Autoregulation of Blood Pressure

Presentation Healthcare Notes on Auto Regulation of BP, Reactive Hyperemia , Active Hyperemia & Action of Chemical Mediators For Medical & Biology Students in word / doc / pdf/ ppt Format Free Download

Autoregulation of BP: 

This occurs according to the needs of the specific tissue. This is called as Oxygen Demand Theory for local blood flow control. This occurs by several mechanisms:

a. Reactive Hyperemia: 

When the blood supply to a tissue is blocked for a few seconds to several hours and then is unblocked, the flow through the tissue usually increases to four to seven times normal; the increased flow will continue for a few seconds if the block has lasted only a few seconds but sometimes for as long as many hours if the blood flow has been stopped for an hour or more. This phenomenon is called reactive hyperemia. Reactive hyperemia is al­most certainly another manifestation of the local "metabolic" blood flow regulation mechanism; that is, lack of flow sets into motion all of those factors that cause vasodilation.

b. Active Hyperemia: 

When any tissue becomes highly active, such as an exercising muscle, a gastroin­testinal gland during a hypersecretory period, or even the brain during rapid mental activity, the rate of blood flow through the tissue increases. Here again, by simply applying the basic principles of local blood flow control, one can easily understand this so-called active hyperemia 

c. Action of Chemical Mediators: 

The most important of these is a vasodi­lator substance called endothelial-derived relaxing fac­tor, which is composed principally, if not entirely, of nitric oxide that has a half-life in the blood of only 6 seconds. Rapid flow of blood through the arteries causes "shear-stress" on the endothelial cells because of viscous drag of the blood against the vascular walls. This stress contorts the endothelial cells in the direc­tion of flow and causes greatly increased release of nitric oxide. The nitric oxide then relaxes the arterial wall, causing it to dilate.

Multiple other stimuli also can cause nitric oxide to be released from the endothelium. These stimuli in­clude acetylcholine, bradykinin, ATP, and others. The nitric oxide in turn causes the local blood vessel to dilate. For instance, when acetvlcholine is secreted bv autonomic nerve endings, it first causes nitric oxide release from the endothelial cells; then the nitric oxide dilates the local blood vessel.

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