Lecture 16: CV Control 1 Flashcards
What are the effector mechanisms responsible for regulating cardiac function?
- Circulating catecholamines
- RAAS
- ADH
- Natriuertic peptides
What are the afferents for regulating CV control?
- Stretch sensitive mechanoreceptors in the atria and vessels.
Write some notes on arterial baroreceptors:
Carotid sinus; CN9
Aortica arch: CN10
Threshold: 30-50mmHg (drop below doesnt change)
Saturation: Above 150-180mmHg
Rate sensitivity: responds better to pulsatile than steady pressure.
They are slowly adapting receptors so will go back to basal if sustained increase in pressure.
What factors can change the sensitivity of baroreceptors?
- SNS activity can change vessel SM, which in turn modifies pressure sensitivity.
- Endothelial release of NO or PG markedly increase baroreceptor sensitivity.
- Endothelin decreases sensitivity.
Describe the arterial baroreflex:
Decrease in pressure = decrease firing
= Increased SNS output to:
- heart
- Vessels
- Adrenal glands = increased catecholamine circulation
- Decrease vagal output
Graded response depending on change in pressure.
Changes in baroreceptor firing also:
- Changes ADH levels within minutes
- RAAS levels but over hours.
Describe cardiac receptors:
- Myelinated vagal afferents
- Fire during atrial systole and end of atrial filling.
- Informative of cardiac filling and are indirectly influence by venous return and thus blood volume.
- “low pressure or volume receptors’
Also a number of c-fibres throughout all chambers. Aggregate firing with increased cardiac volumes.
What are the effects of changed cardiac receptor firing?
- Increased firing reduces SNS to heart and BV
- Increased vagal firing
- Decreased circulating catecholamines
- Reduced ADH, ANG
BUT qualitatively
- More pronounced neurohormonal effect and regulation of ECF volume.
Where are the osmoreceptors located? What do they sense?
Supraoptic and paraventricular nuclei
- Sense effective changes in plasma osmolality by altering their volume.
= ADH release
= Changes in water and potent vasoconstrictor
Where are the chemoreceptors located and what do they sense?
Aortic arch and carotid bodies
- Increase PaCO2, H+ conc.
- Decreased PaO2 (most sensitive to)
Central chemoreceptors in hindbrain
- More sensitive to PaCO2..
How do peripheral chemoreceptors respond to decreased PaO2?
Results in increased SNS to heart and BV i.e Conserves O2 for essential organs
What are some other receptors that are important for the regulation of cardiac function?
- Nocioceptors, pulmonary receptors can have sig. CV effects
But not homeostatic therefore wont be consiered.
What are the major centres of brainstem CV control located?
Venterolateral medulla - Tonic activity and reflex control of ANS supply to heart and blood vessels.
Preganglionic sympathetic nerves located in intermediolateral column of thoracic spine are ultimate pathway for SNS drive to CVS. Activity driven by cell bodies in RVLM. CVLM neurons inhibit this activity.
NTS is major relay for sensory CVS info.
Whats the origin of the PSNS to the heart?
Vagal nuclei: Dorsal vagus nucleus and nucleus ambiguous (Cardiac vagal nuclei)
Whats the role of higher centres in the CVS control?
- So much more complicated than simple reflexes
i.e Rapid distension of atria = increased SNS to heart, reduced to kidney. (brainbridge)
i.e exercise increases SNS activity to vascular beds, reducing blood flow to gut but it increases to skin (converse to expected)
What is the CNS ischeamic response?
- When arterial pressure falls, perfusion decrease
- Hypoxia and hypercapnia centres activate VLM and together with vasomotor centres increase cardiac vagal nuclei activity
= Increases SNS output = huge vasoconstriction and increased cardiac vagal activity decreases HR.
