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Nathan Goodyear

Effect of Medroxyprogesterone Acetate on Endothelium-Dependent Vasodilation in Postmeno... - 0 views

circ.ahajournals.org/...1773.long

estrogen estradiol endothelium hormone HRT BHRT medroxyprogesterone acetate medroxyprogesterone

shared by Nathan Goodyear on 14 Oct 13 - No Cached
  • Nathan Goodyear on 14 Oct 13
     
    Estradiol has been shown to have positive health effects on vascular endothelium.  The synthetic progestin, medroxyprogesterone acetate, negates this.  
Nathan Goodyear

Endothelium and control of vascular function. State of the Art lecture. - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...2661425

vitamin C NO nitric oxide blood pressure CV cardiovascular disease hypertension endothelium

shared by Nathan Goodyear on 20 Dec 17 - No Cached
  • Nathan Goodyear on 20 Dec 17
     
    vitamin C, absorbed via the endothelium, increases NO.  This will have a positive effect in lowering the blood pressure.
Nathan Goodyear

Differential regulation of endothelium behavior by progesterone and medroxyprogesterone... - 0 views

joe.endocrinology-journals.org/...179.abstract

progesterone medroxyprogesterone acetate medroxyprogesterone hormone hormones women cardiovascular disease HRT

shared by Nathan Goodyear on 04 Feb 14 - No Cached
  • Nathan Goodyear on 04 Feb 14
     
    No surprise that progesterone and the synthetic progestin medroxyprogesterone acetate (MPA) have different effects on the vascular endothelium. MPA inhibits NO production, whereas Progesterone maintains NO production.  MPA promoted platelet adhesion whereas Progesterone did not--significant implication in plaque formation.
Nathan Goodyear

SARS-CoV-2 Spike Protein Impairs Endothelial Function via Downregulation of ACE2 - 0 views

www.ncbi.nlm.nih.gov/...PMC7724674

COVID-19 COVID endothelium spike protein ACE2 COVID19 SARS-CoV-2

shared by Nathan Goodyear on 28 Aug 21 - No Cached
  • Nathan Goodyear on 28 Aug 21
     
    S protein damages endothelium
Nathan Goodyear

Testosterone: a vascular hormone in health and disease - 0 views

joe.endocrinology-journals.org/...R47.full

testosterone hormone health disease hormones men male cardiovascular disease CVD

shared by Nathan Goodyear on 13 May 13 - No Cached
  • Testosterone has beneficial effects on several cardiovascular risk factors, which include cholesterol, endothelial dysfunction and inflammation
  • In clinical studies, acute and chronic testosterone administration increases coronary artery diameter and flow, improves cardiac ischaemia and symptoms in men with chronic stable angina and reduces peripheral vascular resistance in chronic heart failure.
  • testosterone is an L-calcium channel blocker and induces potassium channel activation in vascular smooth muscle cells
  • ...54 more annotations...
  • Animal studies have consistently demonstrated that testosterone is atheroprotective, whereas testosterone deficiency promotes the early stages of atherogenesis
  • there is no compelling evidence that testosterone replacement to levels within the normal healthy range contributes adversely to the pathogenesis of CVD (Carson & Rosano 2011) or prostate cancer (Morgentaler & Schulman 2009)
  • bidirectional effect between decreased testosterone concentrations and disease pathology exists as concomitant cardiovascular risk factors (including inflammation, obesity and insulin resistance) are known to reduce testosterone levels and that testosterone confers beneficial effects on these cardiovascular risk factors
  • Achieving a normal physiological testosterone concentration through the administration of testosterone replacement therapy (TRT) has been shown to improve risk factors for atherosclerosis including reducing central adiposity and insulin resistance and improving lipid profiles (in particular, lowering cholesterol), clotting and inflammatory profiles and vascular function
  • It is well known that impaired erectile function and CVD are closely related in that ED can be the first clinical manifestation of atherosclerosis often preceding a cardiovascular event by 3–5 years
  • no decrease in the response (i.e. no tachyphylaxis) of testosterone and that patient benefit persists in the long term.
  • free testosterone levels within the physiological range, has been shown to result in a marked increase in both flow- and nitroglycerin-mediated brachial artery vasodilation in men with CAD
  • Clinical studies, however, have revealed either small reductions of 2–3 mm in diastolic pressure or no significant effects when testosterone is replaced within normal physiological limits in humans
  • Endothelium-independent mechanisms of testosterone are considered to occur primarily via the inhibition of voltage-operated Ca2+ channels (VOCCs) and/or activation of K+ channels (KCs) on smooth muscle cells (SMCs)
  • Testosterone shares the same molecular binding site as nifedipine
  • Testosterone increases the expression of endothelial nitric oxide synthase (eNOS) and enhances nitric oxide (NO) production
  • Testosterone also inhibited the Ca2+ influx response to PGF2α
  • one of the major actions of testosterone is on NO and its signalling pathways
  • In addition to direct effects on NOS expression, testosterone may also affect phosphodiesterase type 5 (PDE5 (PDE5A)) gene expression, an enzyme controlling the degradation of cGMP, which acts as a vasodilatory second messenger
  • the significance of the action of testosterone on VSMC apoptosis and proliferation in atherosclerosis is difficult to delineate and may be dependent upon the stage of plaque development
  • Several human studies have shown that carotid IMT (CIMT) and aortic calcification negatively correlate with serum testosterone
  • t long-term testosterone treatment reduced CIMT in men with low testosterone levels and angina
  • neither intracellular nor membrane-associated ARs are required for the rapid vasodilator effect
  • acute responses appear to be AR independent, long-term AR-mediated effects on the vasculature have also been described, primarily in the context of vascular tone regulation via the modulation of gene transcription
  • Testosterone and DHT increased the expression of eNOS in HUVECs
  • oestrogens have been shown to activate eNOS and stimulate NO production in an ERα-dependent manner
  • Several studies, however, have demonstrated that the vasodilatory actions of testosterone are not reduced by aromatase inhibition
  • non-aromatisable DHT elicited similar vasodilation to testosterone treatment in arterial smooth muscle
  • increased endothelial NOS (eNOS) expression and phosphorylation were observed in testosterone- and DHT-treated human umbilical vein endothelial cells
  • Androgen deprivation leads to a reduction in neuronal NOS expression associated with a decrease of intracavernosal pressure in penile arteries during erection, an effect that is promptly reversed by androgen replacement therapy
  • Observational evidence suggests that several pro-inflammatory cytokines (including interleukin 1β (IL1β), IL6, tumour necrosis factor α (TNFα), and highly sensitive CRP) and serum testosterone levels are inversely associated in patients with CAD, T2DM and/or hypogonadism
  • patients with the highest IL1β concentrations had lower endogenous testosterone levels
  • TRT has been reported to significantly reduce TNFα and elevate the circulating anti-inflammatory IL10 in hypogonadal men with CVD
  • testosterone treatment to normalise levels in hypogonadal men with the MetS resulted in a significant reduction in the circulating CRP, IL1β and TNFα, with a trend towards lower IL6 compared with placebo
  • parenteral testosterone undecanoate, CRP decreased significantly in hypogonadal elderly men
  • Higher levels of serum adiponectin have been shown to lower cardiovascular risk
  • Research suggests that the expression of VCAM-1, as induced by pro-inflammatory cytokines such as TNFα or interferon γ (IFNγ (IFNG)) in endothelial cells, can be attenuated by treatment with testosterone
  • Testosterone also inhibits the production of pro-inflammatory cytokines such as IL6, IL1β and TNFα in a range of cell types including human endothelial cells
  • decreased inflammatory response to TNFα and lipopolysaccharide (LPS) in human endothelial cells when treated with DHT
  • The key to unravelling the link between testosterone and its role in atherosclerosis may lay in the understanding of testosterone signalling and the cross-talk between receptors and intracellular events that result in pro- and/or anti-inflammatory actions in athero-sensitive cells.
  • testosterone functions through the AR to modulate adhesion molecule expression
  • pre-treatment with DHT reduced the cytokine-stimulated inflammatory response
  • DHT inhibited NFκB activation
  • DHT could inhibit an LPS-induced upregulation of MCP1
  • Both NFκB and AR act at the transcriptional level and have been experimentally found to be antagonistic to each other
  • As the AR and NFκB are mutual antagonists, their interaction and influence on functions can be bidirectional, with inflammatory agents that activate NFκB interfering with normal androgen signalling as well as the AR interrupting NFκB inflammatory transcription
  • prolonged exposure of vascular cells to the inflammatory activation of NFκB associated with atherosclerosis may reduce or alter any potentially protective effects of testosterone
  • DHT and IFNγ also modulate each other's signalling through interaction at the transcriptional level, suggesting that androgens down-regulate IFN-induced genes
  • (Simoncini et al. 2000a,b). Norata et al. (2010) suggest that part of the testosterone-mediated atheroprotective effects could depend on ER activation mediated by the testosterone/DHT 3β-derivative, 3β-Adiol
  • TNFα-induced induction of ICAM-1, VCAM-1 and E-selectin as well as MCP1 and IL6 was significantly reduced by a pre-incubation with 3β-Adiol in HUVECs
  • 3β-Adiol also reduced LPS-induced gene expression of IL6, TNFα, cyclooxygenase 2 (COX2 (PTGS2)), CD40, CX3CR1, plasminogen activator inhibitor-1, MMP9, resistin, pentraxin-3 and MCP1 in the monocytic cell line U937 (Norata et al. 2010)
  • This study suggests that testosterone metabolites, other than those generated through aromatisation, could exert anti-inflammatory effects that are mediated by ER activation.
  • The authors suggest that DHT differentially effects COX2 levels under physiological and pathophysiological conditions in human coronary artery smooth muscle cells and via AR-dependent and -independent mechanisms influenced by the physiological state of the cell
  • There are, however, a number of systematic meta-analyses of clinical trials of TRT that have not demonstrated an increased risk of adverse cardiovascular events or mortality
  • The TOM trial, which was designed to investigate the effect of TRT on frailty in elderly men, was terminated prematurely as a result of an increased incidence of cardiovascular-related events after 6 months in the treatment arm
  • trials of TRT in men with either chronic stable angina or chronic cardiac failure have also found no increase in either cardiovascular events or mortality in studies up to 12 months
  • Evidence may therefore suggest that low testosterone levels and testosterone levels above the normal range have an adverse effect on CVD, whereas testosterone levels titrated to within the mid- to upper-normal range have at least a neutral effect or, taking into account the knowledge of the beneficial effects of testosterone on a series of cardiovascular risk factors, there may possibly be a cardioprotective action
  • The effect of testosterone on human vascular function is a complex issue and may be dependent upon the underlying androgen and/or disease status.
  • the majority of studies suggest that testosterone may display both acute and chronic vasodilatory effects upon various vascular beds at both physiological and supraphysiological concentrations and via endothelium-dependent and -independent mechanisms
  • Nathan Goodyear on 13 May 13
     
    Good deep look into the testosterone and CVD link.
Nathan Goodyear

Uptake, recycling, and antioxidant actio... [Free Radic Biol Med. 2002] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...12086686

alpha lipoic acid oxidative damage oxidative stress antioxidant

shared by Nathan Goodyear on 20 Feb 13 - No Cached
  • Nathan Goodyear on 20 Feb 13
     
    Alpha lipoic acid is shown to protect the vascular endothelium against oxidative damage.
Nathan Goodyear

alpha-Lipoic acid and ascorbate prevent LDL... [Mol Cell Biochem. 2008] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...18026819

alpha lipoic acid vitamin C oxidized LDL LDL cholesterol CVD cardiovascular disease

shared by Nathan Goodyear on 20 Feb 13 - No Cached
  • Nathan Goodyear on 20 Feb 13
     
    Alpha lipoic acid and vitamin C shown to protect against oxidized LDL.  When discussing the negative effects of LDL, the real risk associated with LDL is whether it is oxidized or not.  Alpha lipoic acid and Vitamin C prevent this and thus protect the vascular endothelium.
Nathan Goodyear

Analysis of the vascular responses in a murine model of polycystic ovary syndrome - 0 views

joe.endocrinology-journals.org/...205.abstract

PCOS polycystic ovarian syndrome CVD DHT

shared by Nathan Goodyear on 24 Jul 13 - No Cached
  • Nathan Goodyear on 24 Jul 13
     
    Animal model of PCOS provides insight to changes in vascular response.  In this animal mode, DHT resulted in a decrease in vasorelaxation of arterial endothelium.
Nathan Goodyear

Lipopolysaccharide (LPS) potentiates hydrogen peroxide toxicity in T98G astrocytoma cel... - 0 views

www.ncbi.nlm.nih.gov/...PMC2631585

LPS lipopolysaccharides microglia astrocytes brain H2O2 inflammation

shared by Nathan Goodyear on 21 Sep 17 - No Cached
  • Nathan Goodyear on 21 Sep 17
     
    good review of proposed mechanism of how LPS aids in cell death of astrocytes in vivo: LPS damages the endothelium of the BBB, leading to increase permeability.  This exposes astrocytes to LPS directly.  LPS suppressed genetic expression of antioxidant genes.  LPS stimulates cytokine production, including the production of H2O2 from microglial cells in the brain.  An up regulation of iNOS occurs and in the presence of weakened ability to protect against NO and its metabolites occurs.  
Nathan Goodyear

The SARS-CoV-2 Spike protein disrupts human cardiac pericytes function through CD147-re... - 0 views

www.biorxiv.org/...2020.12.21.423721v2

spike proteins COVID-19 covid19 SARS-CoV-2

shared by Nathan Goodyear on 07 Sep 21 - No Cached
  • Nathan Goodyear on 07 Sep 21
     
    Surprise, surprise, the spike proteins damage endothelium.
Nathan Goodyear

Circulating Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) Vaccine Antige... - 0 views

academic.oup.com/...6279075

COVID-19 COVID SARS-CoV-2 covid19 spike protein

shared by Nathan Goodyear on 07 Sep 21 - No Cached
  • Nathan Goodyear on 07 Sep 21
     
    Spike proteins reach blood stream in 11/13 vaccinated. The implications on the endothelium and myocardium is significant.
Nathan Goodyear

Beyond the male sex hormone: deciphering the metabolic and vascular actions of testoste... - 0 views

joe.endocrinology-journals.org/...C1.full

AR androgen receptors androgen receptor testosterone androgen receptors Diabetes metabolic syndrome MetS CVD cardiovascular disease men hormone hormones male

shared by Nathan Goodyear on 08 May 13 - No Cached
  • androgen deprivation therapy results in unfavorable changes in body composition, insulin resistance, and dyslipidemia and predisposes men to develop atherosclerosis and an increased risk of cardiovascular mortality
  • The hypogonadal–obesity cycle hypothesis was originally proposed by Cohen in 1999 to explain the relationship between low testosterone levels and metabolic disease. It was based on the finding that obesity impairs testosterone levels by increasing the aromatization of testosterone to estradiol, while low testosterone levels promote increased fat deposition
  • adipocytokines contribute to low testosterone levels as well as to the processes underlying metabolic syndromes and type 2 diabetes
  • ...15 more annotations...
  • hypogonadal–obesity–adipocytokine hypothesis
  • The presence of estradiol and the adipocytokines TNF-α, IL6, and leptin (as a result of leptin resistance in obesity) inhibits the hypothalamic–pituitary–testicular axis response to decreasing androgen levels
  • An increasing number of studies have illustrated the potential for applying metabolomics to the field of androgen research
  • As early as the 1940s, the therapeutic use of testosterone was reported to improve angina pectoris in men with coronary artery disease
  • most of the epidemiological studies reported increased cardiovascular risk and mortality in men with low testosterone levels
  • long-term testosterone replacement appears to be a safe and effective means of treating hypogonadal elderly men
  • a recent interventional trial showed that testosterone treatment was associated with decreased mortality when compared with no testosterone treatment in an observational cohort of men with low testosterone levels
  • a number of short-term studies conducted support the notion that testosterone therapy reduces the cardiovascular risk
  • The majority of animal studies support the hypothesis that the actions of testosterone on vascular relaxation are both endothelium-dependent and -independent vasodilatory effects
  • Endothelial-dependent actions of testosterone increase the expression or activity of endothelial nitric oxide synthase and enhance nitric oxide production, which in turn activates cyclic guanosine monophosphate to induce vasorelaxation in smooth muscle cells
  • Endothelial-independent mechanisms of testosterone are believed to occur primarily via inhibition of voltage-operated Ca2+ channels and/or activation of K+ channels in smooth muscle cells
  • Testosterone may also inhibit intracellular Ca2+ influx via store-operated Ca2+ channels by blocking the response to prostaglandin F2α
  • testosterone has demonstrated anti-inflammatory effects to protect against atherogenesis in animal studies
  • both genomic AR activation to modulate gene transcription and non-genomic activation to modulate the rapid intracellular signaling pathways of ion channels may mediate testosterone effects on vascular function and inflammation.
  • Butenandt & Ruzicka first showed how testosterone is synthesized and responsible for masculine characteristics in the early 1930s
  • Nathan Goodyear on 08 May 13
     
    Awesome review on the current understanding of Testosterone and Diabetes, metabolic syndrome, and CVD.  This article even goes into the literature on androgen receptors.
Nathan Goodyear

Vitamin C Improves Endothelium-Dependent Vasodilation by Restoring Nitric Oxide Activit... - 0 views

circ.ahajournals.org/...2222

eNOS NO nitric oxide vitamin C hypertension

shared by Nathan Goodyear on 16 Jan 17 - No Cached
  • Nathan Goodyear on 16 Jan 17
     
    vitamin C, in small study in patient with/without hypertension, found to increase endothelial vasodilation via increasing eNOS activity.
Nathan Goodyear

SpringerPlus | Full text | Testosterone-derived estradiol production by male endotheliu... - 0 views

www.springerplus.com/...214

aromatase activity aromatase estradiol estrogen atherosclerosis hormone hormones male ER-alpha ER alpha

shared by Nathan Goodyear on 04 Oct 13 - No Cached
  • Nathan Goodyear on 04 Oct 13
     
    Mouse study, but aromatase activity and ER alpha required for atherosclerosis in male mice.
Nathan Goodyear

Equine Estrogens Impair Nitric Oxide Production and Endothelial Nitric Oxide ... - 0 views

hyper.ahajournals.org/...405.long

premarin estradiol HRT BHRT eNOS NO nitric oxide endothelium

shared by Nathan Goodyear on 14 Oct 13 - No Cached
  • Nathan Goodyear on 14 Oct 13
     
    This is the perfect study to compare synthetic, unnatural hormones with bioidentical hormones.  Premarin was compared with bioidentical estradiol.  Premarin reduced the endothelial NO synthase transcription and activity by 30-50% compared to Estradiol.   Thus, premarin results in a lower NO production and thus greater endothelial dysfunction compared to Estradiol.
Nathan Goodyear

Medroxyprogesterone interferes with ovarian steroid ... [Nat Med. 1997] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...9055861

progesterone estradiol medroxyprogesterone vascular endothelium hormone hormones HRT BHRT medroxyprogesterone acetate

shared by Nathan Goodyear on 14 Oct 13 - No Cached
  • Nathan Goodyear on 14 Oct 13
     
    head to head study in rhesus monkeys finds that medroxyprogesterone acetate negates the positive vascular effects of estradiol.  This is in contrast to the bioidentical progesterone.
Nathan Goodyear

Androgen Exposure Increases Human Monocyte Adhesion to Vascular Endothelium and Endothe... - 0 views

circ.ahajournals.org/...2317.long

DHT VCAM-1

shared by Nathan Goodyear on 06 Nov 13 - No Cached
  • Nathan Goodyear on 06 Nov 13
     
    DHT shown to increase VCAM-1 adhesion to endothelial cells.  This was a cell culture study of human umbilical vein endothelial cells exposed to postmenopausal female serum and then DHT.  Not exactly physiologic.
Nathan Goodyear

Effect of Medroxyprogesterone Acetate on Endothelium-Dependent Vasodilation in Postmeno... - 0 views

circ.ahajournals.org/...1773

MPA synthetic medroxyprogesterone progestins

shared by Nathan Goodyear on 18 Nov 10 - No Cached
  • Nathan Goodyear on 18 Nov 10
     
    medroxyprogsterone acetate (synthetic progestin) increase vascular function in postmenopausal women
Nathan Goodyear

Effect of Medroxyprogesterone Acetate on Endothelium-Dependent Vasodilation in Postmeno... - 0 views

circ.ahajournals.org/...1773

MPA synthetic progestins heart cardiac medroxyprogesterone

shared by Nathan Goodyear on 18 Nov 10 - No Cached
  • Nathan Goodyear on 18 Nov 10
     
    synthetic progestin (MPA) off sets beneficial estrogen heart benefits
Nathan Goodyear

Thyroid Function Is Intrinsically Linked to Insulin Sensitivity and Endotheli... - 0 views

jcem.endojournals.org/...3337

thyroid function IR insulin resistance vascular disease

shared by Nathan Goodyear on 01 Feb 11 - No Cached
  • Nathan Goodyear on 01 Feb 11
     
    thyroid, insulin, and vascular function all linked; no linear thinking here
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