• artery
  • Only ACE inhibitor treatment normalised resistance vessel contractility and endothelium-dependent relaxation suggesting that factors other than blood pressure reduction play an important role in restoring resistance artery endothelial function. (bl.uk)
  • In addition, stepwise multiple regression analysis of all subjects showed that HbA1c level was an independent determinant for the l -arginine-induced vascular response of each artery. (ahajournals.org)
  • inhibitor
  • In this study, we use 2 mouse models of vascular calcification, mice with gene deletion of matrix Gla protein, a bone morphogenetic protein (BMP)-inhibitor, and Ins2Akita/+ mice, a diabetes model. (nih.gov)
  • Treatment of SHRs with either an ACE inhibitor, a vasodilator or a calcium antagonist prevented the rise in blood pressure and normalised vascular structural alterations. (bl.uk)
  • The protein acts as an inhibitor of vascular mineralization and plays a role in bone organization. (wikipedia.org)
  • systemic
  • 5 6 7 In isolated ophthalmic arteries, NO is an important modulator of vascular tone, 8 and systemic NO-synthase inhibition decreases choroidal blood flow in animals 9 and humans. (ahajournals.org)
  • Vascular responses after the intravenous administration of l -arginine were recently demonstrated to be a likely consequence of an increase in the endothelial production of NO. 15 Accordingly, we compared the effects of l -arginine and NO donation with nitroglycerin on systemic, retinal, and renal hemodynamics in patients with and those without microalbuminuria. (ahajournals.org)
  • enzyme
  • Once produced in endothelial cells, NO diffuses across the vascular smooth muscle cell membranes and activates the enzyme soluble guanylate cyclase (sGC), which catalyzes the conversion of guanosine triphosphate into cyclic guanosine monophosphate (cGMP). (wikipedia.org)
  • atherosclerosis
  • Vascular calcification is a regulated process that involves osteoprogenitor cells and frequently complicates common vascular disease, such as atherosclerosis and diabetic vasculopathy. (nih.gov)
  • adhesion
  • Mouse anti-human monoclonal antibodies against vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin were obtained from Becton-Dickinson, and isotype mouse IgG1 and IgG2 not directed against endothelial cell antigens were obtained from ICN Immunobiologicals. (ahajournals.org)
  • relaxation
  • Treatment also prevented the development of impaired endothelium-dependent relaxation. (bl.uk)
  • cGMP, in turn, activates protein kinase G (PKG), which promotes multiple phosphorylation of cellular targets lowering cellular Ca2+ concentrations and promoting vascular relaxation. (wikipedia.org)
  • Type
  • There are several types of vascular disease, (which is a subgroup of cardiovascular disease), the signs and symptoms depend on which type, among them are: Erythromelalgia - a rare peripheral vascular disease where syndromes includes burning pain, increased temperature, erythema and swelling, of mainly the hands and feet are affected. (wikipedia.org)
  • The physical exam may be different depending on the type of vascular disease. (wikipedia.org)
  • brain
  • Additionally, endothelial-specific deletion of Gpr116 resulted in a significant increase of the brain vascular leakage. (diva-portal.org)
  • brain endothelium expresses tight junctions and transporters which are absent from other endothelia. (open.ac.uk)
  • This blog contains research & information on lifestyle, nutrition and health for those with MS, as well as continuing information on the understanding of the endothelium and heart-brain connection. (blogspot.com)
  • PKG-II has been detected in renal cells, zona glomerulosa cells of the adrenal cortex, club cells in distal airways, intestinal mucosa, pancreatic ducts, parotid and submandibular glands, chondrocytes, and several brain nuclei, but not in cardiac and vascular myocytes. (wikipedia.org)
  • therefore
  • NE is detected in the endothelium of murine atherosclerotic plaques and, therefore, this is a plausible mechanism to promote local IL-1β release in the vasculature. (bmj.com)