First of all, the control of vascular tone is mainly by the action of alpha 1 receptors which are innervated, these are the main effectors of the sympathetic nervous system adrenergic effects. Beta 2 receptors in vascular smooth muscle are not innervated and basically will only cause vasodilation by stimulation from circulating epinephrine produced in the adrenal medulla(neuro-humoral). If you directly(direct agonist) stimulate B2 receptors you will get vasodilation but they are not used for this reason, thats actually an adverse effect of these bronchodilators. Having said that, Blocking beta2 receptors is not directly producing the opposite effect, they are not in charged of vasoconstriction, in some cases, Non- selective beta blockers are actually used in cases of hypertension. Blocking B2 doesn't mean you are stimulating alpha1 receptors who are the ones in charge of vasoconstriction; only in patients with vasospastic pathologies like Reynaud's you would see maybe an exacerbation or possibly as a reaction to prolonged decrease of cardiac output.
The main action in the heart is by blocking B1 receptors, when you decrease contractility you decrease demands of O2, you are also decreasing heart rate and that has a direct effect increasing diastolic interval which is the time when blood flows from the coronary arteries to the cardiac muscle so you are actually INCREASING perfusion to the heart. Also by blocking B receptors you are decreasing the sympathetic outflow stimulation in 2 ways: in the CNS you are decreasing the release of neurotransmitters and in the kidneys by blocking B1 you are inhibiting the production of renin thus decreasing the RAAS.....
I hope that explains to you why beta blockers don't cause coronary vasospasm and they don't reduce de O2 supply to the heart. 😉
