Lack of evidence for peripheral alpha1- adrenoceptor blockade during long-term treatment of heart failure with carvedilol
Toshihiko Kubo, MD, PhDa,
Eduardo R. Azevedo, MDa,
Gary E. Newton, MD, FACCa,
John D. Parker, MD, FACCa and
John S. Floras, MD, DPhil, FACC*,a
a Division of Cardiology, Mount Sinai Hospital and the University of Toronto, Toronto, Canada

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Figure 1 Effects of carvedilol on muscle sympathetic nerve activity (MSNA) (A, n = 10) and calf hemodynamics (B and C, n = 8) in response to handgrip (HG) exercise. Before treatment, HG significantly increased MSNA and calf vascular resistance (CVR), and significantly decreased calf vascular conductance (CVC). Carvedilol had no effect on the reflex sympathoneural response to HG, or on calf hemodynamic responses to this vasoconstrictor stimulus. Individual data and means ± SE values are expressed. *p < 0.01 compared with control values; p < 0.05 compared with control values.
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Figure 2 Gain of the transfer function from muscle sympathetic nerve activity (MSNA) to blood pressure (BP) before and four months after carvedilol treatment (n = 13). Carvedilol did not alter neuroeffector transfer function gain in any frequency band. Values are means ± SE. Open bars = before treatment; solid bars = after four months treatment. Very low frequency (VLF) = 00.05 Hz; low frequency (LF) = 0.050.15 Hz; high frequency (HF) = 0.150.5 Hz.
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