The arterial elastance Ea, mentioned in the question, is not related to the properties of the arterial wall.
It is the hemodynamic parameter. Ea is defined as follows:
Ea = MAP / SV
MAP - Mean arterial pressure
SV - Stroke volume.
This parameter is a good indicator of the afterload of the heart.
In heart failure, this Ea will be higher than normal. Vasodilators target arteriolar smooth muscle to dilate the arterioles, thereby decreasing systemic vascular resistance. Reduction in systemic vascular resistance lowers the hemodynamic parameter Ea.
So, the following are the questions.
1. Is the hemodynamic parameter Ea usually monitored for patients with heart failure?
2. If this Ea is high, is vasodilator drug therapy the common medical therapy to reduce this Ea?
Rajagopalan Ganesan
,You ask an interesting question. Vasodilators target arteriolar smooth muscle because their goal is to increase blood flow from arteries to veins and thus to shift volume from the arterial side to the venous side. The objective is to reduce arterial pressure by reducing V in (V-Vo)/C, where C is the arterial compliance and Vo is the unstressed volume of the arterial lumen. You are thinking differently (always a good idea). I believe you are thinking, "Why not change the properties of the arterial wall so that the large arteries can accommodate more volume without increasing pressure and creating more work for the left heart? This is a reasonable idea, but it requires that you be able to estimate the contributions of all the components of the arterial wall to arterial compliance or elastance. I believe you will find that arterial compliance is dominated by elastin and collagen, not by arterial smooth muscle tension. If I'm right about this, a vasodilator cannot significantly alter arterial compliance.
You will see this is a complex question because we are considering a case in which both volume and compliance are changing, but I bet you have the math skills to do the theory. What you need is an experiment with which to test your theory. A simple experiment would be to obtain a length of unbranched rodent aorta, tie off the peripheral end, and measure a pressure-volume curve with and without an effective dose of vasodilator in the physiological salt solution you use to inflate the arterial "balloon."
If the pressure-volume curve changes substantially when the vasodilator is present, then your idea has merit. If the two pressure-volume curves are nearly superimposable, then it appears that your vasodilator has negligible effect on arterial elastance (compliance).
What do you think?
Diminishing the afterload on the heart is the cornerstone in the treatment of heart failure and vasodilators work that way. But pure vasodilators type hydralazine cause reflex stimulation of the secretion of adrenaline and fluid retention to counter the fall in blood pressure and this is very bad for a failing heart (higher heart rate with higher oxygen need etc..). The vasodilators with proven clinical benefit all have an inhibitory effect on the adrenergic stimulation: ACEI an ARB's. Beta blockers have multiple longterm beneficial effects, one of it is also vasodilation. By lowering the heart frequency the stroke volume rises what stimulates the carotid bodies, causing reflex vasodilation and BP lowering.