L20 Regulation of Cardiovascular function

Question 1

What maintains the electrolyte compositions of ECF (plasma and interstitial fluid - similar) and ICF- different

Answer 1

Various transporters, NaKATPase and conc gradient created maintain difference between ECF and ICF

Question 2

How does a change in ECF volume (increase) affect cardiovascular performance

Answer 2

1. Increase in ECF volume
2. increases filling pressure of the heart (venous return)
3. increase cardiac output and arterial pressure

Question 3

What is the relationship between plasma osmolality and ADH release

Answer 3

Once plasma osmolality increases past a certain threshold there is a proportional linear relationship.

Question 4

What are the steps from receptor to release of ADH and what are the main effects of ADH/AVP/Vasopressin

Answer 4

1a) Cells in supra-optic and paraventricular nuclei of hypothalamus (close to fenestrated capillaries) sense
- increase in osmolarity (1% change)
OR
1b) decreased ECF volume >10% sensed by cardiac receptors (less sensitive, needs firing over threshold, as <10% then only increased renal symp activity)

2. This modulates synthesis and release of ADH by posterior pituitary

Increased plasma osm also stimulates thirst centres in hypothalamus

ADH: aquaporins in collecting duct. In high conc can cause direct vasoconstriction

Question 5

How exactly do osmoreceptor neurons sense osmolality

Answer 5

1. Actin filaments in osmoneuron arranged in lattice formation (unlike others)
2. Filaments connect to ion channels on cells surface membrane
3. Change in osmolarity drag water out of neuron–> shrink–> reduce cell volume
4. Lattice opens the ion channels which increase firing rate –> project to pituitary to increase synthesis and release of ADH

Question 6

What are the responses to reduction in ECF volume sensed by cardiovascular receptors

Answer 6

1. Increased thirst mechanism via CNS
2. Decreased water and Na excretion due to
   - increased ADH release
   - increased renal symp tone (NA) –> increases
   - RAAS system
3. Decreased capillary bed filtration pressure: due to reduced BP from aorta (lower CO), the BP falls more rapidly, so there is an increase in precapillary resistance which favours reabsorption of fluid back into circulation from interstitial space

Question 7

How long does it take to restore blood components after acute blood loss

Answer 7

• RBC: complete 4-8 wks
• Bulk of plasma proteins restored by hepatic synthesis in 3-4 days
• Preformed albumin can be transferred in circulation immediately

Question 8

What is the difference between hypotensive, non hypotensive haemorrhage and haemorrhagic shock

Answer 8

Hypotensive haemorrhage: blood loss >10%, causing graded fall in systemic arterial pressure

Non hypotensive haemorrhage: blood loss <10%, causing MAP maintained although pulse pressure is reduced

Haemorrhagic shock: blood loss is extreme and remains uncompensated for long periods and replacement of volume deficit may not restore CVS homeostasis

Question 9

What is the response to baroreceptors from lying down to standing

Answer 9

Dip in arterial pressure due to pooling of blood in the legs (central blood pool), causes baroreceptor to increase HR and TPR to get SV back to normal.

Question 10

Why are systemic arterial baroreceptors important

Generally 2nd line receptors

Answer 10

The Baroreflex helps to reduce the variability of BP level preventing lots of random spikes of BP, by having large range of variability in HR.

This is important because variable blood pressure increases change of stroke, so not just baseline BP important.

Question 11

Which receptor is involved in potentially causing Hypertension: cardiac or baroreceptor and why

Answer 11

Denervation of cardiac receptors causes the baseline BP to shift, but not denervation of baroreceptors

Baroreceptors don’t really play a role in helping stop hypertension (due to rightward shift reset: regulate at a new range in hypertension)