Different vasopressors have different functions and these functions dictate why we choose certain pressors at certain times. We’re all familiar (hopefully) with the fact that epinephrine is a positive inotrope as well as a vasopressor while phenylephrine is pure vasoconstrictor. This is why we choose epi over phenylephrine when we need inotropy and why phenylephrine will actually make hypotension secondary to cardiogenic shock worse.
These differences in function are dictated by the different receptors on which the pressor drugs act. In addition to different functions, some vasopressors with the same general effect (vasoconstriction) act on different targets (catecholamine vs non-catecholamine) and so can have a synergistic effect. Adding vasopressin to norepinephrine for a patient in septic shock, for example, can help even beyond the fact that norepi is at its limit. This is why adding vasopressin before maxing out norepi is often beneficial. Additionally, vasopressin is less affected by blood pH, so it will work in patients with extreme acidosis where norepi will not.
Eddy Joe Gutierrez has a great Instagram post on this with a nice slide showing how the different pressors work.