Neurohumoral Factors of Arterial Pressure– Blood Vessels and Pressure

00:00 So now we have talked through a lot of factors, we went through a lot of anatomical things, we went through local factors. Let's end by talking about a few neurohumoral factors. Some of these are going to be spread across the couple of different organ systems that we'll discuss and so you might see some of these mechanisms come up in some future topics but I think it's important to talk about them now as well because you'll get a good feel for how these systems are interrelated. So let's go through them. The autonomic nervous system is probably the most important second by second changer of systemic vascular resistance as well as a number of the other parameters we have discussed such as heart rate and inotropy. The sympathetic nervous system is your fight or flight response or I like to refer to it as the flight or aggressive conflict mediation or the parasympathetic nervous system which is more that relax and digest.

01:10 In the cardiovascular component, we always need to keep in mind that there the baroreflex might be involved. The baroreflex is going to govern arterial pressure and it does that by sensing blood pressure and sending important signals to cause there to either be a change in heart rate or vascular resistance. Hormonal factors such as circulating catecholamines can become very important and the main ones here are things like epinephrine released from the adrenal medulla, the renin-angiotensin-aldosterone system or RAAS system, anti-diuretic hormone or arginine vasopressin as well as our natriuretic peptides, ANP which is atrial natriuretic peptide and BNP which is brain natriuretic peptide. I know it says brain but it really is released by the ventricles. So let's go through this sympathetic activation. If you cause there to be an increase in the sympathetic nervous system, you get vasoconstriction. This is mediated by an alpha-adrenergic response. Alpha-adrenergic receptors are what we call GCPRs, G-coupled-protein receptors, and it will stimulate a very specific portion or G protein that increases IP3 and another substance known as DAG. This will cause there to be a constriction or release of calcium in the smooth muscle. The sympathetic nervous system also increases cardiac output. It does this by increasing heart rate which is a positive chronotropic mechanism and increasing stroke volume by increasing the strength of the contraction as well as sometimes even increasing the amount of preload. Why did we go through systemic vascular resistance and cardiac output? Because these are the two variables multiplied together to equal mean arterial blood pressure. What is the mediator of the cardiac responses? These are beta-adrenergic receptors. These are also G-couple-protein responses but instead of G alpha q we use G alpha s and that increases cyclic AMP. The last item related to the increase in blood volume is through beta-adrenergic responses and activation of the renin angiotensin-aldosterone system. This should increase blood volume to increase cardiac preload. Now the parasympathetic nervous system works a little bit more indirectly. This is going to decrease cardiac output and it does this primarily by decreasing heart rate. So if you decrease cardiac output and keep all other variables the same, arterial pressure will drop. The mechanism by which cardiac output changes is through muscarinic receptors, these are M2-related receptors and these are coupled to a G alpha i protein that decrease cyclic AMP. So it's kind of working in the opposite of a beta-adrenergic receptor. The one thing to be very cognizant about with a parasympathetic nervous system response is it can cause fainting. This is known as a vasovagal response and this is oftentimes seen on an individual who maybe was scared or a response in which you get a drop in both blood pressure and heart rate at the same time.