HELP! SNS regulation of BP

[Lnursing]

Hi! I am having trouble understanding the SNS regulation of blood pressure.

So in response to low arterial pressure, the SNS becomes activated which causes the release of norepinephrine and epinephrine. Norepinephrine acts on the alpha receptors to cause systemic vasoconstriction, which increases SVR, which will lead to an increase in blood pressure. I am having trouble understanding epinephrine's action on the beta receptors. So with decreased arterial pressure, SNS is stimulated and epinephrine released; epinephrine stimulates the beta receptors which causes an increase in heart rate, speed of conduction and force of contraction, but also causes vasodilation. This is the part I am confused about. With vasodilation, wouldn't the BP decrease? Or is the vasodilation used to accommodate an increased heart rate and increased cardiac output to protect the blood pressure from becoming too high? Any help and clarification would be great!

Thanks!

[Rose_Queen, BSN, MSN, RN]

[h=2]From Encyclopedia Britannica

Physiological actions[/h]The actions of epinephrine are complex, owing to its stimulatory effects on α- and β-adrenergic receptors (or adrenoceptors, so named for their reaction to the adrenal hormones), which produce various responses, depending on the specific receptor and the tissue in which it occurs. Hence, epinephrine causes constriction in many networks of minute blood vessels but dilates the blood vessels in the skeletal muscles and the liver. In the heart, it increases the rate and force of contraction, thus increasing the output of blood and raising blood pressure. In the liver, epinephrine stimulates the breakdown of glycogen to glucose, resulting in an increase in glucose levels in the blood. It also acts to increase the level of circulating free fatty acids. The extra amounts of glucose and fatty acids can be used by the body as fuel in times of stress or danger, when increased alertness and exertion are required. The physiological actions of epinephrine are terminated by metabolic breakdown with catechol-O-methyltransferase (COMT) or monoamine oxidase (MAO), by reuptake into nerve endings, and by diffusion from active sites.