4. Regulation of Blood pressure Flashcards
Blood pressure
Hydrostatic pressure in arterial system pushing blood through the capillary beds to organs / tissues.
results from: Co x TPR
- > Systolic pressure (maximum 90 - 240 mmHg)
- > Diastolyc pressure (minimum 60 - 140 mmHg)
- > Pulse pressure (SP - DP)
- > major cardiovascular variable regulated by body -> arterioles major resistance vessel
- > closely regulated as too low (brain / other tissues not receive adequate flow) and too high (extra work for heart + risk of vascular damage)
-> blood vessels don’t burst but tend to leak
Haemodynamics
Study of how blood flows
- > variety of factors influence haemodynamics
- Vessel length (L)
- vessel radius (R)
- viscosity of blood (V)
Flow (Q) = Pressure differece (delta p) / Resistance (R)
CO = (mean arterial p (beginning of tube) - central venule p (end of tube)) / TPR
Factor affecting Blood pressure
BP = CO xTPR
Regulation of blood pressure is achieved by controlling the determinants of BP:
1.)
Cardiac Output
Heart Rate:
-> determined by sino-atrial node, “pacemaker” -> regulated by nervous activity
- > Parasympathetic stimulation (low temperature)
- > Sympathetic nerve stimulation (adrenalin - high temperature)
Control:
- > Stroke volume
- > amount of blood ejected by ventricle during single beat
- > difference between end diastolyc + end systolic volumes (EDV (preload, contractility, afterload) - ESV(filling time, venous term))
Systolic pressure
- > influenced by stroke volume which is th eamount of blood ejected from heart per heart beat
- > Increase in SV increases pressure, therefore increasing pulse pressure
- > left ventricular ejection velocity
- > loss of arterial compliance, e.g. increase stiffness, increases pressure ->
Diastolic pressure
-> increase in HR and decrease in pulse pressure
Total peripheral resistance
Primary resistance in arterioles -> important in regulating blood pressure
Affected by:
- > radius of arterioles
- > vasolidation increase radius - resistance falls
- > vasoconstriction reduces radius - resistance increases
A - Vascular Tone
constriction or tone of blood vessels alter resistance + pressure (hypertension)
Modulated by the action of vasoconstrictors and vasodilators
Vasodilators
-> endothelial cells determine dilation + constriction
- > Sheer stress : Ca 2+ ions released due to the stress -> enzyme Nitric oxide centase released (nitric oxide - very small enzyme and can go from one cell to another very quickly - doesn’t care about obstacles but not very stable hence it can’t affect much in the body, just the neighbouring cells)
- > nitric oxide activates + releases G cyclase -> G cyclase a signalling molecules, activating GTP -> cGMP, activating PHG -> cannot contract and hence relaxation occurs
- > G protein has a receptor but activates ATP -> cAMP -> RKA -> Relaxation
- > Vasodilators such as Bradykinins or ADP can have a bigger impact by releasing Ca 2+
- > EDF recognise hypertension (high BP) -> relaxation
=> Nitric oxide synthesised by nitric oxide syntahse (NOS) from L-arganine + oxygen
- > eNOS in endothelium (constitutive) - > iNOS induced in monocytes in response to inflammation - > nNOS in neurons
=> Peptide hormones: reduce BP
Vasoconstrictos
e.g. angiotensin II, thrombin -> all have own receptors (Endothelin, TX A2, PG H2 -> molecules released) -> picked up y smooth muscle cells -> Ca 2+ influx -> constriction
Superoxide another molecule -> present in free radicals -> 1.) gets rid of nitric oxide produced by endothalial cells
=> Endothelin 1 is 21 amino acid peptide released by EC
=> Prostaglanding A2 + H2 released from platelets + EC
=> Superoxide radicals react with NO
Blood flow, pressure + Viscosity
- > blood flow related to pressure
- > blood viscosity -> dependent on amount of colloidal (non-soluble) material in blood, e.g. lipoproteins, RBC alter viscosity
- > volume fraction of colloidal material increases viscosity
=> colloidal partical such as lipoproteins are in suspension due to attractive + repulsive van der waals + electrostatic forces -> there is a balance - come together and don’t go further away from each other
=> alteration in electrolytes can neutralise these charges allowing the
=> Oxidation neutralises the charge of the surface of these particles -> e.g. smoking oxidises lipoproteins -> allows them to come together easier -> remember: Lana
Aggragation of lipoproteins
- > separated -> 4 times the volume (vol. fraction)
- > aggregation: stuck together -> volume fraction 4 + all the dead volume between them -> increased volume fraction hugely
Blood Volume
- > decrease in blood volume -> loss of blood, e.g. haemorrhage / chronic bleeding
- > dehydration + fall in CO - > Increase in Blood volume
Neuronal regulation of BP
- > major cardiovascular control centre in in medulla of brain
- > VASOMETER CENTRE one of the subgroups within control centre -> consists of group of
Baroreceptors
- > pressure sensors
- > located in walls of large arteries in neck and thoracic regions
- > rapid response system for dealing with change in BP
- > Stimulated by stretch of arterial walls caused by rise in BP
- >