Original Articles
Seasonal variation of endothelin-1, angiotensin II, and plasma catecholamines and their relation to outside temperature,☆☆

https://doi.org/10.1067/mlc.2002.127169Get rights and content

Abstract

Circannual rhythmicity in plasma catecholamines is well known, but no chronobiologic data are available on endothelin-1 and angiotensin II. This study was designed to investigate in healthy human subjects whether endothelin-1 and angiotensin II exhibit seasonal variations. Furthermore, we assessed the relation of both variables to plasma catecholamines, to environmental temperature, and to relative humidity in northern Germany, a region of a temperate climate. Plasma concentrations of endothelin-1, angiotensin II, epinephrine, and norepinephrine were prospectively determined in venous blood from 10 healthy subjects at monthly intervals during 13 consecutive months. The single-cosinor method was applied to evaluate the seasonal rhythmicity of these parameters and to assess their temporal relation to both relative humidity and ambient temperature. Whereas relative humidity did not significantly change throughout the year, outdoor temperature was lowest in January and highest in August. Endothelin-1 levels displayed a significant variation, with a sinusoid pattern throughout the year: nadir values occurred in January, peak values in July. Angiotensin II demonstrated a significant correlation with endothelin-1 and paralleled its rhythmicity. In contrast, the two plasma catecholamines exhibited an opposite pattern. We noted a significant inverse correlation between endothelin-1 and norepinephrine. Outside temperature correlated positively with endothelin-1 and angiotensin II levels and correlated negatively with levels of both catecholamines. This is the first study to report a seasonal variation of endothelin-1 and angiotensin II in normal subjects. According to our data, environmental temperature is the climate variable most closely related to the rhythmicity of endothelin-1, angiotensin II, epinephrine, and norepinephrine. (J Lab Clin Med 2002;140:236-41)

Section snippets

Subjects

Ten clinically healthy normotensive nonsmoking subjects (mean age 39 ± 13 years) participated in the study. None of the subjects had a history of cardiovascular, endocrine, or renal disease or was taking any medication. Plasma values for angiotensin II, epinephrine, and norepinephrine were normal in all individuals. Venous blood was obtained while the patient lay in a supine position in a quiet room, 30 minutes after arrival, at the same time of day (8:30 a.m.) at monthly intervals for 13

Plasma variables

Plasma endothelin-1 concentrations displayed significant seasonal variation, with peak values in July and trough values in January (mean 3.9 pg/mL [range 1.8-8.6] vs 1.7 [0.8-3.8; P <.0001; Fig 1).

. Plasma endothelin-1 concentrations in 10 healthy subjects throughout the year: original observations and cosinor fit with mean and 95% range.

Angiotensin II paralleled the rhythmicity of endothelin-1, with the highest levels in July and nadir levels in January (36.2 pg/mL [16.3-80.4] vs 21.3

Discussion

This longitudinal study of healthy subjects demonstrates a seasonal variation, with a sinusoid pattern, of endothelin-1 and angiotensin II, as well as plasma epinephrine and norepinephrine. Environmental temperature was the climatic variable most closely related to the rhythmicity of endothelin-1, angiotensin II, epinephrine, and norepinephrine concentrations.

A circannual rhythmicity of plasma norepinephrine concentration and urinary norepinephrine excretion has been linked to the effect of

Acknowledgements

We thank Dr Alexander von zur Mühlen, Hannover, for the determination of plasma catecholamine concentrations and Dr Steffen Albrecht, Dresden, for the determination of angiotensin II concentrations.

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    Supported by a grant from the Deutsche Gesellschaft für Angiologie and by grant 01ZZ9604 from the Bundesministerium für Bildung und Forschung.

    ☆☆

    Reprint requests: Hans-J. Kruse, MD, Universitatsklinikum Carl Gustav Carus, Medizinische Klinik III, Fetscherstrasse 74, 01307 Dresden, Germany; e-mail: [email protected].

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