regulation 3 Flashcards
Sympathetic stimulation directly activates:
VSMC contraction
independent of membrane depolarization
Sympathetic stimulation mechanism
- Sympathetic terminals release NE
- NE activates aARs on VSMCs
- aARs in VSMCs are coupled to Gq
- Gq activation causes IP3 production.
- IP3 increases cytosolic Ca2+
(by activating SR Ca2+ release via IP3 receptors)
Minor case in skeletal muscle:
Circulating epinephrine can activate b2ARs on VSMCs,
This causes vasodilation through cAMP/PKA inhibition of MLCK.
Baroreceptor reflex =
SHORT TERM and rapid negative feedback mechanism for sudden changes in blood pressure.
Baroreceptors are
pressure-sensitive NEURONS
High pressure baroreceptors
- in aortic arch and carotid sinus
2. respond to increases in arterial pressure by increasing firing rate
Stretch of arterial walls activates
mechanosensitive eNac Na+ channels on baroreceptor cell membranes.
Inward current causes depolarization, triggers APs in neurons
Carotid sinus baroreceptors project to the:
“cardiovascular control center” in the medulla via glossopharyngeal nerve.
Aortic arch baroreceptors project via the:
vagus nerve.
Low pressure baroreceptors
- in atria and vena cavae,
2. mediate “Bainbridge Reflex” (increase HR in response to stretch).
CV control center Feedback response via
changes in autonomic regulation of the heart and vasculature
Classic Baroreceptor Reflex
- Increase in pressure increase firing rate of baroreceptors.
- CV control centers decrease sympathetic and increase parasympathetic output.
- In heart this causes decreases heart rate and inotropy.
- In vasculature, decreased sympathetic tone causes vasodilation
Intrinsic control of the vasculature
- Vasoactive metabolites
- Myogenic response
- Nitric Oxide
- Endothelin
What is the primary mechanism to match blood flow in the capillaries to metabolic demand?
vasoactive metabolites
Vasoactive metabolites produced by metabolically active tissue =
local feedback control of blood flow.