RAAS System, Friend or Foe?
The Renin-Angiotensin-Aldosterone system is a very basic, physiological system that allows mammals, like us, to survive. Looking at it broadly, there are two parallel system, one at the tissue level, and one at the organism level, that allows us to maintain our body fluid levels.
We learn in basic human physiology that in the event of a sudden loss of blood volume, or when the organism needs a BP boost, for extra blood flow (eg. like fleeing from a threat) the RAAS kicks in, to conserve salt and water (aldosterone) and also to vaso-constrict (angiotensin II and aldosterone). This allows the circulation to be extra boosted up, increasing blood flow and metabolism, to maintain survival of the organism.
Like all good physiological control for survival, there is always a "yin" and a "yang". In the event of an overshoot in the response (to the first insult), there is a counter-corrective mechanism to correct. So the Angiotensin II and (I suspect, the aldosterone as well) will act on type 1 and type 2 receptors. One type of the receptor for the pro-action, and the other type 2 receptor, for the counter-action. There is this balancing act at the human body level, and for fine tuning, also at the blood vessel level. That is why, the human body is so complicated. And that is the good side.
What happens when this fine balancing act of the body is deranged? What happens when this RAAS yin-yang balance is diseased, as in hypertension and also heart failure. (It would appear that both hypertension and heart failure, are over-zealous compensation of a deranged RAAS). There is excessive production of Angiotensin II and aldosterone. The counter-correcting mechanism cannot correct adequately and that body suffers from all the deletrious effects of hyper-angiotensin II, and hyper-aldosterone states. Believe me, too much angiotensin II and too much aldosterone, is bad for the body. Like everything else for the human body, too much of a good thing, may not necessarily be a good thing.
Coming back to the RAAS, that is why in hypertension, ACE-I (Angiotensin converting enzyme inhibitors), ARBs (Angiotensin Receptor blockers), and aldosterone antagonist, have proven so useful, both to correct hypertension and heart failure, and also improve the patient outcomes by "extra-BP" lowering effects and extra-CCF improvement effects.
Part of the reason, for this posting is that this weekend (13th July), Novartis is holding a soft launch of another drug, which will affect the RAAS, namely the anti-renin agent, aliskerin. Now, we have agents that can block, virtually the whole of the RAAS. Is that good or bad? Again, good or bad use, lies in the hands of the physician using it. But we are surely doing or best to interfere (for better or worse) in a very unique and fine survival mechanism, that God has given to us.
We learn in basic human physiology that in the event of a sudden loss of blood volume, or when the organism needs a BP boost, for extra blood flow (eg. like fleeing from a threat) the RAAS kicks in, to conserve salt and water (aldosterone) and also to vaso-constrict (angiotensin II and aldosterone). This allows the circulation to be extra boosted up, increasing blood flow and metabolism, to maintain survival of the organism.
Like all good physiological control for survival, there is always a "yin" and a "yang". In the event of an overshoot in the response (to the first insult), there is a counter-corrective mechanism to correct. So the Angiotensin II and (I suspect, the aldosterone as well) will act on type 1 and type 2 receptors. One type of the receptor for the pro-action, and the other type 2 receptor, for the counter-action. There is this balancing act at the human body level, and for fine tuning, also at the blood vessel level. That is why, the human body is so complicated. And that is the good side.
What happens when this fine balancing act of the body is deranged? What happens when this RAAS yin-yang balance is diseased, as in hypertension and also heart failure. (It would appear that both hypertension and heart failure, are over-zealous compensation of a deranged RAAS). There is excessive production of Angiotensin II and aldosterone. The counter-correcting mechanism cannot correct adequately and that body suffers from all the deletrious effects of hyper-angiotensin II, and hyper-aldosterone states. Believe me, too much angiotensin II and too much aldosterone, is bad for the body. Like everything else for the human body, too much of a good thing, may not necessarily be a good thing.
Coming back to the RAAS, that is why in hypertension, ACE-I (Angiotensin converting enzyme inhibitors), ARBs (Angiotensin Receptor blockers), and aldosterone antagonist, have proven so useful, both to correct hypertension and heart failure, and also improve the patient outcomes by "extra-BP" lowering effects and extra-CCF improvement effects.
Part of the reason, for this posting is that this weekend (13th July), Novartis is holding a soft launch of another drug, which will affect the RAAS, namely the anti-renin agent, aliskerin. Now, we have agents that can block, virtually the whole of the RAAS. Is that good or bad? Again, good or bad use, lies in the hands of the physician using it. But we are surely doing or best to interfere (for better or worse) in a very unique and fine survival mechanism, that God has given to us.
1 comment:
it would appear that this may be the holy grail in the treatment of HPT, altering physiology right at the source of the RAAS system, & thereby altering downstream responses as well.
i attended a talk recently on Carduet. i thought it strange that 2 drugs with different physiological effects should be formulated into a single pill to improve patient compliance.
i would think that a fair proportion of patients would not be optimally controlled for BOTH blood pressure & LDL with this formulation, & eventually be put on 2 different pills, each for optimal control of their respective parameters.
what is your experience on this?
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