Well, two things. First, this is not something you need to understand for the MCAT, so I wouldn't be worrying about it. Second, you're not going to have the background knowledge to fully understand it yet, but the basics of it are as follows:
In heart failure (of which there are different flavors) you generally have both left and right sided failure. The definition is basically that the heart is not pumping enough blood to meet the metabolic needs of the body. With left-sided failure, the heart is unable to pump enough blood due to an infarct or some other derangement. Right-sided failure often follows left-sided failure because of volume overload of the right ventricle following pulmonary edema. This leads to backup of blood in the venous circulation.
One of the important results of all this, as Instatwaiter mentioned, is congestion that builds in the kidney. This leads to activation of the renin-angiotensin-aldosterone axis. Aldosterone causes the kidney to reabsorb more sodium and thus more water causing an increase in blood volume. With Angiotensin II there is also an increase in the systemic vascular resistance. Accompanying all this is also a spike in sympathetic outflow, which contributes to the increase in resistance and also tries to augment the action of the heart.
The problem is in most cases the heart can no longer compensate through the Frank-Starling mechanism so the increase in fluid retention does not augment the cardiac output enough to meet the metabolic needs of the body, so you just keep retaining more fluid and keep sympathetic outflow high. The increase in fluid along with the higher hydrostatic pressure due to backup of blood leads to the edema (peripheral and pulmonary).
The simple answer to your first question is no, the extra volume does not "expand the renal artery and promote excretion." There is congestion of the kidney and this leads to renin-AII-aldosterone activation which leads to further fluid retention.