Lecture 14 Flashcards
What did NO used to be called?
EDRF
What is the NO mechanism?
Increased flow increases induces shear stress which increases calcium influx. This binds to calmodulin which activates eNOS. eNOS produces NO from L-arginine. NO moves to the underlying smooth muscle cells and acts on guanyl cyclase which convers GTP to cGMP. This activates PKG which induces relaxation.
What is NO broken down by?
Free radicals.
What breaks down cGMP?
PDE-5
What do PDE-5 inhibitors cause. give an example.
Viagra. Inhibits PDE-5 from breaking down cGMP so increases vasodilation/relaxation.
What is tonic control
A continuous level of contraction that maintains pressure and blood flow.
What is an inhibitor of eNOS?
L-NMMA. This is reversible by the addition of L-arginine. NAME
What is on the surface of the endothelial cells?
The glycocalyx
Name three things that activate eNOS
Calcium calmodulin, shear stress and PKB.
What is essential hypertension?
An abnormal NO production with no obvious cause
What is secondary hypertension?
Increased ADMA from the kidneys.
What happens to NO in diabetes 1 and 2?
Less NO production
What increases in septic shock?
iNOS production which produces too much NO. there is a big drop in blood pressure.
What occurs to the vascular smooth muscle is pathophysiology?
less contractile, less myosin, shifts from L type calcium channels to T type.
What occurs to pulse pressure with age?
Increases, pulse propagates more rapidly.
