Letter to the Editor - Hypertension

Response to Role of Angiotensinogen and Relative Aldosterone Excess in Salt-Sensitive
Hypertension
Angela J. Woodiwiss and Gavin R. Norton
Hypertension. 2012;59:e58; originally published online April 30, 2012;
doi: 10.1161/HYPERTENSIONAHA.112.195560
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Letter to the Editor
Letters to the Editor will be published, if suitable, as space permits. They should not exceed 1000 words
(typed double-spaced) in length and may be subject to editing or abridgment.
Response to Role of Angiotensinogen and Relative
Aldosterone Excess in Salt-Sensitive Hypertension
We thank Satoh and colleagues for their interest in our work
published recently in Hypertension. 1 In response to the Letter to the
Editor by this group, 2 we acknowledge that, as compared with
aldosterone concentrations alone, the aldosterone/renin ratio (ARR)
may be more reproducible and, hence, could be used as an index of
inappropriate aldosterone activity. With respect to our recent work, 1
further analysis did indeed show that plasma angiotensinogen (AGT)
concentrations were related to ARR in participants with urinary
Na /K above the median (r0.21; P0.0005) but not in those with
urinary Na /K below the median (r0.03; P0.52; P0.005 for
comparison of the relationships).
Regarding the question by Satoh et al 2 on the impact of AGT on
ARR-blood pressure (BP) relations, it is important to note that this
relationship, as reported previously by us in the same community
sample, 3 is driven largely by a negative relationship with plasma
renin. Indeed, only a modest positive relationship between serum
aldosterone concentrations and BP was evident. 3 In contrast, however,
as also reported previously by our group, 3 the relationship of
the interaction between ARR with urinary Na /K and BP is driven
largely by serum aldosterone and not plasma renin concentrations. 3
We have, therefore, emphasized previously that, in this ethnic group,
one should envisage aldosterone effects on BP as being dependent on
salt intake. 3 Thus, the question that Satoh et al 2 may have is whether
circulating AGT concentrations influence the interactive effect noted
between ARR and urinary Na /K as a determinant of BP. This was
indeed the case, because this relationship was more marked in those
with AGT concentrations above the median (r0.26; P0.0001)
versus those below the median (r0.12; P0.01; P0.05 for
comparison of partial r values). This interactive effect translates into
higher adjusted mean systolic BP values in individuals with AGT,
ARR, and urinary Na /K above the median.
With reference to the question by Sato et al 2 of whether ARR is
associated with BP dipping, although we do indeed have ambulatory
BP data on some of the participants in our study, not all of those with
high-quality ambulatory BP data have high-quality urine for evaluation
of urinary Na /K , as well as plasma AGT concentrations.
Hence, we are not statistically powered to assess the impact of AGT
on nondipping.
In conclusion, we believe that our study 1 provides evidence to
suggest that, in the absence of primary aldosteronism, AGT is an
important determinant of renin-angiotensin-aldosterone system activation
and BP, under the condition of high-Na , low-K diets and
subsequent renin suppression.
Sources of Funding
Medical Research Council of South Africa, the Circulatory Disorders
Research Trust, the Hypertension Society of Southern Africa, the
University Research Council of the University of the Witwatersrand,
the National Research Foundation of South Africa, and the Carnegie
Corporation.
None.
Disclosures
Angela J. Woodiwiss
Gavin R. Norton
Cardiovascular Pathophysiology and Genomics Research Unit
School of Physiology
University of the Witwatersrand
Johannesburg, South Africa
1. Michel FS, Norton GR, Majane OH, Badenhorst M, Vengethasamy L,
Paiker J, Maseko MJ, Sareli P, Woodiwiss AJ. Contribution of circulating
angiotensinogen concentrations to variations in aldosterone and blood pressure
in a group of African ancestry depends on salt intake. Hypertension. 2012;59:
62–69.
2. Satoh M, Kikuya M, Ohkubo T, Imai Y. Role of angiotensinogen and
relative aldosterone excess in salt-sensitive hypertension. Hypertension.
2012;59:e57.
3. Scott L, Woodiwiss AJ, Maseko MJ, Veliotes DGA, Majane OHI, Paiker
J, Sareli P, Norton GR. Aldosterone-to-renin ratio and the relationship
between urinary salt excretion and blood pressure in a community of
African ancestry. Am J Hypertens. 2011;24:951–957.
(Hypertension. 2012;59:e58.)
© 2012 American Heart Association, Inc.
Hypertension is available at http://hyper.ahajournals.org
DOI: 10.1161/HYPERTENSIONAHA.112.195560
Downloaded from http://hyper.ahajournals.org/ e58 by guest on August 30, 2013