Lecture 15: Regulation Of Peripheral Blood Flow Flashcards
How is arteriolar radius controlled?
Radius is dependant on contractile state of smooth muscle in arteriolar wall
- vasoconstriction: increased contraction ➡ decreased radius
- vasodilation: decreased contraction ➡ increased radius
Smooth muscle contraction. Remind me how it works again?
When Ca2+ enters the cell it binds to calmodulin to form the Ca-calmodulin complex. This activates MLCK which causes the phosphorylation of myosin light chain ➡ this makes myosin ATPase active ➡ crossbridge cycling ➡contraction
What is hyperemia?
Higher than normal blood flow
Arteriolar radius and distribution of blood flow
- Flow of blood through an organs is regulated by changing arteriolar resistance in that organ.
- distribution of cardiac output between different organs can be changed according to need
- arteriolar resistance is regulated both intrinsically and extrinsically
What is the functions of varying arteriole radius?
2
- Regulating mean arterial pressure (extrinsic)
2. Controlling blood flow to individual capillary beds (intrinsic)
List the intrinsic factors influencing arteriolar radius?
1) arteriolar tone
2) active hyperemia
3) reactive hyperemia
4) myogenic response
Regulation of arteriolar resistance
Intrinsic regulation
A) arteriolar tone
Arteriolar tone= contraction of arteriolar smooth muscle in the absence of extrinsic input
- spontaneous, slow depolarisation of smooth muscle cells ➡ calcium influx and contraction
- makes it possible to locally decrease resistance below resting value
Regulation of arteriolar resistance
Intrinsic regulation
B) active hyperemia
Also what are the mechanisms of active hyperemia?
Active hyperemia= increased blood flow in response to increase metabolic activity
- increased blood flow to contracting muscles, secreting glands, active intestinal epithelium
- changes assosiated with increased metabolic activity generally cause vasodilation.
- ⬆carbon dioxide
- ⬆potassium
- ⬆ hydrogen ions
- ⬇ in tissue oxygen concentration
Mechanism of active hyperemia
CBF slide 17
Regulation of arteriolar resistance
Intrinsic regulation
C) reactive hyperemia
Also what are the mechanism of reactive hyperemia
Reactive hyperemia= increased blood flow die to previous restriction in blood flow eg blockage
-quickly restores normal chemical balance to deprived tissue
-changes assosiated with blockage of blood flow cause vasodilation ie metabolises increases and oxygen decreases
-Changes associated with release of blockage cause vasoconstriction ie increased blood flow due to lower resistance, metabolises removed, oxygen increases
-blockages can be
-pathological (eg clots)
-physiological (eg blockage of flow during cardiac or skeletal muscle contraction.)
Mechanisms of reactive hyperemia?
CBF slide 20
What is the differences between active vs reactive hyperemia?
Slide 22
Arteriolar radius
Intrinsic regulation
Myogenic response. Explain
Myogenic response = contraction of arteriolar smooth muscle in response to stretch.
-Stretch sensitive Ca2+ channels open➡ contraction
-maintains a relatively constant flow even in different arterial pressures because of they are sensitive to stretch.
-safeguards blood supply to brain, kidneys, heart
Eg ⬆arteriolar stretch ➡⬆arteriolar SM contraction ➡⬆ resistance ➡⬇flow (negative feedback)
Arteriolar radius
Extrinsic regulation
Neuronal regulation ➡ sympathetic control of arteriolar radius
Postganglionic sympathetic neuron ➡ noradrenaline ➡ a adrenergic receptors ➡ vasoconstriction.
There is a baseline (tonic) activity of the sympathetic NS all the time.
Increased sympathetic activity ➡ increased noradrenaline release➡ vasoconstriction.
Decreased sympathetic activity ➡ decreased noradrenaline released➡ vasodilation.
Arteriolar radius
Extrinsic regulation
Hormonal control of radius
What are the 3 main hormones involved in regulation of arteriolar radius?
Adrenaline ➡ vasoconstriction or dilation depending on receptor
Antidiuretic hormone
Angiotensin 2
Both function to vasoconstrict
How does adrenalin control arteriolar radius?
Released from the renal medulla in response to sympathetic activity.
-action depends on type of adrenergic receptors in different vascular beds
-GI tract, mostly a (alpha) receptors ➡ vasoconstriction
-skeletal muscles, mostly B (beta) receptors ➡ vasodilation
BETA MAKES IT BIGGER!
ADH, Angiotensin 2 and control of arteriolar radius
- Both stimulate vasoconstriction of arterioles
- both also involved in increasing water reabsorption in the kidney ➡ blood volume
- affects peripheral resistance and blood volume, therefore regulators of arterial pressure