Blood pressure is the pressure in the circulatory system that is produced when the heart beats. Whenever something is held in a container it exerts some kind of pressure, so blood exerts pressure on the tubes that it is passing through. The blood vessels have elasticated walls, so if the heart is beating hard, the walls stretch more and the pressure in the system is a bit higher. It is usually split into systolic and diastolic pressures to reflect the difference when the heart is and isn't beating (respectively).
The systolic pressure is the highest pressure that the blood reaches in the arteries when the ventricles are contracting (i.e. the highest pressure in systole). Rather predictably it occurs during systole. The diastolic pressure is the lowest pressure that the blood reaches in the arteries when the ventricles are relaxed (i.e. the lowest pressure in diastole).
Blood pressure is affected by a range of things, but the equation which determines blood pressure is as follows:
Blood pressure (BP) = Cardiac output (CO) x Total peripheral resistance (TPR)
Cardiac output is the amount of blood leaving the heart in any given time, and is a reflection of the 'work' done by the heart. Total peripheral resistance is largely contributed by the arterioles, and is the total resistance against the blood flow that is contributed by the peripheral circulation (i.e. all the blood vessels in the body). The higher the TPR or the CO, the higher the blood pressure will be. This is why efforts to control blood pressure either try to slow the heart rate (reducing CO) or cause vasodilatation (reducing TPR).
Vasoconstriction and vasodilatation (or vasodilation) are basically just contraction and relaxation of blood vessels. You can almost work it out from the word - vaso (i.e. talking about blood vessels), and then constriction or dilation.
That's all simple enough, but the reason it's important to know is that vasoconstriction and vasodilatation are an important part of controlling blood pressure. They're probably not the most important part - as we'll see next - but inevitably they play their role.
As the blood vessels constrict, there is less room for the blood to go through and so the pressure goes up; both the systolic blood pressure and diastolic blood pressure will be increased. Conversely, as the vessels dilate, there is more room for the blod to go through, and so the pressures go down.
In actual fact, vasoconstriction and vasodilatation happen completely independantly of attempts to change blood pressure in a normal person. For instance, when you want more blood to get to a particular set of capillaries (e.g. one of your muscles starts working, so you need to get more blood to it), it's worth causing vasodilatation to make sure enough supplies get there.
The blood vessels contract in response to a range of vasoconstrictors (e.g. noradrenaline, or angiotensin II) which act via a G-protein coupled receptor to activate phospholipase C and a cation channel. The activation of phospholipase C converts PIP2 into IP3, which enables calcium to released from the sarcoplasmic reticulum. The activation of the cation channel enables an influx of sodium and calcium, which depolarises the membrane, opening voltage-gated calcium channels (i.e. channels which are opened when the voltage changes) and allowing the influx of calcium. All this, of course, increases the calcium inside the cell.
So how does high intracellular calcium lead to muscle contraction?
For the smooth muscle in the tunica media to contract, there needs to be some phosphorylated myosin in the equation, and this is made my phosphorylating dephosphorylated myosin using the enzyme myosin light chain kinase. This enzyme is made up of a complex which includes calmodulin and four calcium ions - so when calcium is high in the cell, this works fine, the myosin can get phosphorylated, and the muscle contracts.
Of course, this means that it's relatively simple to achieve vasodilatation - at least in theory. That is, if you manage to reduce the intracellular calcium then there's not enough to form the complex needed for myosin light chain kinase to work, and the myosin won't get phosphorylated - what is more, myosin phosphatase kicks in to dephosphorylate any myosin which has got a phosphate group attached!! So vasodilatation simply needs to get the intracellular calcium levels reduced.
This happens quite easily when nitric oxide does its stuff. Endothelial Nitric Oxide Synthase (eNOS) is stimulated by raised calcium, but vasodilators (e.g. bradykinin) and by increased flow in a blood vessel. When eNOS produces nitric oxide, this then goes into the smooth muscle cell and activates guanylate cyclase. This is an enzyme which transforms GTP into cyclic GMP (cGMP).
cGMP activates potassium (K+) channels which lead to membrane hyperpolarisation, and therefore close the voltage-gated calcium channels which would otherwise let more calcium in. The cGMP also activates pumps which pump calcium back into the sarcoplasmic reticulum and out of the cell. Phosphodiesterase (PDE) then turns cGMP into GMP, which stops it going too far. All in all this leads to reduced intracellular calcium, which of course was what we decided we needed to do if we wanted to get the muscle to relax.
People moan a lot about blood pressure, and people worry about it being too high or too low ... it's enough for anyone to think that we've got nothing on board to control blood pressure. But in fact blood pressure is extremely important for every minute of the day, and it's mainly because the head is above the heart. Naturally, then, blood is going to fall out of the head - not into it! But we need blood to deliver oxygen from the lungs to the brain so that the brain can work, and in order to keep blood going into the brain, we need the blood pressure to stay up.
Since blood pressure is basically CO x TPR, the body can do one of two things to change the BP and make sure it stays high enough: either change the cardiac output, or change the resistance in the blood vessels against which the heart is beating. So that means to increase the blood pressure the body can either cause the heart to beat faster, or it can cause vasoconstriction. To reduce the pressure, it can cause the heart to beat less forcefully, or cause vasodilatation.
First of all, the body needs to detect what the blood pressure is and whether or not it needs to be any higher. Then a signal needs to be sent to change the blood pressure accordingly.
The two main detectors are the pressure receptors, and the juxtaglomerular apparatus. The pressure receptors are the first part of the baroreceptor reflex which uses the nervous system to change the way the heart is beating. Stretch receptors in the aortic arch and each carotid sinus send the relevant signals to the lower part of the brain so that the heart is affected appropriately. The juxtaglomerular apparatus is the first part of the renin-angiotensin system. This releases a signal in the form of a hormone, renin, which causes a change in blood pressure by through vasoconstriction or vasodilatation, and by changing the blood volume.
So, the blood pressure is controlled by nerves changing how well the heart is beating, and by hormones changing the resistance in the blood vessels and the blood volume.
Blood pressure is usually measured using a sphygmomanometer, which sounds like a complicated word but is actually quite simple. The manometer bit means something which records pressure, and the sphygmo bit refers to the pulse. So a sphygomomanometer is something which measures the pressure of the pulse.
The standard instrument involves a pressure cuff with a balloon to inflate and a dial to show what the pressure is; a manual meter needs a stethoscope to listen over the artery, whereas automatic meters listen for you and give the result on a digital display. In either circumstance, the cuff should be wrapped in such a way that when it is inflated, the pressure will be applied over an artery. So, to place it properly, you should feel for a pulse (e.g. the brachial pulse) and place the cuff over it.
The cuff is inflated to a pressure greater than the systolic pressure, so that the artery it is surrounding is flattened. A valve attached to the cuff is then used to slowly deflate the cuff, while the stethoscope is used to listen in for Korotkoff sounds. While the cuff is slowly deflating, the onset of Korotkoff sounds signals a pressure equal to the systolic pressure; when the sounds go again, it shows you've reached a pressure equal to the diastolic pressure. Click here to find out why that works.
The reading should usually be repeated a couple of times, and if someone is particularly keen on assessing someone's blood pressure, it should be taken while the subject is sitting and standing. This is because when someone stands up, their blood pressure would normally drop and the body's coping mechanisms need to be working well in order to make sure this doesn't happen. Taking the blood pressure measurement standing up as well as sitting down is therefore a useful measure of how well these mechanisms are working.
Korotkoff sounds are the sounds which can be heard when someone is measuring a person's blood pressure, caused by turbulent flow in an artery. They were named after the man who discovered them, Nikolai Korotkoff (1874-1920), who appreciated that the sounds were quite separate from the sounds of heart valves closing, and recognised that they would be very useful for measuring blood pressure.
In a normal artery, there shouldn't be any disruption to flow - arteries have been designed to allow blood to flow through normally. However, when the blood pressure cuff is inflated during measurement, the artery is flattened from the pressure. This change to the shape of the artery disrupts the blood coming through, causing turbulence, a bit like you get on an aeroplane flight.
When liquid travelling through a tube faces turbulence, it causes vibrations which can be picked up as sound. Because these sounds are transmitted along the artery, placing a stethoscope over the artery just next to the blood pressure cuff allows these sounds to be heard. These sounds are what we call Korotkoff sounds.
But why are they useful for telling us the blood pressure? Well, first of all you need to understand blood pressure and know the difference between systole and diastole. Put simply, when the heart is in systole, it is pumping it's hardest; when it is in diastole, it is relaxed. So, during systole you have the highest pressure in the arteries, and during diastole you have the lowest pressure.
If you pump the blood pressure cuff so that it is at a higher pressure than the systolic pressure, the artery will be completely flattened all the time, so there won't be any flow and you won't be able to hear any sounds of turbulent flow. If you start to reduce the pressure, then the artery will start to open up but still be a bit flattened, so there will be turbulence and you'll hear the sound. When you drop the pressure in the cuff below diastolic pressure, then the pressure in the arteries will be higher than in the cuff even during relaxation - so even the lowest pressure in the arteries is still high enough to keep the artery from being flattened at all. If the artery can't be flattened, there won't be any turbulence; so the sounds disappear again.
It makes a lot of sense, then, to blow up the blood pressure cuff until you can't feel the pulse anymore, and then slowly reduce the pressure in the cuff. When the sounds start, you know that enough blood is getting through to cause the sounds - so you must be below the highest, systolic pressure; and when the sounds stop, you know that there's no flattening of the artery - so you must be below the lowest, diastolic pressure. These are the principles which have governed blood pressure measurement since Nikolai Korotkoff invented the technique in 1905.