neural control of the heart Flashcards
what are the 4 central processing centres
- medullary cardiovascular centor
- hypothalamus
- motor cortex
- higher centres ie limbic system
what can emotional stress do to alter CVS
limbic centre outflow = override reflex
input to both hypothalamus and medulla
what is the CVS centre component
- RVLM: sympathoexcitatory neurons, synapse to preganglionic neuron at IML. tonic activity
- CVLM: inhibit RVLM neuron, inhibit preganglionic neuron at the spinal cord. no tonic outflow, no direct cvs innervation
what is special about the motor cortex
what is the function of the nerve originating here?
origins of sympathetic cholinergic nerve
fight flight: skeletal muscle arteriole and skin overlying it ONLY
- great reduction in TPR
where is the vagal outflow and how does it interact with the medullary centre
- dorsal motor vagal nuclei
- reciprocal relationship with the RVLM
- no tonic discharge, activated by afferent
what structures do the
parasympathetic
sympathetic innervate
parasympathetic:
NODAL AND ATRIAL only = affects rate not contractility
little blood vessel innervation = no change in TPR
sympathetic: atrial, ventricle ALL blood vessels, nodal tissue
= rate contractility and TPR increases
different sympathetic response of 1. arterioles
2. veins
a1 a2 receptors
- concentric VSM arrangement = arterioles = TPR
- longitudinal VSM arrangement = veins = compliance
3 ways to alter heart rate
- steepness of pacemaker potential (K conductance in pacemaker phase)
- threshold level
- degree of hyperpolarisation
how does sympathetic activity affet CVS (LEFT AND RIGHT)
left: ventricle innervation = contractility
right: nodal innervation: increases heart rate
relationship between sympathetic innervation and funny channels
b1 receptor: AC = cAMP
Na funnel channels: hyperpolarisation activated and cAMP gated
= cAMP opens Na channels sooner no need to wat for hyperpolarisation = steep pacemaker potential
mechanism of vagal influence on heart rate
increases K conductance in BOTH repolarisation and pacemaker potential phase
- Ach dependent K channels activated, on top of the normal ones
- increase K conductance
= hyperpolarisation and sooner repolarisation and shallow slope - increases AV conductance