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15 Cards in this Set

  • Front
  • Back
Sequence of Blood Vessels
Heart->Aorta->Arteries (Conductance)->Arterioles (Resistance)->Capillaries (Exchange)->Tissue->Venules->Veins (Capacitance)->Heart
Distribution of Blood Volume at Rest
Lungs: 9%
Heart: 7%
Arteries: 15%
Capillaries: 5%
Veins: 64%
Blood Vessel Anatomy
Intima: layer of endothelial cells that provide a smooth surface for blood flow. It produces substances that have cardiovascular properties (e.g. NO, prostacyclin) and forms a diffusion barrier which will limit the amt of substances able to get into the wall. Media: smooth muscle cells that aid in vasoconstriction
Adventitia: collagen, connective tissue, etc. that provide support and protection for the vessel.
*Lumen: hole in the middle through which the blood passes
The extent of each blood vessel layer depends on the type of vessel.
1) The aorta has a very tough adventitia and a limited media. It is very stiff b/c has a low elastin/collagen ratio.
2) Arterioles have a very extensive media so can easily change diameter.
3) All vessels have 3 components except for capillaries, which have only an intimal layer.
4) Veins are thinner with little adventitia and media. During muscle contraction, the muscle squeezes the veins, pushing the blood to the heart. Valves keep blood from going backwards in the extremities. Veins have a greater elastin/collagen ratio; they are less stiff and so can stretch and hold much blood; therefore they are called capacitance vessels and have higher compliance than arteries.
What affects the amount of blood that a given vessel can hold?
The stiffness of the vessel wall, the adventitial layer: the elastin to collagen ratio.
Function of Nitrous Oxide (Furchgott, Ignaro, Murad)
NO is an endogenous physiological mediator of vasorelaxation and inhibition of platelet function and thrombosis. NO is also used as a signal molecule in the brain, the immune system, skeletal muscle and the kidney.
Nitrous Oxide Synthase (NOS) Inhibitors
These inhibitors are structural analogs of L-arginine and work as competitive inhibitors. When administered, these agents induce several actions, including hypertension and thrombosis. Some examples include NG-monomethyl-L-arginine (L-NMMA), N-nitro-L-arginine-methyl ester (L-NAME).
Nitrous Oxide Synthase (NOS) Isoforms
eNOS (endothelial NOS): responsible for vascular relaxation; constitutively expressed, and Ca2+ is a principal regulator of the formation of NO.
nNOS: found in neurons and muscle and is also activated by neurons
iNOS (inducible NOS): activated during inflammation/immunity
1) NO plays a major role in regulating ____ and ____.
2) Endothelium-derived NO is produced in both ____ and ____ cells.
3) NO produced by endothelium has a half-life of ____.
1) systemic blood pressure, organ blood flow
2) arterial and venous endothelial cells
3) a few seconds, so its effects are short-lived
What can an intravenous injection of an NOS inhibitor cause and how can this be reversed?
This can cause immediate hypertension that can be reversed by an injection of excess arginine, demonstrating the important role that the continuous production of NO plays in maintaining basal vascular tone.
What is the stimulus for the continuous production of NO?
The stimulus is the shear force production on the endothelial cell surface generated by local blood flow that opens endothelial K+ channels, and the resulting hyperpolarization opens endothelial Ca2+ channels, thereby allowing Ca2+ influx into endothelial cells to activate eNOS. The receptors for these agents are localized on the endothelial cells surface.
Where does the NO produced by eNOS go, and what does it do?
The NO diffuses both abluminally to interact with the underlying smooth muscle and also luminally to interact with the nearby platelets and neutrophils to inhibit their adhesion and ADP-induced platelet aggregation via the formation of cGMP which causes a decrease in platelet Ca2+ levels.
What is atherosclerosis and how is it treated?
In atherosclerosis, plaques reduce blood flow in the arteries. This decreases O2 supply to the heart, causing chest pain (angina pectoris) and sometimes even myocardial infarction. Treatment with nitroglycerin provides NO, causes dilation of the blood vessels, and increases blood flow and O2 supply, thus protecting the heart from damage and cell death. Therefore, nitroglycerin is often used in patients with angina pectoris.
cGMP Effects
These effects are probably mediated by cGMP-dependant kinase, all of which tend to produce relaxation.
1) Reduces the affinity of MLCK for Ca-CM by promoting phosphorylation of MLCK.
2) Phosphorylates phospholamban causing phospholamban to dissociate from the Ca2+-ATPase. Thus the pump activity is increased, as is the rate of Ca2+ transport out of the cytosol. This effect may occur at both the SR and sarcolemmal Ca2+ pump.
3) Phosphorylates K+ channels, increasing K+ conductance, thus promoting cellular repolarization or hyperpolarization. These close L-type voltage dependent Ca2+ channels, reducing Ca2+ influx.
What agents stimulate endothelial production of Nitrous Oxide by acting on Nitric Oxide Synthase, which converts L-arginine into Citrulline?
Shear Stress, Estrogen, ACh, Insulin, Bradykinin, Exercise