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Abstract
Aim. To study if gene alterations affecting renal sodium reabsorption associate with susceptibility to licorice-induced hypertension.
Methods. Finnish subjects (n = 30) with a previously documented incident of licorice-induced hypertension were recruited for the study using a newspaper announcement. Their previous clinical and family histories as well as serum electrolyte levels were examined. DNA samples from all individuals were screened for variants of the genes encoding 11β-hydroxysteroid dehydrogenase type 2 (11βHSD2) and α-, β-, and γ-subunits of the epithelial sodium channel (ENaC).
Results. Upon licorice predisposition, the patients had a mean blood pressure of 201/118 mmHg. Circulating potassium, renin, and aldosterone levels were low. No significant DNA variations were identified in the 11βHSD2 gene. Four subjects were heterozygous for β- and γENaC variants previously shown to be associated with hypertension. Furthermore, a novel G insertion (2004–2005insG) in the SCNN1A gene encoding the αENaC was identified in two subjects. The frequency of these ENaC variants was significantly higher in subjects with licorice-induced hypertension (6/30 i.e. 20%) than in blood donors (11/301 i.e. 3.7%, P = 0.002).
Conclusions. Defects of the 11βHSD2 gene do not constitute a likely cause for licorice-induced hypertension. Variants of the ENaC subunits may render some individuals sensitive to licorice-induced metabolic alterations and hypertension.
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Acknowledgements
We thank Dr Leena Mykkänen for help in collection of pedigree data and Mrs Susanna Saarinen for technical assistance. This study was supported by The Academy of Finland, Sigrid Juselius Foundation, and The Finnish Foundation for Cardiovascular Research. Authors HEM and KP contributed equally to this work.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.