Contrasting effects of phentolamine and nitroprusside on neural and cardiovascular variability.

The relative contributions of a central neural oscillator and of the delay in alpha-adrenergic transmission within the baroreflex loop in the predominance of low-frequency (LF) cardiovascular variability during sympathetic activation in humans are unclear. We measured R-R interval (RR), muscle sympathetic nerve activity (MSNA), blood pressure (BP), and their variability in 10 normal subjects during sympathetic activation achieved by BP lowering with sodium nitroprusside (SNP) and alpha-adrenergic blockade using phentolamine. SNP and phentolamine induced comparable reductions in BP (P > 0.25). Despite tachycardia and sympathetic activation with both SNP and phentolamine, LF variability in RR, MSNA, and BP increased during SNP and decreased during phentolamine (SNP: RR +20 +/- 6%, MSNA +3 +/- 5%, systolic BP +9 +/- 6%, diastolic BP +7 +/- 5%; phentolamine: RR -2 +/- 7%, MSNA -34 +/- 6%, systolic BP -16 +/- 8%, diastolic BP -13 +/- 4%, P < 0.05 except systolic BP, where P = 0.09). Thus LF variability is reduced when sympathetic activation is induced by alpha-adrenergic blockade. This suggests that alpha-adrenergic transmission within the baroreflex loop may contribute importantly to the predominance of LF cardiovascular variability associated with sympathetic excitation in humans.

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