DOCA-salt treatment enhances responses to endothelin-1 in murine corpus cavernosumThis article is one of a selection of papers published in the special issue (part 1 of 2) on Forefronts in Endothelin.

Carneiro, Fernando S.; Giachini, Fernanda R.; Lima, Victor Vitorino; Carneiro, Zidonia N.; Nunes, Kênia Pedrosa; Ergul, Adviye; Leite, Rômulo; Tostes, Rita C.; Webb, R.

doi:10.1139/y08-031

Cited by 27 publications

(4 citation statements)

References 34 publications

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“…49 Moreover, the DOCA/salt hypertension model exhibits increased caspase-1 and IL-1β activity in the kidney, 50 and it is characterized by ET-1 overexpression. 6,51 As observed in the present study, ET-1 does not need previous stimulation with LPS to increase pro-caspase-1 and pro-IL-1β, and the increased caspase-1 and IL-1β are in agreement with direct stimulation of NF-κB.…”

Section: Discussionsupporting

confidence: 86%

NLRP3 activation contributes to endothelin‐1‐induced erectile dysfunction

Fais

Costa

Mendes

et al. 2022

J Cellular Molecular Medi

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In the present study, we hypothesized that endothelin (ET) receptors (ET A and ET B ) stimulation, through increased calcium and ROS formation, leads to Nucleotide Oligomerization Domain-Like Receptor Family, Pyrin Domain Containing 3 (NLRP3) activation. Intracavernosal pressure (ICP/MAP) was measured in C57BL/6 (WT) mice.Functional and immunoblotting assays were performed in corpora cavernosa (CC) strips from WT, NLRP3 −/− and caspase −/− mice in the presence of ET-1 (100 nM) and vehicle, MCC950, tiron, BAPTA AM, BQ123, or BQ788. ET-1 reduced the ICP/MAP in WT mice, and MCC950 prevented the ET-1 effect. ET-1 decreased CC ACh-, sodium nitroprusside (SNP)-induced relaxation, and increased caspase-1 expression.BQ123 an ET A receptor antagonist reversed the effect. The ET B receptor antagonist BQ788 also reversed ET-1 inhibition of ACh and SNP relaxation. Additionally, tiron, BAPTA AM, and NLRP3 genetic deletion prevented the ET-1-induced loss of ACh and SNP relaxation. Moreover, BQ123 diminished CC caspase-1 expression, while BQ788 increased caspase-1 and IL-1β levels in a concentration-dependent manner (100 nM-10 μM). Furthermore, tiron and BAPTA AM prevented ET-1-induced increase in caspase-1. In addition, BAPTA AM blocked ET-1-induced ROS generation. In conclusion, ET-1-induced erectile dysfunction depends on ET A -and ET B -mediated activation of NLRP3 in mouse CC via Ca 2+ -dependent ROS generation.

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Section: Discussionsupporting

confidence: 86%

NLRP3 activation contributes to endothelin‐1‐induced erectile dysfunction

Fais

Costa

Mendes

et al. 2022

J Cellular Molecular Medi

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“…Penile VSM cells are able to synthesize ET-1 as well as respond to stimulation with ET-1(18). In addition, both ET-A and ET-B have been reported to be expressed in cavernosal tissue (19–22). In the penis, ET-1 induces corpus cavernosum vasoconstriction through the ET A receptor and subsequent activation of the inositol triphosphate (IP 3 ) / Ca 2+ signaling pathway (Ca 2+ sensitive) and the RhoA/Rho-kinase signaling pathway (Ca 2+ independent) (23).…”

Section: C- Ed In Hypertensionmentioning

confidence: 99%

“…Concurrently, ET-1 was shown to increase ROS generation via NADPH oxidase activation. Data from our laboratory has shown that ET-1 mediates not only penile vasoconstriction, but also contraction of the internal pudendal artery, the major artery providing blood flow to the penis (22, 25). We have also revealed that the corpora cavernosum from DOCA-salt hypertensive rats exhibit increased contractile responses to ET-1when compared with their normotensive counterpart controls (22).…”

Section: C- Ed In Hypertensionmentioning

confidence: 99%

New insights into hypertension-associated erectile dysfunction

Nunes

Labazi

Webb³

2012

Current Opinion in Nephrology and Hypertension

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Purpose of review Erectile dysfunction (ED) is recognized as a quality of life disorder that needs to be treated. Currently, it is estimated to affect as many as 30 million American men. Thirty percent of hypertensive patients complain of ED. The understanding of common mechanisms involved in the etiology of ED associated with hypertension, and the investigation of antihypertensive drugs that impact ED, will provide important tools toward indentifying new therapeutic targets that will improve the quality of life for patients in these conditions. Recent findings Hypertension and ED are closely intertwined diseases which have endothelium dysfunction as a common base. During hypertension and/or ED, disturbance of endothelium derived factors can lead to an increase in vascular smooth muscle (VSM) contraction. Hypertension can also lead to ED as a consequence of high blood pressure (BP) or due to antihypertensive treatment. However, growing evidence suggests ED as an early sign for hypertension. Also, some PDE-5 inhibitors used to treat ED can improve BP, but the link between these conditions has not been totally understood. Summary This review will discuss the interplay between hypertension and ED, exploring newest insights regarding hypertension-associated ED, as well as the effect of antihypertensive drugs in ED patients.

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“…In the vasculature, ET-1 elicits reactive oxygen species (ROS), production by NADPH oxidase enzyme, which in turn releases ET-1, favouring a prohypertensive [ 158 , 159 ]. Animal model studies reveal ET-1 to be essential in salt-sensitive hypertension-related ED [ 160 , 161 ]. Furthermore, ET-1 generated Ca 2+ influx alteration, prompting smooth muscle contraction in isolated penile tissue [ 162 ].…”

Section: Gender Differences In Et-1 Functionalitymentioning

confidence: 99%

Endothelin-1 axes in the framework of predictive, preventive and personalised (3P) medicine

et al. 2021

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Endothelin-1 (ET-1) is involved in the regulation of a myriad of processes highly relevant for physical and mental well-being; female and male health; in the modulation of senses, pain, stress reactions and drug sensitivity as well as healing processes, amongst others. Shifted ET-1 homeostasis may influence and predict the development and progression of suboptimal health conditions, metabolic impairments with cascading complications, ageing and related pathologies, cardiovascular diseases, neurodegenerative pathologies, aggressive malignancies, modulating, therefore, individual outcomes of both non-communicable and infectious diseases such as COVID-19. This article provides an in-depth analysis of the involvement of ET-1 and related regulatory pathways in physiological and pathophysiological processes and estimates its capacity as a predictor of ageing and related pathologies, a sensor of lifestyle quality and progression of suboptimal health conditions to diseases for their targeted prevention and as a potent target for cost-effective treatments tailored to the person.

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DOCA-salt treatment enhances responses to endothelin-1 in murine corpus cavernosumThis article is one of a selection of papers published in the special issue (part 1 of 2) on Forefronts in Endothelin.

Cited by 27 publications

References 34 publications

NLRP3 activation contributes to endothelin‐1‐induced erectile dysfunction

NLRP3 activation contributes to endothelin‐1‐induced erectile dysfunction

New insights into hypertension-associated erectile dysfunction

Endothelin-1 axes in the framework of predictive, preventive and personalised (3P) medicine

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