Renin-angiotensin-aldosterone system (RAAS)

Renin-angiotensin-aldosterone system (RAAS)

‍There are peripheral baro-receptors stimulated by arterial stretch, are located within the aortic arch and carotid sinus.

Aortic arch receptors: are innervated by the vagus nerve.

Carotid sinus receptors: are innervated by the glossopharyngeal.

The main role of the RAAS system is to maintain blood pressure, and it functions to do this in two ways.

1. Blood pressure = Cardiac output X total peripheral resistance. Angiotensin II is a potent vasoconstrictor and increases TPR.
   
   
2. Cardiac output = Heart rate x Stroke Volume. Aldosterone and ADH increase circulating volume = Increased preload = Increased stroke volume.
   

Let’s follow the system through and assume there is a drop in blood pressure.

1. A drop-in blood pressure → reduced arterial stretch → receptors ‘fire’ less. As result there is:
   
   Increased sympathetic flow
   ‍Decreased parasympathetic flow.
   ‍
2. Sympathetic activation → release of renin from juxta-glomerular cells.
   ‍
3. Renin then cleaves angiotensinogen (produced by the liver) to angiotensin I.
   ‍
4. Angiotensin I is converted in the lung to angiotensin II via the enzyme ACE.
   ‍
5. Angiotensin II, among its other functions, stimulates: The release of ADH and Aldosterone.

Aldosterone

1. Aldosterone is released from the zona glomerulosa, in response to:
   
   Renin, angiotensin II, high levels of potassium, ACTH and adrenergic stimulation.
   

2. Aldosterone causes sodium retention in exchange for excreting K+/H+ in the distal convoluted tubule.

Anti-diuretic hormone (ADH)

1. Synthesised by the hypothalamus (by the paraventricular and supraoptic neurons) and stored in the posterior pituitary.
   

2. Secreted In response to an increase in serum osmolarity (high levels of solutes and lower levels of water).
   

3. ADH acts on the distal convoluted tubule and collecting ducts within the kidneys binding to principal cells.
   

4. This triggers the vesicles to bind to the basolateral surface and apical membranes, to increase the number of aquaporin channels allowing more water (but not sodium) to be resorbed.
   

5. When serum osmolarity is low, less ADH is released and so less water is reabsorbed.