ECF fluid regulation 1 Flashcards
Two major ECF osmoles
Na+ and Cl-
Major ICF osmoles
K+ salts
Regulation of ECF volume = ?
Regulation of body Na+
How many litres of water is in the body
42l
Distribution of body water
ECF = 1/3 (14l) ICF = 2/3 (28l)
Distribution of ECF
Interstitial Fluid ~4/5
Plasma ~1/5
What can cause hypovolaemia (low ECF)
Vomiting
Diarrhoea
Excess sweating
Severe bleeding
Response to low ECF (hypovolaemia)
Reduced Pulse Volume => reduced venous P => reduced Venous Return => reduced Atrial P => reduced end diastolic volume => reduced systolic volume => reduced cardiac output => reduced BP => reduced carotid sinus baroreceptor inhibition of sympathetic discharge.
Effect of sympathetic discharge
increased Sympathetic discharge => increased Vaso Constriction => increased Total Peripheral Resistance => increases BP towards normal
Effect of sympathetic discharge on kidney
Increased arterial constriction
Increased renin
Effect of increased renin
Increased angiotensin II => increased NaCl and water reabsorption at PROXIMAL TUBULE
Increased angiotensin II => increased Aldosterone => increased reabsorption of NaCl at DISTAL TUBULE
What are the changes in proximal tubule Na+ reabsorption due to
changes in the rate of uptake by the peritubular capillaries (greater reabsorpitive forces)
What does angiotensin II do to the hydrostatic and oncotic pressure of the peritubular capillaries
Increases oncotic pressure
Decreases hydrostatic pressure
What regulates reabsorption of Na+ at the distal tubule
The cortical steroid hormone Aldosterone
The smooth muscle of the media, just before it enters the glomerulus, contains what specialised cells
Juxtaglomerular cells aka JG cells (Large epithelial with plentiful granules)
What’s the name of the histologically specialized loop of the distal tubule
The Macula Densa
What makes up the juxtaglomerular apparatus
Juxtaglomerular cells and the Macula Densa
What kind of enzyme is Renin and what does it do
Proteolytic enzyme
Cleaves the alpha2-globulin part off angiotensinogen => angiotensin I
How does angiotensin I become angiotensin II and where does most of this conversion occur
Angiotensin I + ACE enzyme
As the blood passes through the pulmonary circut
What 3 things increase renin release
Decrease in pressure in afferent arterioles of glomeruli
Increased Sympathetic nerves activity via beta-1 effect
Decreased NaCl delivery at the Macula Densa
What 2 things decrease renin release
ADH
Angiotensin II negative feedback
4 reasons angiotensin II is important in the body’s response to hypovolaemia
Stimulates aldosterone release => increases NaCl and water retention
Very potent vasoconstrictor
Acts on hypothalamus to secrete ADH => increases water absorption in collecting duct
Stimulates thirst and salt appetite (in hypothalamus)
Main determinant of [ADH] in normality and severe hypovolaemia
Normality = Osmolarity Severe hypovolaemia (risk to brain perfusion) = plasma volume Will tolerate disturbed osmolarity to perfuse brain
