The Cost of Compensation

So, we've discussed a few of the ways that the body knows the blood pressure and blood flow has changed, and also how it goes about making those changes.

It the arteries, the baroreceptors that exist in the aorta and carotid arteries sense changes in blood pressure (which the communicate to the brain).  If a change needs to occur, it can be a nervous change, an endocrine (or hormonal) change, or a structural change (in order of speed).  All matters of change could occur, we are only listing the types.

In regards to blood flow, the system is less developed.  Direct changes occur in tissues, known as metaboreflexes.  Metaboreflexes occur in response to changes in oxygen, nutrient and waste levels in the tissue and cause vasodilation or vasoconstriction.  When vasodilation or vasoconstriction has a profound effect at the heart, indirect changes as a result of changes in blood flow occur, piggy-backing on the baroreceptors of the blood pressure detection system to cause big changes.

Something we haven't discussed is how changes in the veins are measured.  Well, there are technically baroreceptors in the major veins as well.  However, they are much more forgiving of change and are not termed as baroreceptors to avoid any confusion with the more important baroreceptors of the arteries.


So, that leads us to our final consideration (for now) when thinking about these reflexes of change in blood pressure or blood flow.  What is the cost?  Well, actually, it's good that you ask!  There is always a cost to compensation in the CV System.  


For example, when changes in the nervous system occur, what are the costs?  Well, if the sympathetic nervous system is stimulated to increase heart rate and contractility to provide more oxygen (via blood) to tissues, what has to work harder?  Right!  Both the heart and the lungs have to work harder.  Increasing the work of either tissue is going to increase the amount of waste that tissue produces.  This, in the long term, can result in damage to the tissues, which can later lead to apoptosis (or cell death).

How about the negative consequences of renin activation in the endocrine system?  Well, when renin increases, it not only leads to salt retention in the kidneys, but it also leads to the production of the hormone angiotensin II in the kidneys.  Guess what, chronic increases in angiotensin II levels can lead to deterioration of the heart via the hormone triggering remodeling.  


Finally, how about hypertrophy?  First and foremost, hypertrophy is known to shorten the lifespan in humans.  Why?  Well, hypertrophy, overtime, is going to cause less flexibility in the heart wall.  This means that preload and afterload are going to have to increase to overcome the increased pressure required for the heart to either fill or contract (for ejection of blood).

As you can see, in the short term, these adaptations are essential to keep the animal alive.  However, in chronic situation, all of these adaptations come with consequences.  These consequences (if sustained) will eventually lead to heart disease if not controlled.

- JD