Suppression
Angiotensin
Category: Natural chemicals
Type
Voluntary
Introduction and description
Angiotensin is a peptide hormone that causes blood vessels to constrict. In combination with adenosine, angiotensin controls what blood gets to our bodies in a general way. By balancing the flow in various ways we can regulate how much blood gets to the various organs in our system. It is thus useful in normal bodily function in a number of ways, for example:
- Conserving heat - as by restricting the amount of blood flowing through our veins and arteries less heat is lost when we are very cold and it is cold outside.
- Conserving energy - We have no need of so much blood when we are resting as such it enables the flow to be down regulated, conserving glucose and oxygen. When we are deeply relaxed angiotensin will be in operation.
- Injury - It helps when we are wounded by helping to either constrict flow [so we don't bleed to death] or by its absence enable flow [so our immune system can work to get protective blood cells to the site of injury].
- 'Fight and flight' - Angiotensin is part of the sympathetic nervous system, this means that if we need to 'fight and flight' and more glucose and oxygen needs to get to our muscles, angiotensin release is restricted and adenosine is released. In effect these act like balancing hormones, whilst adenosine acts like a vasodilator, angiotensin acts like a vasoconstrictor.
- Mineral balance- Angiotensin stimulates the release of aldosterone, another hormone, from the adrenal cortex, which then, via the kidneys, alters the balance of sodium, calcium, chloride and potassium in our system so that muscles and cells can work more effectively. The description of the physical nervous system and how it works show that the correct functioning of all our cells relies on the right balance of these essential minerals, and angiotensin has a hand in this balance, restricting supply of them or not as the case may be. Aldosterone 'causes the conservation of sodium, and secretion of potassium' according to Wikipedia, but I suspect that the balancing act is far more complex and sophisticated. Imbalance here would serve to affect muscle and other cell mineral balance leading to such things as stiffness, pain and weak or ineffective muscles. As the heart is a muscle, it could affect the heart too
- Water retention and release - Arginine vasopressin (AVP), also known as vasopressin, or antidiuretic hormone (ADH), is a hormone that helps regulate water in the body via the kidneys. Angiotensin affects ADH levels. Note that there is the tendency in medical descriptions for this activity to somehow be regarded as 'bad', but water plays such a key role in our systems that whether water is retained or released has a key effect on every part of us. If we use the flight and fight response, for example, the last thing we want is to have to wee mid flight, so water is retained until we are back to parasympathetic activity. Burning glucose produces water as a byproduct, so in this case we need to get rid of all this water once we are resting. The action is eminently logical. Unfortunately western fight and flight response – known as stress – often goes on for weeks which is why we suffer from oedema.
The following rather simplistic picture shows the main sequence of flows and the effect of release of angiotensin.
ACE
As can be sen from the diagram, Angiotensin I is converted to angiotensin II by the enzyme angiotensin-converting enzyme (ACE, or kinase), primarily through ACE within the kidney.
ACE also has a high density in the lung. ACE is a target for inactivation by ACE inhibitor drugs, which decrease the rate of angiotensin II production.
ACE inhibitor drugs are supposedly major drugs against hypertension, but of course this assumption is highly simplistic and ignores the other effects of angiotensin when it comes to mineral balance and muscle action and effectiveness. They may cause
- oedema - there ia an observation for this that I have provided for ACE inhibitors
- coughing and bronchoconstriction - also see the ACE inhibitor entry
- Mineral imbalance - see the two references below. via the mineral imbalance you can get
- Arrythmias
The action of angiotensin II itself is targeted by angiotensin II receptor antagonists, which directly block angiotensin II AT1 receptors.
References and further reading
- “ Electrolyte disorder, especially hyperkalemia, is observed after the administration of RAAS inhibitors.” Ref Renin-angiotensin-aldosterone system inhibitors and electrolyte disturbances - Kato H, Kobayashi K, Uchida S. Department of Internal Medicine, School of Medicine, Teikyo University. PMID: 23012800
- "Hyperkalaemia, an elevated extracellular fluid potassium concentration, is a common electrolyte disorder .... it may be associated with electrocardiogram (ECG) changes. Hyperkalaemia occasionally leads to life-threatening cardiac arrhythmias". Management of hyperkalaemia. Maxwell AP, Linden K, O'Donnell S, Hamilton PK, McVeigh GE. Regional Nephrology Unit, Belfast City Hospital PMID: 24087806