Recommended
More Related Content
What's hot
What's hot (20)
Viewers also liked
Viewers also liked (20)
Similar to Endothelial Dysfunction Y O U S R Y Y Yeasured
Similar to Endothelial Dysfunction Y O U S R Y Y Yeasured (20)
More from M.YOUSRY Abdel-Mawla
More from M.YOUSRY Abdel-Mawla (20)
Recently uploaded
Recently uploaded (20)
Endothelial Dysfunction Y O U S R Y Y Yeasured
- 1. ENDOTHELIAL DYSFUNCTION ( ED ) in ERECTILE DYSFUNCTION( ED ) ED = ED M.Y.ABDEL_MAWLA,MD Zagazig Faculty of Medicine,EGYPT
- 2. Causes of Erectile Dysfunction( ED ) Endothelial dysfunction ED Smoking Hypogonadism Endocrine Disorders Hypertension Hyperlipidemia Alcohol abuse Drug abuse Anemia Trauma/surgery to pelvis or spine Peyronie’s disease Vascular surgery Depression
- 5. LUMEN Tunica adventitia Tunica media Tunica intima
- 7. Note the individual Endothelial Cells
- 10. Vasoconstriction and dilatation Normal Vasoconstriction Vasodilatation
- 11. Vasoconstriction Vasodilatation Vasoconstriction and dilatation ↓ Resistance to flow ↑ Resistance to flow
- 12. Endothelial Apoptosis Normal Apoptosed
- 13. The Endothelium As an Endocrine Organ
- 20. (L-NMMA) = N(G)-mono-methyl-L-arginine
- 23. NO induces synthesis of cGMP by stimulation of GC leading to relaxation of myosin (muscle protein)
- 26. (L-NMMA) = N(G)-mono-methyl-L-arginine
- 27. (L-NMMA) = N(G)-mono-methyl-L-arginine (L-NMMA) = N(G)-mono-methyl-L-arginine
- 29. Regulatory Functions of the Endothelium Normal Dysfunction Vasodilation Vasoconstriction NO, PGI2, EDHF, BK, C-NP ROS, ET-1, TxA2, A-II, PGH2 Thrombolysis Thrombosis Platelet Disaggregation NO, PGI2 Adhesion Molecules CAMs, P,E Selectins Antiproliferation NO, PGI2, TGF- , Hep Growth Factors ET-1, A-II, PDGF, ILGF, ILs Lipolysis Inflammation ROS, NF- B PAI-1, TF- α , Tx-A2 tPA, Protein C, TF-I, vWF LPL Vogel R
- 33. Endothelin peptides Endothelin-1, a 21-amino-acid peptide, is the predominant isoform of the endothelin peptide family that includes ET-2, ET-3, and ET-4 Endothelin-1 is produced primarily by endothelial cells but can also be synthesized by vascular smooth muscle cells (VSMCs) and by macrophages The action of ET-1 are mediated by 2 receptor subtypes, ETA and E TB receptors
- 42. Endothelium-dependent vasodilator and vasoconstrictor mechanisms
- 51. The Mechanism of the Assocation Between Endothelium&Erectile Dysfunction
- 53. The roles of two forms of nitric oxide synthase in cavernosal smooth muscle relaxation and the initiation and maintenance of penile erection Watts Permission obtained from National Academy of Sciences © Hurt KJ et al . (2002) Proc Natl Acad Sci USA 99: 4061–4066.
- 55. Endothelial dysfunction in DM
- 73. Endothelial mechanoreceptors changes in hypertension –induced stress
- 76. Can We Measure Endothelial Function ??
- 80. What is the Treatment. for Endothelial Dysfunction ??
- 88. THANK YOU
Editor's Notes
- Figure 4-21. Endothelium-dependent vasodilator and vasoconstrictor mechanisms: modification in hypertension. Normal endothelial cells secrete both vasodilators-the most prominent of which are nitric oxide (NO), prostacyclin (PGI2), and endothelium-derived hyperpolarizing factor (EDHF)-and vasoconstrictors, including endothelin and endothelium-derived contracting factor (EDCF) [22]. Vessel tone is dependent on the balance between these factors and on the ability of the smooth muscle cell to respond to them. A, In normotensive vessels there is a predominance of vasodilator secretion. These substances may also contribute to the inhibition of smooth muscle cell growth or hypertrophy. The relative concentrations of the vasoconstricting/vasodilating agents are indicated by the relative sizes of the arrows and bold type in the illustration. B, In hypertension, release of vasoconstrictor substances may predominate [4]. In addition, vasodilator release may be decreased or, alternatively, the vasodilator itself may be inactivated by superoxide anion. Under certain circumstances, endothelin also can be growth-promoting, thereby contributing to smooth muscle cell hypertrophy or hyperplasia and intimal thickening. The biochemical pathways activated by endothelial agonists and by contracting and relaxing factors acting on smooth muscle can also be affected in hypertension. NO, produced by the conversion of L-arginine to citrulline, traverses the endothelial cell membrane, and activates the smooth muscle cell guanylate cyclase to generate intracellular cGMP. PGI2 and EDCF are produced via cyclo-oxygenase action on arachidonic acid. PGI2 relaxes vessels by increasing smooth muscle cell cAMP; the mechanism of action of EDCF is unknown. Endothelin is made and modified by endothelium. It then stimulates the phospholipase C pathway in smooth muscle to produce the second messengers inositol trisphosphate (IP3) and diacylglycerol (DG), which in turn activate the Ca2+ and protein kinase C (PKC) signaling pathways. This leads to phosphorylation of the myosin light chain (MLC-P), causing contraction. Alterations of any of these signals could easily augment contraction or decrease the ability of the vessel to dilate.