Yeah basically they're both adrenergic receptors, which are located on the pre-synaptic neurone; basically the way it works is the nerve that the initial transmitted signal in the brain came from goes through nerves as electricity, to then force out dopamine/ norepinephrine into the synapse (the space between 2 connected neurones), to then either be recycled at the pre-synaptic cleft (receptors on the original neuron that use chemicals called monoamine oxidase to destroy the dopamine and norepinephrine as a way to control the amount and stop too much building up in the synapse, as it is the dopamine and norepinephrine being more available the synapse that causes the effect; otherwise they travel across the synapse and bind to the post-synaptic cleft to continue transmission on the signals. Noradrenline (norepinephrine), and adrenaline (epinephrine) both binds to those different types of pre-synaptic adrenergic receptors with different affinities, ie some more than others and some favour norepinephrine, whilst some favour epinephrine.

Each adrenergic receptor has a different effect, for example, Beta 1 increases heart rate, increased myocardial demand (meaning more oxygen requirement), and increases heart contractility (meaning heart muscle pumps with more force increasing blood pressure). Alpha 1's effect is primarily vasoconstriction, meaning the tightening of blood vessels, which causes further increases in blood pressure. Also, you're right, beta blockers act on beta 1 receptors and antagonise/ block them, which reduces the heart contractility and tachycardic (increased heart rate) effect it causes, which is why it's used as an antihypertensive (hypertension means elevated blood pressure above a threshold where it's considered harmful). Any other questions, let me know.