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(Hypertension. 2009;53:e2.)
© 2009 American Heart Association, Inc.
Letters to the Editor |
Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Milan, Italy, and, Istituto Auxologico Italiano, Milan, Italy
Istituto Auxologico Italiano, Milan, Italy
Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Milan, Italy
Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Milan, Italy, and, Istituto Auxologico Italiano, Milan, Italy
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
We appreciate the interest of Yano and Kario1 in our study documenting the neuroadrenergic abnormalities characterizing different nighttime ambulatory blood pressure (BP) profiles. In their letter, the authors make 2 major points. First, they underline that our findings support the data that they collected throughout
-blocker administration in reverse dippers.2 Second, they disagree with the lack of "correlation between extreme dipper status and morning sympathetic activation" inferred from our data.
As far as the first comment is concerned, we are pleased that the authors share our thinking on this issue. However, we would like to emphasize that our microneurographic evidence provides direct demonstration of the adrenergic overdrive seen in extreme dippers, which was indirectly inferred in the study by Kario et al3 by the finding of a potentiated BP fall in response to doxazosin administration. We emphasize that information obtained by indirect approaches assessing sympathetic function has not always been confirmed by direct techniques in the past. A typical example is represented by the data showing that
-blockade may attenuate the BP response to acute cigarette smoking,4 a finding suggesting the occurrence of an adrenergic overdrive during smoking. However, microneurographic nerve recordings have shown that central sympathetic outflow is inhibited during smoking and that only peripheral secretion of norepinephrine (on which
-blockade may act) is increased.5
The second point made by Yano and Kario1 refers to the fact that, in our study, no correlation between extreme dipping status and sympathetic activation at awakening has been found. We emphasize, however, that
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