I hope this answers your question:
So the heart is an electrically excitable tissue: it pumps due to action potentials that start from specialized heart cells called nodal cells and these nodal cells spread the action potential to surrounding heart cells. These nodal cells are found throughout the heart and they make up what's called the conducting system. These nodal cells don't need neural or hormonal input for them to spread action potentials, they have this mechanism to spontaneously start action potentials on their own called a pacemaker potential, BUT they can be influenced by neural (think sympathetic and parasympathetic) or hormonal input. These external inputs change the frequency (the pace) of the heart beat by influencing the pacemaker potential of the nodal cells.
The sympathetic nerve fibers send out epinephrine which cause the pacemaker potential to occur at a faster rate, that's why during exercise (when epinephrine is released... hopefully) the heart beats faster. Parasympathetic nerve fibers send out acetylcholine which causes the pacemaker potential to occur at a slower rate, thus slowing down the heart. What does this mean in regards to the cardiac cycle? It influences how much blood (the volume) is ejected during the cycle. The volume of blood that is ejected from the ventricles, called cardiac output (CO), which is also how many liters/min, is determined by 2 other factors: stroke volume (volume of blood ejected during each ventricle during systole) and heart rate (CO = HR x SV). And therein lies a part of the answer to your question: when heart rate decreases because of parasympathetic stimulation, cardiac output should also decrease, granted stroke volume stays constant.
I unfortunately do not know how acetylcholine affects blood pressure. I've read a paper of how acetylcholine induced relaxation in hypertensive rats, but I'm not sure of the mechanism, like how it affects systolic or diastolic BP.
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