brain, could contribute to the genesis and maintenance of AD. R00GM118885, R01HL149762, R00HL151889, and NHLBI (R00HL151889) This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
    Type of Medium: Online Resource
    ISSN: 1548-9213 , 1548-9221
    URL: Article
    DOI: 10.1152/physiol.2023.38.S1.5731729
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 3115360-4
    detail.hit.zdb_id: 2005759-3
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  • 5
    Online Resource
    Online Resource
    Low-dose 1,3-butanediol reverses age-associated vascular dysfunction independent of ketone body β-hydroxybutyrate
    American Physiological Society ; 2022
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 322, No. 3 ( 2022-03-01), p. H466-H473
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 322, No. 3 ( 2022-03-01), p. H466-H473
    Abstract: With an aging global population, identifying novel therapeutics are necessary to increase longevity and decrease the deterioration of essential end organs such as the vasculature. Secondary alcohol, 1,3-butanediol (1,3-BD), is commonly administered to stimulate the biosynthesis of the most abundant ketone body β-hydroxybutyrate (βHB), in lieu of nutrient deprivation. However, suprapharmacological concentrations of 1,3-BD are necessary to significantly increase systemic βHB, and 1,3-BD per se can cause vasodilation at nanomolar concentrations. Therefore, we hypothesized that 1,3-BD could be a novel antiaging therapeutic, independent of βHB biosynthesis. To test this hypothesis, we administered a low-dose (5%) 1,3-BD to young and old Wistar-Kyoto (WKY) rats via drinking water for 4 wk and measured indices of vascular function and metabolism posttreatment. We observed that low-dose 1,3-BD was sufficient to reverse age-associated endothelial-dependent and -independent dysfunction, and this was not associated with increased βHB bioavailability. Further analysis of the direct vasodilator mechanisms of 1,3-BD revealed that it is predominantly an endothelium-dependent vasodilator through activation of potassium channels and nitric oxide synthase. In summary, we report that 1,3-BD, at a concentration that does not stimulate βHB biosynthesis, could be a nutraceutical that can reverse the age-associated decline in vascular function. These results emphasize that 1,3-BD has multiple, concentration-dependent mechanisms of action. Therefore, we suggest alternative approaches to study the physiological and cardiovascular effects of βHB. NEW & NOTEWORTHY 1,3-Butanediol (1,3-BD) is often administered to stimulate the biosynthesis of the most abundant ketone body, β-hydroxybutyrate (βHB), and its purported salubrious effects. Here, we report that a low dose of 1,3-BD (5%) is sufficient to reverse age-associated vascular dysfunction, independent of βHB. Therefore, low-dose 1,3-BD could be a novel therapeutic to increase blood flow and improve the quality of life in the elderly.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00486.2021
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2022
    detail.hit.zdb_id: 1477308-9
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  • 6
    Online Resource
    Online Resource
    Reply to De Mey et al.
    American Physiological Society ; 2022
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 322, No. 4 ( 2022-04-01), p. H683-H684
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 322, No. 4 ( 2022-04-01), p. H683-H684
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00086.2022
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2022
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Mitochondrial N -formyl peptides induce cardiovascular collapse and sepsis-like syndrome
    American Physiological Society ; 2015
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 308, No. 7 ( 2015-04-01), p. H768-H777
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 308, No. 7 ( 2015-04-01), p. H768-H777
    Abstract: Fifty percent of trauma patients who present sepsis-like syndrome do not have bacterial infections. This condition is known as systemic inflammatory response syndrome (SIRS). A unifying factor of SIRS and sepsis is cardiovascular collapse. Trauma and severe blood loss cause the release of endogenous molecules known as damage-associated molecular patterns. Mitochondrial N-formyl peptides (F-MIT) are damage-associated molecular patterns that share similarities with bacterial N-formylated peptides and are potent immune system activators. The goal of this study was to investigate whether F-MIT trigger SIRS, including hypotension and vascular collapse via formyl peptide receptor (FPR) activation. We evaluated cardiovascular parameters in Wistar rats treated with FPR or histamine receptor antagonists and inhibitors of the nitric oxide pathway before and after F-MIT infusion. F-MIT, but not nonformylated peptides or mitochondrial DNA, induced severe hypotension via FPR activation and nitric oxide and histamine release. Moreover, F-MIT infusion induced hyperthermia, blood clotting, and increased vascular permeability. To evaluate the role of leukocytes in F-MIT-induced hypotension, neutrophil, basophil, or mast cells were depleted. Depletion of basophils, but not neutrophils or mast cells, abolished F-MIT-induced hypotension. Rats that underwent hemorrhagic shock increased plasma levels of mitochondrial formylated proteins associated with lung damage and antagonism of FPR ameliorated hemorrhagic shock-induced lung injury. Finally, F-MIT induced vasodilatation in isolated resistance arteries via FPR activation; however, F-MIT impaired endothelium-dependent relaxation in the presence of blood. These data suggest that F-MIT may be the link among trauma, SIRS, and cardiovascular collapse.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00779.2014
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2015
    detail.hit.zdb_id: 1477308-9
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  • 8
    Online Resource
    Online Resource
    Carotid dysfunction in senescent female mice is mediated by increased α 1A ‐adrenoceptor activity and COX-derived vasoconstrictor prostanoids
    American Physiological Society ; 2023
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 324, No. 4 ( 2023-04-01), p. H417-H429
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 324, No. 4 ( 2023-04-01), p. H417-H429
    Abstract: α-Adrenergic receptors are crucial regulators of vascular hemodynamics and essential pharmacological targets for cardiovascular diseases. With aging, there is an increase in sympathetic activation, which could contribute to the progression of aging-associated cardiovascular dysfunction, including stroke. Nevertheless, there is little information directly associating adrenergic receptor dysfunction in the blood vessels of aged females. This study determined the role of a-adrenergic receptors in carotid dysfunction of senescent female mice (accelerated-senescence prone, SAMP8), compared with a nonsenescent (accelerated-senescence prone, SAMR1). Vasoconstriction to phenylephrine (Phe) was markedly increased in common carotid artery of SAMP8 [area under the curve (AUC), 527 ± 53] compared with SAMR1 (AUC, 334 ± 30, P = 0.006). There were no changes in vascular responses to the vasoconstrictor agent U46619 or the vasodilators acetylcholine (ACh) and sodium nitroprusside (NPS). Hyperactivity to Phe in female SAMP8 was reduced by cyclooxygenase-1 and cyclooxygenase-2 inhibition and associated with augmented ratio of TXA2/PGI2 release (SAMR1, 1.1 ± 0.1 vs. SAMP8, 2.1 ± 0.3, P = 0.007). However, no changes in cyclooxygenase expression were seen in SAMP8 carotids. Selective α 1A -receptor antagonism markedly reduced maximal contraction, whereas α 1D antagonism induced a minor shift in Phe contraction in SAMP8 carotids. Ligand binding analysis revealed a threefold increase of α-adrenergic receptor density in smooth muscle cells (VSMCs) of SAMP8 vs. SAMR1. Phe rapidly increased intracellular calcium (Ca i 2+ ) in VSMCs via the α 1A -receptor, with a higher peak in VSMCs from SAMP8. In conclusion, senescence intensifies vasoconstriction mediated by α 1A -adrenergic signaling in the carotid of female mice by mechanisms involving increased Ca i 2+ and release of cyclooxygenase-derived prostanoids. NEW & NOTEWORTHY The present study provides evidence that senescence induces hyperreactivity of α 1 -adrenoceptor-mediated contraction of the common carotid. Impairment of α 1 -adrenoceptor responses is linked to increased Ca 2+ influx and release of COX-derived vasoconstrictor prostanoids, contributing to carotid dysfunction in the murine model of female senescence (SAMP8). Increased reactivity of the common carotid artery during senescence may lead to morphological and functional changes in arteries of the cerebral microcirculation and contribute to cognitive decline in females. Because the elderly population is growing, elucidating the mechanisms of aging- and sex-associated vascular dysfunction is critical to better direct pharmacological and lifestyle interventions to prevent cardiovascular risk in both sexes.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00495.2022
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2023
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 9
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    Exposure to stimulatory CpG oligonucleotides during gestation induces maternal hypertension and excess vasoconstriction in pregnant rats
    American Physiological Society ; 2016
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 310, No. 8 ( 2016-04-15), p. H1015-H1025
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 310, No. 8 ( 2016-04-15), p. H1015-H1025
    Abstract: Bacterial infections increase risk for pregnancy complications, such as preeclampsia and preterm birth. Unmethylated CpG DNA sequences are present in bacterial DNA and have immunostimulatory effects. Maternal exposure to CpG DNA induces fetal demise and craniofacial malformations; however, the effects of CpG DNA on maternal cardiovascular health have not been examined. We tested the hypothesis that exposure to synthetic CpG oligonucleotides (ODNs) during gestation would increase blood pressure and cause vascular dysfunction in pregnant rats. Pregnant and nonpregnant female rats were treated with CpG ODN (ODN 2395) or saline (Veh) starting on gestational day 14 or corresponding day for the nonpregnant groups. Exposure to CpG ODN increased systolic blood pressure in pregnant (Veh: 121 ± 2 mmHg vs. ODN 2395: 134 ± 2 mmHg, P 〈 0.05) but not in nonpregnant rats (Veh: 111 ± 2 mmHg vs. ODN 2395: 108 ± 5 mmHg, P 〉 0.05). Mesenteric resistance arteries from pregnant CpG ODN-treated rats had increased contractile responses to U46619 [thromboxane A 2 (TxA 2 ) mimetic] compared with arteries from vehicle-treated rats [E max (%KCl), Veh: 87 ± 4 vs. ODN 2395: 104 ± 4, P 〈 0.05]. Nitric oxide synthase (NOS) inhibition increased contractile responses to U46619, and CpG ODN treatment abolished this effect in arteries from pregnant ODN 2395-treated rats. CpG ODN potentiated the involvement of cyclooxygenase (COX) to U46619-induced contractions. In conclusion, exposure to CpG ODN during gestation induces maternal hypertension, augments resistance artery contraction, increases the involvement of COX-dependent mechanisms and reduces the contribution of NOS-dependent mechanisms to TxA 2 -induced contractions in mesenteric resistance arteries.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00834.2015
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2016
    detail.hit.zdb_id: 1477308-9
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  • 10
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    Online Resource
    B lymphoma Moloney murine leukemia virus insertion region 1 homolog: the Janus-faced polycomb protein that will break your heart
    American Physiological Society ; 2019
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 316, No. 2 ( 2019-02-01), p. H257-H259
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 316, No. 2 ( 2019-02-01), p. H257-H259
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00726.2018
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2019
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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