Mammalian blood pressure is represented by the following formula: blood pressure (BP) = cardiac output (CO) X total  peripheral resistance (TPR).  CO is the product of heart rate (HR) and stroke volume (SV); whereas, TPR is represented by the formula [8 eta (n) length (l)]/ pi (insert symbol for Pi) radius⁴ (r⁴)]. An increase in either component of CO will result in  increased BP. The only variable in TPR that is easily changed is r⁴.  An increase in the radius of any blood vessel will result in a  decrease in BP; likewise, a decrease in radius will result in an increase in BP.
 

Both the heart and blood vessels are supplied by sympathetic innervation (Guyton, p.194).  Adrenergic receptors on the heart
are B₁'s; however, arterioles possess both alpha,'s and Beta₂'s which cause vasocanstriction and vasodilation, respectively
(Guyton, pp. 671-673). Sympathetic stimulation of the heart increases both HR and SV thereby increasing CO and BP.
Sympathetic stimulation of the arterioles results in vasoconstriction and increased TPR since the alpha's outnumber the beta's
(Guyton, p. 673).
 

Normal HR and BP were 66 beats/minute and 153/148 mmHg, respectively. After treatment with an alpha-blocker
phentolamine), the BP decreased to 123/115 mmHg; HR was unchanged. Upon treatment with the adrenergic agonist,
epinephrine, HR increased to 154 beats/minute and BP decreased to 48/38 mmHg. The effect of sympathetic stimulation of the
heart was obvious; however BP decreased significantly. Thus, of the two components that regulate BP, the effects of CO are
minuscule when compared to TPR.
 

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