Potassium has many ways of entering or exiting the cells.
One factor that blocks potassium entry is B blockers whilst b-agonists aid the entry of K into the cell. That's why one of the treatment modalities of hyperkalemia is b-agonists.
Now, as far as hypoglycemia is concerned:
The sympathetic system employs many insulin counterregulatory hormones such as the catecholamines which promote glycogenolysis and glyconeogenesis when glucose levels are low. This effect is largely mediated through b-agonist effects of epinephrine and norepinephrine on the a-cells of the pancreas which secrete glucagon as well as the liver. If you block the b-receptors you hamper the ability of the body to raise the levels of glucose when deemed necessary, thus, exacerbating any hypoglycemic state. This is particularly important for diabetic patients who take insulin. If they take b-blockers they are prone to hypoglycemic episodes, and on top of that they lack most of the hypoglycemic symptomatology i.e tremors, diaphoresis, which are signs of sympatheticotonia, making the pt unable to know that he currently suffers from hypoglycemia.
Hope I have covered you!