All the systems you name are interrelated, but they are not simply backups of one another. Nature doesn't create too many strictly repetitive systems - each system has something unique about it.
For example, if you go back and look at my response to you in this thread:
http://emtlife.com/showthread.php?t=9449&highlight=renal+baroreceptors
You'll notice that I underlined the speeds of each of these systems way back then. The important point is that some of these systems are responsible for responding to acute changes in BP or volume, while others control the long term "set point" of BP or volume.
A good analogy would be to consider the control of a eating: the control of the size of a single meal is controlled in a different way than control of your overall intake over the course of many days.
To go through your list here:
renin-angiotensin: this response takes some time to develop, but it can maintain a change in activity for a long time (like months/forever). The activity of this system plays a large part in regulation of "normal" blood pressure by controlling body fluid intake and output (and thus net fluid volume) and long-term vasoconstrictoin. Regulation of the renin/ang system helps create the "set point" of blood pressure and volume.
baroreceptors: one set is responsible for BP, another for volume. These respond to acute changes in BP or volume. "change" is defined relative to the "set point" just discussed. Over time these adapt to new set points: E.g. if someone has chronically elevated BP, the baroreceptors adapt to the higher blood pressure, and consider the high pressure "normal."
You can see the utility of having both control mechanisms. Having both gives your body the ability to set its "normal" pressure (via renin-angiotensin) and then respond to acute changes via the systems mediated by the baroreceptors. For this reason, ACE inhibitors are given, because they affect the pathway that regulates the "set point", as opposed to giving something that blocks the baroreceptors input to the brain, or sympathetic output in general.
Of course hypertension is not necessarily due to an excess of the renin-ang system. That is possible, but there are other etiologies. Regardless, there is a base level of activity in the system that can be repressed by ACE inhibitors, thus lowering BP. This makes ACE inhibitors are really nice for doctors because they can be prescribed without ever figuring out what the source of the hypertension is - they treat hypertension of any cause.
Keep in mind, that regardless of cause, the baroreceptors will eventually adapt to a chronically high blood pressure, no longer interpret e.g. 200/100 as "high", and fail to attempt to lower blood pressure. Thus, the system does not necessarily feedback-regulate itself. Physiologically it should, but hypertension is by definition a pathological condition, and thus medications are used to “tweak” the malfunctioning systems.
As for ANP - again a couple of things are at work. ANP secretion depends on atrial baroreceptors. I can't confirm that these adapt to chronically high blood pressure/volume, but I bet they do. Might be something worth your while to research, though.
Second, ANP works primarily by mediating changes in blood volume (the natriuresis in the name). Thus, it is poorly suited to deal with rapid changes in pressure or volume, and works more over time. Also, ANP (along with aldosterone and VP/ADH) are extremely important for regulating osmotic homeostasis, and all three are more potently influenced by electrolytic imbalance than volume/pressure problems. K+ in particular is extremely tightly controlled by aldosterone and ANP for good reason. These are not simply duplicate BP control mechanisms – they have individualized important roles to play in other areas of body fluid homeostasis.
Thus, while the systems seem to be repetitive, you can understand why they all exist if you consider the speed/duration of each reaction, along with the other responsibilities of the system.
