Short Term and Long Term Control of Blood Pressure

Other inputs to the medullary cardiovascular centres

•Cardiopulmonary baroreceptors

-Sensing central blood volume

•Central chemoreceptors

-Sensing arterial pCO₂ and pO₂

•Chemoreceptors in muscle

-Sensing metabolite concentrations

•Joint receptors

-Sensing joint movement

•Higher centres

-Hypothalamus and cerebral cortex

•Mean arterial pressure must be kept in the right range

•The arterial baroreflex is responsible for the short term control of arterial blood pressure

•The medullary cardiovascular centres listen to other inputs as well though

•Long term control of blood pressure is different

*carotid body are chemoreceptors

*aortic arch and carotid sinus are baroreceptors

increased sympathetic tone generally leads to increased contractility, increased heart rate, vasoconstriction (of veins and venules and arterioles)

increased parasympathetic tone generally leads to decreased heart rate, no effect on contractility or venoconstriction

vasoconstriction increases MAP

arteriolar constriction increases TPR

venoconstriction increases VR (venous return) and CO (cardiac output)

Valsalva manoeuvre = forced expiration against a closed glottis

late phase II : constriction to increase VR and arteriole resistance?

IV : big increase in EDV, SV therefore large increase in MAP

baroreceptors reflex still active, send info to medullary cardiovascular receptors to bring pressure down

causes activation of muscarinic centres to slow down pacemaker cells

gradually BP comes down to baseline levels

valsalva manouevre used as a test of autonomic function

reduced in older people and autonomic neuropathy

unable to detect changes in MAP

during Phase II BP continue to fall as no detection

if they do valsalva manouevre on the toilet causes strain to heart

can increase risk of myocardial infarction

control of supraventricular tachycardia

changes in posture and the Valsalva manoeuvre are both good examples of the arterial baroreflex in action

baroceptor reflex becomes activated between phase I and phase II

blood flow through the capillaries is large total cross sectional area and low velocity (from previous lecture)

billions of capillaries causing large cross sectional area

skeletal muscle pump

respiratory pump (exercise increases depth of respiration, negative thoracic pressure increasing driving force pushing blood back to venous and venules increases venous return therefore increasing EDV)

increased venomotor tone

patterned flight socks

^all increase end diastolic volume

Long Term Control of Blood Pressure

kidney controlled

functions of kidney:

excretion of waste products

maintenance of ion balance

regulation of pH

regulation of osmolarity

regulation of plasma volume

controlling plasma volume is used to regulate MAP

reabsorption : water and ions moving from the tubule into capillaries

secretions is opposite way, from blood to filtration?

less water, left behind is solutes in loop of henle = high osmolarity

descending limb water going to stay there

how permeable we make the duct determines how much water will be reabsorbed

renin-angiotensin-aldosterone system (RAAS)

juxtaglomerular (granular) cells release renin

macula densa detects changed in Na+/Cl+

renin converts angiotensinogen (inactive) to angiotensin I to the more active angiotensin II

ADH synthesised in hypothalamus and released from posterior pituitary

Decrease in blood volume

Increase in osmolarity of interstitial fluid

Circulation angiotensin II

^all trigger ADH release, these are all signs of low plasma volume and/or MAP

alpha one, a1 receptors cause smooth muscle contraction and arteriolar constriction and increase total peripheral resistance,

binding of adrenaline and noradrenaline to alpha one causes arteriolar constriction?

the arterioles supplying cardiac muscle and skeletal muscle mostly express B2 receptors

preload is described as stretch on the myocardium before contraction

how much blood filling into ventricles before contraction, how stretched?