Control of BV Flashcards
How does long-term regulation of blood pressure occur ? Describe the mechanism involved.
Overall, through the control of body fluid volume by the kidneys (when arterial pressure increases, urine production increases and vice versa).
Increase Extracellular fluid V → Increased BV → Increased mean circulatory filling P → Increased venous return of blood to heart → Increased CO → (→ autoregulation → increased total peripheral resistance →) Increased Arterial P → Increased urine output → Deceased extracellular fluid V (etc., up until decreased arterial P)
What are the main determinants of the long term regulation of blood pressure ? Why are these said to be determinants of the long term regulation of blood pressure ?
1) The renal output curve for salt and water
2) The level of salt and water intake
Because it is impossible to change long-term mean arterial blood pressure without changing one or both of these!
What is the effect of increase intake of water and salt on BP in the long term ?
Increases BP
Show, in graphical form, the effect of an increase of arterial pressure on urinary output. What is the name of this curve ? How may we change its shape ?
Refer to slide 5 in lecture on ‘“Control of Blood Volume”
Renal function curve
By modifying the permeability of kidneys to water and sodium, changing blood flow going to the kidneys (through ADH, and renin?).
Show, in graphical form, the effect of an increase in water and salt intake on arterial pressure. Then, in graphical form, show how the body deals with this.
Refer to slide 6 in lecture on “Control on Blood Volume”
Explain the process through which the body deals with increased water and salt intake. Why is this necessary ?
By modifying the kidney’s permeability to salt and sodium, thereby changing the blood flow going to the kidneys.
Because otherwise, would get a large increase in blood pressure (this allows to maintain blood pressure even with increased salt and water intake)
Why is it problematic if kidney function becomes compromised (wrt to blood volume etc.).
Because then we cannot change the permeability of it to salt and water (i.e. changing the shape of the curve). This means that we cannot adjust blood pressure if there is increased salt and water intake, possibly resulting in hypertension.
What are other names for Antidiuretic hormone ?
Vasopressin, Arginine vasopressin
Where and in response to what, is ADH released ?
Released by the pituitary gland in response to:
1) ↑ Osmo tic Pressure
• Sensed by hypothalmic osmoreceptors (i.e. higher ion concentration → receptors dehydrated → receptors shrink → signals high osmolarity, needs to be diluted
VICE VERSA)
2) Hypovolemia (10% loss or greater)
• Atrial baroreceptors normally inhibit ADH release
• ↓ volume leads to ↓ firing rate, so ↑ ADH release
3) Hypotension
• ↓ arterial baroreceptor firing
• ↑ sympathe tic ac tivity and ↑ ADH release
What is ADH’s function ? How does it fulfill this function ?
1) “Regulates the amount of water in your blood (if increased ADH, increases blood volume, cardiac output and arterial pressure)”
2) Can also cause vasoconstriction (and hence increase total peripheral resistance) in response to severe hypovolemic shock (because high ADH release)
Increases blood volume by
– ↑ water permeability in renal collecting ducts (leads to ↓ urine production because water pushed out by filtration can come back in)
Make a diagram, explaining all the elements which contribute to the regulation of blood osmolarity.
↓ Blood volume → ↓ Atrial baroreceptor firing rate → Hypothalamus
↑ Blood osomatic Pressure (via osmoreceptors) → Hypothalamus
Hypothalamus → Hypothalamic thirst center → ↑ Fluid intake (increases intake of fluid)
Hypothalamus → Posterior pituitary → ↑ ADH output → ↓ Kidney Fluid Loss (decreases loss of fluid)
All these us to get BV back to normal
What does RAAS stand for ?
Renin-angiotensin- aldosterone system
What kind of enzyme is renin ?
Proteolytic enzyme
Where, and in response to what is renin released ?
Renin is released from the juxtaglomerular cells in the kidneys in response to:
1) Sympathetic nerve activation
• Mediated by baroreceptor feedback (when BV or BP dropping)
2) Renal artery hypotension (low flow to kidneys)
• Independent of baroreceptor feedback
3) Decreased sodium in kidney distal tubules
What is the main difference between ADH and renin, with respect to osmotic balance ?
Renin is more blind to osmotic balance (more associated with if correct volume in the system or not)
Draw a diagram to illustrate the role of RAAS in the regulation of blood volume.
Refer to slide 11 in lecture on “Control of Blood Volume”
Describe the main elements of the RAAS.
Decreased arterial Pressure → Renin released from kidney juxtoglomerular cells → → Renin (from kidneys) binds to angitensinogen (in liver, since veinous blood from both kidneys and liver will mix) and converts it to angiotensin 1 → Blood will be going to pulmonary circulation and coming into contact with ACE enzyme which converts Angiotensin 1 into Angiotensin 2 → Angiotensin 2 stimulates retention of water and salt (through release of aldosterone from the adrenal glands), stimulates vasoconstriction of renal arteries (increased total peripheral resistance, leads to decreased blood flow via kidneys, preventing loss of fluid via urine) and stimulates release of ADH from pituitary (decreased urine production), all of which result in increased arterial pressure → Angiotensin 2 can be inactivated by Angiotensinase
How may angiotensin 2 be inactivated ?
Through Angiotensinase
Describe any systems in place to oppose effects of the RAAS system (help counteract volume overload).
Atrial-natriuretic hormone (a.k.a. Atrial-natriuretic peptide), a 28-amino acid peptide synthesized and stored in muscle cells of the atria.
Released in response to stretch of the atria
Define hypovolemia. What are the main types of hypovolemia ?
Loss of blood volume (resulting in drop of blood pressure)
• ↓ whole blood, e.g. hemorrhage
• ↓ plasma, e.g. burns
• ↓ sodium, e.g. vomiting
What are the different classes of shock ?
– Class 1, 10-15% blood loss
– Class 2, 15-30% blood loss
– Class 3, 30-40% blood loss
– Class 4, >40% blood loss
Describe the effect of a hemorrhage on cardiac output.
Hemorrhage → ↓ Blood Volume → ↓ Venous Pressure → ↓ Venous Venous Return → ↓ Atrial Pressure → ↓ EDV → ↓ Stroke Volume → ↓ CO
Describe the immediate (reflex) response to hypovolemia. What is the problem with this response in the long term ?
Baroreceptor Reflex (Degree of volume loss affects how successful)
1) Increase Stroke Volume (to increase CO): 1) increase veinous return leading to increased EDV through vasoconstriction 2) if EDV stays the same, can influence force of contraction by calcium channels (sympathetic NS stimulation)
2) Increase Heart Rate (to increase CO): Through sympathetic innervation (Using just stroke volume and heart rate, CO back to 2/3 of what it was prior to hemorrhage)
3) Increase force of contraction (to increase MABP): via sympathetic innervation (vasoconstriction)
Problem: This does not solve the problem with the BV, only with the BP (that’s where angiotensin and everything kicks in)
How much blood loss can immediately reflex response to hypovolemia fully compensate for ?
10%
