Control of Blood Pressure

Second last post on the heart. Almost there!

List the actions of local metabolites, autonomic nerves, adrenaline and vasopressin on blood vessels.
Describe the role of vasopressin in control of blood pressure.
Explain how long term regulation of blood pressure depends on regulation of ECF volume.

I've already described the action of local metabolites in my previous post, so let's get on to the other stuff!

As I've also already touched on several times before, adrenaline and noradrenaline released by the sympathetic nervous system cause vasoconstriction. But there's another interesting point that I want to tell you. The sympathetic nervous system also stimulates chromaffin cells to reduce adrenaline and noradrenaline, as mentioned here. More adrenaline than noradrenaline is released, however. Adrenaline actually has a higher affinity for β₂ receptors than for alpha receptors, which is helpful: activation of β₂ receptors causes vasodilation, so adrenaline is helping out with the vasodilation of vessels supplying skeletal muscles and the heart! And it helps these places preferentially: the skeletal muscles and heart have more β₂ receptors than anywhere else in the body. Cool, right?

Oh, and another important point is that the parasympathetic nervous system has very little to no effect on blood vessels, as they don't have receptors for acetylcholine.

Vasopressin is a hormone that can have a longer-term effect on blood pressure. As I will discuss when I get onto the renal stuff, vasopressin causes retention of water. Retention of water means more fluid, which means more blood, which means an increase in blood pressure. Angiotensin II, which is part of the RAAS pathway for conservation of salts (yes, I'll get onto this during the renal stuff, don't you worry), also causes retention of water, which increases blood pressure. (This is because taking in salt increases osmolarity, which drags water back into the body too. Once again, this will all make more sense when I cover renal physiology.) Aside from these effects, vasopressin and angiotensin II can both directly cause vasoconstriction.

Define inotropy/inotropic.
Draw and describe the effect of inotropic agents on the cardiac function curve.
Describe the actions of autonomic stimulation on the heart.

As mentioned briefly before, inotropic agents are agents that affect the strength of contraction. (Chronotropic agents affect the heart rate.)

Now for a refresher on the cardiac function curve! (Yup, it's this incredibly boring graph again...)

An increase in inotropy will increase the stroke volume (and hence cardiac output) at a given left ventricle end-diastolic volume, and vice versa.

The sympathetic nervous system, which innervates the whole heart, is both inotropic and chronotropic: it increases heart rate and force of contraction.

The parasympathetic nervous system is much more limited in its effects. It only stimulates the atria (as well as the sinoatrial and atrioventricular nodes), and the Purkinje system. (That means that most of the ventricles do not receive parasympathetic stimulation.) It has chronotropic effects (slows the heart), but very little inotropic effect.

Define baroreceptor and describe the baroreceptor reflex.
Describe the function of the baroreceptor reflex at rest, on standing and in haemorrhage.
Define and describe the Central Ischaemic Response.

Baroreceptors are pressure receptors (baro = pressure). They are located in the aortic arch and carotid sinus. (As mentioned before, these are also locations of the peripheral chemoreceptors.) The receptors in the carotid sinus are more receptive than those in the aortic arch.

When baroreceptors detect a change in blood pressure, their rate of firing changes. This is picked up by the cardiovascular control centre in the medulla of the brain, which alters the ratio between sympathetic and parasympathetic activity to the heart and blood vessels, restoring original blood pressure.

One example of where this happens is during standing up. When we stand up, blood volume shifts towards the feet and away from our heads, which isn't good for our heads. The fall in blood pressure is detected by baroreceptors, which send out fewer action potentials in response to the drop in blood pressure. The decrease in action potentials is picked up by the medulla and the ratio of sympathetic to parasympathetic activity changes accordingly, so that we don't faint every time we stand up.

The Central Ischaemic Response is pretty much an emergency response to very low blood pressure (<60mmHg). It is like the baroreceptor reflex, but much more potent: it can drive blood pressure up to 200mmHg and cut off blood from everywhere except the heart, lungs and brain. For emergencies only!