Nonselective beta-blockade enhances pressor responsiveness to epinephrine, norepinephrine, and angiotensin II in normal man

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Abstract
Nonselective .beta.-blockers increase peripheral vascular resistance and, sometimes, blood pressure (BP); increased responsiveness to circulating pressor agents could be one of the underlying mechanisms. Heart rate (HR) and BP responses to graded i.v. infusions of epinephrine, norepinephrine and angiotensin II were recorded after placebo and then after 4 wk of .beta.-blocker treatment (nadolol or propranolol, 240 mg/day) in 10 healthy young men. Adequacy of .beta.-blockade was demonstrated by a mean 31% decrease in HR response to bicycle exercise, with no differences between the 2 .beta.-blockers. Under placebo conditions epinephrine lowered diastolic BP and raised HR; these effects were reversed during treatment with .beta.-blockers. .beta.-Blockade potentiated BP responses to norepinephrine and angiotensin II: 35% less norepinephrine and 52% less angiotensin II were required to increase mean BP by 15 mm Hg. A final study 2 wk after .beta.-blocker cessation revealed the absence of the lasting effect. These results confirm the concept of unopposed .alpha.-constriction for epinephrine and also demonstrate increased BP responses to norepinephrie and angiotensin II during chronic .beta.-blockade.