regulation of blood pressure

what are the 2 circulations

1. pulmonary circulation = 24/8

2. systemic circulation = 120/80 (requires increased pressure because it is a longer circuit)

what is MAP

diastolic pressure + 1/3 pulse pressure

- normally around 93

- the pressure that propels blood to the tissues

what are the results of hypotension

- circulatory/vessel collapse

- tissue ischaemia/hypoxia

- no kidney filtration

- MAP<60 = syncope

what are the results of hypertension

- retinal and renal damage

- edema

- aneurysm

- heart hypertrophy

- for MAP>160, cerebral edema can occur

what are the main factors influencing BP

1. blood volume = managed by kidneys

2. total peripheral resistance = managed by vessels + SNS

3. cardiac output = managed by vessels + SNS

what is the formula for BP and CO

BP = CO x TPR

CO = HR x SV

therefore, BP = HR x SV x TPR

where are the cardiovascular centres located

medulla oblongata (brain stem)

what receptors sense increased BP

- baroreceptors in the carotid body and aortic arch, where there is highest pressure

what 3 centres do baroreceptors send signals to

1. vasomotor

2. cardio-inhibitory cetre

3. cardio-acceleratory centre

what does the vasomotor centre do

- determines how much SNS output goes to the smooth muscle

- therefore acts upon blood vessels to manage vasoconstriction + dilation

what does the cardio-inhibitory centre do

- manages parasympathetic output

- acts upon the heart

- slows down the heart - contractility + speed

what does the cardio-acceleratory centre do

- manages the sympathetic output

- acts on the heart

- increases heart rate and contractility

what are the baroreceptor reflexes

- when MAP increases, there is greater stretch on the high-pressure receptors

- this increases the sensory firing from the baroreceptors to the brainstem

- SNS decreases and rate of vasomotor impulse also decreases (this increases vessel diameter and reduces total peripheral resistance to lower BP)

- rapid response, within seconds

- when MAP is low, there is reduced baroreceptor firing

- the vasomotor centre increases SNS stimulation of smooth muscle to cause vasoconstriction

- the cardio-acceleratory system is also stimulated to increase cardiac output

neurotransmission of SNS

1. noradrenaline is released onto the Beta-1 receptors of the heart = increased cardiac output

2. Noradrenaline released onto smooth muscle of blood vessels causes vasoconstriction or dilation (alpha1 = constriction, beta2 = dilation)

3. activation of RAAS system also increases BP

intrinsic BP regulation by kidney

- blood volume is altered as increased BP + renal blood flow also increases water and sodium excretion (there is not enough time for these to be reabsorbed into the body)

- this maintains homeostasis naturally

extrinsic BP regulation by kidney

- involves RAAS

- antidiuretic hormone

- atrial natriuretic hormone = opposes the actions of RAAS to lower BP

what is the primary site of action of aldosterone and what is the function

distal convoluted tubule

- here, it stimulates sodium and hence water resorption

- this increases BP

where does ADH act and what is the function

- ADH acts on Vasopressin 2 receptors in the collecting duct, and vasopressin 1 receptors in blood vessels to cause vasoconstriction

- it inserts aquaporins along the length

- this increases water resorption to increase BP

what is the function of aldosterone

- it is secreted from the adrenal cortex

- it is involved in sodium/water resorption as well as K+/H+ excretion

- it is regulated by:

- Angiotensin II

- increased potassium

- ANP

- adrenocorticotropic hormone

how does RAAS work

- first, BP is low

- this can be sensed by juxtaglomerular cells in the afferent arteriole, or SNS can just stimulate beta1 receptors on the cells. Decreased sodium can also be detected by macula densa cells in the distal convoluted tubule.

- renin is needed to convert Angiotensinogen into Angiotensin I

- Angiotensin I then gets converted into Angiotensin II, using ACE

what are the functions of Angiotensin II

- stimulates release of ADH

- stimulates vasoconstriction of blood vessels

- stimulates adrenal cortex to produce aldosterone

- acts on the cells of the renal tubule to increase sodium and water resorption

- it also constricts the efferent arteriole to increase GFR

- it also stimulates the hypothalamic thirst center

functions of ACE

- Converts angiotensin I into angiotensin II

- it also degrades bradykinin into inactive metabolites

- this is why people on ACE inhibitors get a cough (accumulation of bradykinin in the lungs)

nitric oxide

- gas synthesised in all endothelial cells

- causes relaxation of all vascular smooth muscle

- acts via cGMP second messenger system = caused potassium efflux (hyperpolarisation) to make it harder for the smooth muscle to contract

- effects are brief as it is quickly destroyed