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Nathan Goodyear

PLOS ONE: Low Mercury Concentration Produces Vasoconstriction, Decreases Nitric Oxide B... - 0 views

www.plosone.org/...10.1371%2Fjournal.pone.0049005

Hg mercury NO RAS renin angiotensin system ROS hypertension oxidative stress vasoconstriction

shared by Nathan Goodyear on 16 Sep 14 - No Cached
  • Nathan Goodyear on 16 Sep 14
     
    Animal model found that low Hg decreased NO availability.  The result is vasoconstriction induced by ROS and hypertension. The hypertension is the result of an activation of the renin angiotensin system.  The importance here is that low Hg levels induced this change.
Nathan Goodyear

Nutrition Journal | Full text | Homocysteine and reactive oxygen species in metabolic s... - 0 views

www.nutritionj.com/4

homocysteine atherogenesis CVD metabolic syndrome metabolic syndrome

shared by Nathan Goodyear on 23 Jul 12 - No Cached
  • Nathan Goodyear on 23 Jul 12
     
    homocysteine contributes to atherogenesis and CVD via: increased ROS, induces endothelial dysfunction, increases platelete adhesion and thrombosis, increases smooth muscle cell proliferation, endothelial cell cytotoxicity, increases LDL oxidation, vasoconstriction, increased MCP-1 and IL-8, and induces endothelial HMG CoA reductase.
Nathan Goodyear

Inflammation-induced vasoconstrictorhyporeactivity is caused by oxidative stress -- Ple... - 0 views

content.onlinejacc.org/...1656

IV intravenous vitamin C inflammation LPS endotoxemia

shared by Nathan Goodyear on 29 Feb 12 - No Cached
  • Nathan Goodyear on 29 Feb 12
     
    IV vitamin C shown to reduce the inflammatory associated complications (vasoconstriction, HTN...) found due to LPS in E. Coli endotoxemia
Nathan Goodyear

Lead-induced hypertension: possible role of e... [Am J Hypertens. 1993] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...8110424

lead Pb hypertension CVD cardiovascular disease

shared by Nathan Goodyear on 16 Sep 14 - No Cached
  • Nathan Goodyear on 16 Sep 14
     
    Low lead exposure causes vasoconstriction in animal study.
Nathan Goodyear

Cyclooxygenase inhibition reduces blood p... [Clin Exp Hypertens. 2000] - PubMed - NCBI - 0 views

www.ncbi.nlm.nih.gov/...10744360

cyclooxygenase NO Hg mercury heart health COX cardiovascular disease hypertension

shared by Nathan Goodyear on 16 Sep 14 - No Cached
  • Nathan Goodyear on 16 Sep 14
     
    Inhibition of NO production will result in increased COX and thus vasoconstriction in rate model.  Hg has been shown to both inhibit NO synthase and increase COX.
Nathan Goodyear

Endothelial dysfunction of rat coronary arteries after exposure to low concentrations o... - 0 views

www.ncbi.nlm.nih.gov/...PMC3081124

Hg mercury NO cardiovascular disease heart health ROS reactive oxygen species oxidative stress

shared by Nathan Goodyear on 16 Sep 14 - No Cached
  • Nathan Goodyear on 16 Sep 14
     
    low dose, chronic exposure induces ROS and decreased NO availability.  This decrease in NO will result in increase vasoconstriction.  This will have localized effects and will result in increased central pressure as a result of the increased peripheral pressure.  In addition, inhibition of COMT will result in increase in catecholeamines.
Nathan Goodyear

Renin-angiotensin system and cancer: A review - 0 views

www.oatext.com/system-and-cancer-A-review.php

renin angiotensin system cancer

shared by Nathan Goodyear on 10 Sep 18 - No Cached
  • crucial role of the RAS in the development and maintenance of cancer
  • kidneys, which produce renin in response to decreased arterial pressure, reduced sodium in the distal tubule, or sympathetic nervous system activity via the β-adrenergic receptors
  • Renin is secreted from the juxtaglomerular cells into the bloodstream where it encounters angiotensinogen (AGN), normally produced by the liver
  • ...22 more annotations...
  • Renin catalyses the conversion of AGN to angiotensin I (ATI), which is quickly cleaved by angiotensin converting enzyme (ACE) to form angiotensin II (ATII)
  • ATII triggers the release of aldosterone from the adrenal glands, which stimulates reabsorption of sodium and water and thereby increases blood volume and blood pressure
  • ATII also acts on smooth muscle to cause vasoconstriction of the arterioles
  • ATII promotes the release of antidiuretic hormone from the posterior pituitary gland, which results in water retention and triggers the thirst reflex
  • ability of non-CSCs to ‘de-differentiate’ into CSCs due to epigenetic or environmental factors, which further increases the complexity of tumour biology and treatment
  • efficacy of RAS modulators on cancer in both cancer models and cancer patients
  • A localised (‘paracrine’) RAS mechanism has been identified in many types of cancers, and interruption of the control of the RAS is thought to be the basis for its role in cancer
  • Components of the RAS are expressed by these CSCs, supporting the hypothesis of the presence of a ‘paracrine RAS’ in regulating these CSCs
  • Renin is an enzyme normally released by the kidneys in response to falling arterial pressure
  • a study of GBM demonstrating overexpression of PRR coupled with the observation that inhibition of renin reduces cellular proliferation and promotes apoptosis
  • PRR has been found to be vital for normal Wnt signalling
  • A major focus of PRR research is its relationship with Wnt signalling
  • suggest a crucial role for PRR activation on the proliferation of CSCs, possibly via Wnt/β-catenin signalling, leading to carcinogenesis.
  • Angiotensin converting enzyme (ACE), also known as CD143, is the endothelial-bound peptidase which physiologically converts ATI to ATII
  • ACE is crucial in the regulation of blood pressure, angiogenesis and inflammation
  • results suggest that an overactive ACE promotes cancer growth and progression, and an inhibited or low-activity ACE may have cancer-protective effects
  • When bound to ATII or ATIII it causes vasoconstriction by stimulating the release of vasopressin, reabsorption of water and sodium by promoting secretion of aldosterone and insulin, fibrosis, cellular growth and migration, pro-inflammation, glucose release from the liver, increased plasma triglyceride concentration, and reduced gluconeogenesis
  • ATIIR1 is a G-protein-coupled receptor, with downstream signalling involved in vasodilation, hypertrophy and NF-κB activation leading to TNF-α and PAI-1 expression
  • ATIIR1 has well-documented links with cancer, with one study demonstrating its overexpression in ~20% of breast cancer patients
  • the effect of RAS dysregulation has been associated with increased VEGF expression and angiogenesis in cancers
  • In ovarian and cervical cancer, ATIIR1 overexpression has been shown to be an indicator of tumour invasiveness
  • administration of ATIIR1 blockers (ARBs) have been associated with reduced tumour size, reduction in tumour vascularisation, lower occurrence of metastases, and lower VEGF levels
  • Nathan Goodyear on 10 Sep 18
     
    Great review on RAS in cancer.
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