7/ regulation of arteriolar resistance Flashcards
what does arteriolar radius affect?
flow through individual vascular beds and mean arterial pressure
how do you keep the blood flow to each vascular bed sufficient, and keep mean arterial pressure in the right range?
resistance “juggling”
how is resistance “juggling” achieved? (two mechanisms)
two levels of control over surrounding smooth muscle surrounding arterioles:
- intrinsic mechanisms (concerned with meeting the selfish needs of each individual tissue)
- extrinsic mechanisms (concerned with ensuring that the total peripheral resistance of the whole body stays in the right ball park, mainly neural and hormonal, concerned with regulating TPR of the whole body, trying to maintain adequate MAP)
what makes up the neural component of extrinsic control?
- sympathetic nerves (release noradrenaline, binds to alpha 1, causes arteriolar constriction, therefore decrease flow through that tissue, and tends to increase TPR)
- parasympathetic nerves (usually no effect)
what makes up the hormonal component of extrinsic control?
- adrenaline
- angiotensin II
- vasopressin (= antidiuretic hormone)
- atrial natriuretic peptide & brain natriuretic peptide
what does adrenaline do? (hormonal component of extrinsic control of TPR)
- released from adrenal medusa
- binds to alpha 1 receptors
- cases arteriolar constriction
- therefore decreasing flow through that tissue and tends to increase TPR
- but in some tissues (ex: skeletal and cardiac muscle) it also activates B2 receptors
- causes arteriolar dilation
- therefore increasing flow through that tissue and tends to decrease TPR
what does angiotensin II do? (hormonal component of extrinsic control of TPR)
- produced in response to low blood volume
- causes arteriolar constriction
- therefore increases TPR
what does vasopressin do? (= antidiuretic hormone) (hormonal component of extrinsic control of TPR)
- released in response to low blood volume
- causes arteriolar constriction
- therefore increases TPR
what do atrial natriuretic peptide & brain natriuretic peptide do? (hormonal component of extrinsic control of TPR)
- released in response to high blood volume
- causes arteriolar dilation
- therefore decreases TPR
what makes up intrinsic control of TPR?
- active metabolic hyperaemia
- pressure (flow) autoregulation
- reactive hyperaemia
- the injury response
how does active metabolic hyperaemia work? (in regulating TPR intrinsically)
- increase in metabolic activity causes increase in concentration of metabolites (CO2, H+, K+)
- triggers release of EDRF (= paracrines)
- causes arteriolar dilation
- increases flow to wash out metabolites
- an adaptation to match blood supply to the metabolic needs of that tissue
how does pressure (flow) auto regulation work? (in regulating TPR intrinsically)
- decrease MAP (mean arterial pressure) causes decrease in flow
- metabolites accumulate
- triggers release of EDRF
- arterioles dilate and flow is restored to normal
- (or it could be myogenic)
- an adaptation to ensure that a tissue maintains its blood supply despite changes in MAP
how does reactive hyperaemia work? (in regulating TPR intrinsically)
- occlusion of blood supply causes a subsequent increase in blood flow
- an extreme version of pressure autoregulation
how does the injury response work? (in regulating TPR intrinsically)
release of histamine by mast cells triggered by the presence of an antigen
- arteriolar dilation (subsequent increased blood flow and increased permeability) as an immune response
- aids delivery of blood born leucocytes etc to injured area
what special areas are there when it comes to regulation of arteriolar resistance?
- coronary circulation (blood supply is interrupted by systole but still has to cope with increased demand during exercise)
- cerebral circulation (need CONSTANT pressure)
- pulmonary circulation (opposite response to most tissues)
- renal circulation (filtration depends on pressure)
