control of arterial blood pressure 2 (CVS8) Flashcards
extracellular fluid
- ~60% of body weight in a 70kg young man is water (~42L)
- total body fluid = intracellular fluid (2/3rd) and extracellular fluid/ECF (normally 1/3rd of the total)
- fluid which bathes the cells and acts as the go between the blood and body cells
ECFV
extracellular fluid volume= plasma volume (PV) + intersitual fluid volume (IFV)
- > if plasma volume falls, compensatory mechanisms shifts fluid shifts fluid from the interstitial compartment
- > PV and hence steady state blood volume and MAP would be controlled if the ECFV is controlled
fluid compartments
- extracellular fluid (14L) = 20% of body weight and is made up of plasma (3L) and interstitual fluid (11L)
- intracellular fluid (28L) = 40% of body weight
- > extracellular fluid (14L) + intracellular fluid (28L) = 60% of body weight which = water (~42L)
two main factors that affect extracellular fluid volume
- water excess or deficit
2. Na+ excess or deficit
how do our bodies control the 2 factors which affect extracellular fluid volume
- factors= water excess/deficit and Na+ excess/deficit
- hormones can act as effectors to regulate the extracellular fluid volume (including plasma volume) by regulating the water and salt balance in our bodies
- healthy people stay in a stable water salt balance, where water input=water output
stable water salt balance in healthy people
water input=water output
hormones which regulate extracellular fluid volume
- the renin-angiotensin-aldosterone sytem (RAAS)
- atrial natriuretic peptide (ANP)
- antidiuretic hormone, arginine vasopressin (ADH)
the role of the renin-angiotensin-aldosterone system
-plays an important role in the regulation of plasma volume and TPR and hence the regulation of MAP
3 important components of the renin-angiotensin-aldosterone system
- renin
- angiotensin
- aldosterone
steps involved in the renin-angiotensin-aldosterone system
- when there is a decrease in plasma volume (therefore a decrease in BP)
- renin is released from the kidneys and stimulates the formation of angiotensin I in the blood from angiotensinogen (produced in the liver)
- angiotensin I is converted to angiotensin II by angiotensin converting enzyme/ACE (produced by pulmonary vascular endothelium)
- angiotensin II stimulates the release of aldosterone from the adrenal cortex and angiotensin II also causes systematic vasoconstriction increasing TPR and BP, thirst and ADH release are also stimulated by angiotensin II contributing to increasing plasma volume mainly brought about by aldosterone:
- aldosterone (a steroid hormone) acts on the kidneys to increase sodium and water retention which increases plasma volume and furthermore increases BP
regulation of RAAS
- rennin secretion is the rate limiting step in the RAAS
- the rennin-angiotensin-aldosterone system is regulated by mechanisms which stimulate rennin release from the juxtaglomerular apparatus in the kidney, these include:
- >
- renal artery hypotension caused by systematic hypotension (decreased BP)
- > 2.stimulation of renal sympathetic nerves
- > 3.decreased [Na+] in renal tubular fluid which is sensed by macula densa (specialised cells of the kidney tubules)
juxtaglomerular apparatus
region comprimising the macula densa, extraglomerular mesangial cells, and granular cells (which release rennin)
role of the atrial natriuretic peptide (ANP)
- ANP is released in response to atrial distension (hypervolaemic states = fluid overload/medical condition where there is too much fluid in the blood)
- ANP causes excretion of salt and water in the kidneys, thereby reducing blood volume and blood pressure)
- ANP acts as a vasodilator (decreases blood pressure)
- ANP decreases rennin release
- ANP acts as a counter-regulatory mechanism for the Renin-Angiotensin-Aldosterone system (RAAS)
atrial natriuretic peptide
-28 amino acid peptide synthesized and stored by atrial muscle cells (atrial myocytes)
role of the antidiuretic hormone (ADH)
- ADH secretion from posterior pituitary is stimulated by reduced extracellular fluid volume or increase extracellular fluid osmolarity (main stimulus)
- > the normal osmolarity of extracellular fluid is about 280milli-osmoles/l
- plasma osmolarity is monitored by osmoreceptors mainly in the brain in close proximity to hypothalamus
- > increased plasma osmolarity will stimulate the release of ADH
- ADH acts in the kidney tubules to increase the reabsorption of water/conserve water ie concentraes unrine (antidiuresis)
- this increases extracellular and plasma volume and hence increases cardiac output and blood pressure
- ADH/vasopressin also acts on blood vessels to cause vasoconstriction which increases TPR and blood pressure (the effect is only small in normal people but becomes important in hypovolemic shock eg. haemorrhage)
