L10: regulation of body fluid volume Flashcards
How does sodium/salt affect volume?
- an increase in sodium ions will increase blood osmolality which would increase ADH, and increase water reabsorption/retention, so ECF volume increases.
Vice Versa
So ECF volume can be regulated by body sodium content.
Effective circulating volume
- body cannot easily measure total body water volume in all compartments, but can measure blood perfuming tissues or effective circulating volume (ECV).
- effective circulating volume is that part of ECF that is in the arterial system (plasma part of ECF) and is effectively perfuming tissues.
- therefore body directly controls the volume of the intramuscular fluid and this influences the volume of other compartments.
Difference between effective circulating volume and total blood volume
The ‘effective’ volume of blood perfuming organs/tissues can change even with no changes in blood volume. The kidney ‘sees’ the ECV and decides if it is low or high.
The ECV and total blood volume might have different values, e.g., in heart failure, cardiac output decreases so blood will sit in the ventricles, so total volume is more than the volume circulating. Or e.g., liver cirrhosis increases splanchnic vasodilatation increases blood flow to the liver so less flows through the rest of body/tissues, e.g., kidneys.
What is ECV detected by?
- baroreceptors detect changes in pressure (stretch) perfusing through then rather than volume.
- changes in ECV can be detected by:
• systemic arterial baroreceptors in the aortic arch and carotid sinus - cardiovascular physiology.
• renal glomerular afferent arterioles - hence we detect changes in our body water volume by getting the kidneys to scrutinise the blood volume going through it.
Baroreceptors in the afferent arteriole
- every nephron can monitor fluid volume/BP.
- inside the afferent arteriole, the smooth muscle very close to the glomerulus is modified to become baroreceptors - juxtaglomerular cells
- the same cell release renin (enzyme) when blood volume/BP drops, in cases of haemorrhage, sweating or diarrhoea.
(Min 25 diagram)
Chemoreceptors (osmoreceptors) in the DCT
- every nephron can monitor the concentration of sodium in the tubular filtrate
- inside the DCT (sits next to glomerulus see min 22) as it approaches the glomerulus, the tubular cells are modified to become chemoreceptors - macula dense cells
- cause the release of renin from JGCs when filtrate sodium is low.
(Min 25 diagram)
What makes up the juxtaglomerular apparatus?
The chemoreceptors macula densa and the baroreceptor juxtaglomerular cells.
How is renin involved in the renin-angiotensin-aldosterone system (RAAS)?
E.g., BP/fluid volume within afferent arteriole is decreased:
- less blood flows to the kidney so less blood in the afferent arteriole
- this is detected by the baroreceptors (JG cells) due to a decrease in stretch
- the JG cells will release renin, which is secreted into the blood vessel (big so is not filtered), it goes into the efferent into the general blood circulation
- low BP means glomerular hydrostatic pressure will drop, and the filtrate will fall into the PCT at a much slower rate, so there is more time in the PCT to reabsorb lots of sodium to the blood
- so when the filtrate hits the chemoreceptors in the DCT, the macula densa cells will detect lower sodium.
- chemoreceptors send a paracrine signal to the baroreceptors, and more renin is released.
How is angiotensin formed in the RAAS system?
- angiotensinogen is a globulin made by the liver and released in the bloodstream
- renin (enzyme) speeds up the conversion of /cleaves angiotensinogen into angiotensin I (AngI).
- angiotensin I is converted/cleaved into angiotensin In (AngII) using angiotensin converting enzyme (ACE) which is found in the surface of endothelial cells mainly of the lungs and renal cells
What does angiotensin II to cause blood fluid volume to increase again?
- activates the thirst centres in the hypothalamus
- make the adrenal cortex release more aldosterone
- AngII goes to the PCT and stimulates more sodium/chloride reabsorption and thus obligatory water reabsorption
- can stimulate the release of ADH from the posterior pituitary gland to cause aquaporin insertion to increase water reabsorption to increase BP.
- constricts the efferent arteriole to raise glomerular hydrostatic pressure, increasing GFR so ensures the kidneys still filter blood despite a drop in BP.
- helps cardiovascular system vasoconstrict blood vessels, so increases the TPR which raises BP. Increases venule venous return, so increases EDV, thus SV, thus BP.
What is the role of aldosterone in the RAAS system?
- aldosterone will make various parts of the nephron more effective at reabsorbing sodium (especially DCT and CDs).
- water will follow the sodium into the blood vessels to increase the blood pressure
Inhibiting the renin-angiotensin-aldosterone system
- pharmacological inhibition of the actions of RAAS widely used in treatment of patients with hypertension, congestive heart failure, left ventricular dysfunction, pulmonary and systemic oedema, diabetic nephropathy, liver cirrhosis, migraines etc
- can be clinically inhibited in 4 different locations, renin inhibition, ACE inhibitors, AngII receptor antagonists/blockers, aldosterone receptor antagonists
Atrial natriuretic peptide (ANP)
- having too much salt/sodium in your body leads to water retention
- the renal system excretes sodium in the urine and thus restores volume by:
• switching off the RAAS system
• heart releasing atrial natriuretic peptide (ANP) - when blood volume increases, the atria of the heart are stretched - they release ANP. Stored and secreted by cardiac myocytes. ANP goes to nephrons and stops kidneys from reabsorbing sodium, so less water absorbed which goes into urine. Occurs for high BP.
How are the regulation of body osmolality and volume linked?
Osmolality is maintained at the expense of volume changes by ADH.
Volume is maintained by altering sodium sodium content by RAAS system.
