lecture 18

Endothelial Cells Modify Hormones

rednin-angiotensin-aldosterone system

precursor hormone release from liver → angiotensinogen (floating around in blood)

kidney release renin - renin cleaves angiotensinogen (renin is a rate-limitng enzyme)

produced angiotensin I → rapidly converted into Angiotensin II in lungs by ACE

angiotensin II also increases sympathetic nerve action and activity

**endothelial cells are very important bc they have ACE

when there is damage, the exposed collagen reacts with the blood

the platelets in the blood are attracted to the collagen

platelets become activited and send out cytokines → cytokines attract more platelets

weibel palade body in the EC nearby release vWF → enhance platelet aggregation

EC not in the damages area will release factors to prevent paltelet aggregation to occur in their region - PGI2, NO* - inhibit platelet aggregation

  • basally? (i think this means all the time)

ROS impair nitric oxide

arteriole

  • increased blood flow

venule

  • increased fluid into tissue

**maybe watch videos

endothelial cells control infiltration of immune cells (leukocytes) in venules

TIME on x axis ->

infection in tissues → local immune cells release inflammatory factors (in blood)

slow rolling (loose binding)

this activates EC → start expressing receptors for immune cells

weibell palader body releases P selectin (receptor) that inserts into the membrane

e selectin in the cell (not from weibell body) inserted into memrbane

selectins attract immune cells

immune cells start to express receptors that can bind to selectins

arrest

EC’s start expressin gmore firm receptors - receptors are different shapes

adhesion molecules (ICAM and VCAM) CAM = cell adhesive molecule

leukocytes start expressing different receptor too - will bind tightly

diapedesis

immune cells squeezes through with the help of ICAM and PECAM

if you have extended hypoxia, you can get lots of new blood vessel growth

  1. stop tumor growth by preventing angiogenic process froom occurring bc tumors need to develop its own supply

3 and 4: remodeling rather than adaptation

damaged EC’s (dysfunctioinal) provokes immmune cells → activate EC’s

once activated they attract leukocytes

leukocytes infiltrate under EC layer → change into macrophages → then foam cells

  • macrophages consume LDL chol. (esp oxidized) and small dense LDL

fatty sreak formation from foam cells - lipid laden (full of chol.)

  • starts in teen years

activated EC’s also cause SMC migration and proliferation

  • also move underneath EC layer and become macrophages and foam cells

thin cap and big plaque (most dangerous)

more stable but can block artery