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A Phenotyping Regimen for Genetically Modified Mice Used to Study Genes Implicated in Human Diseases of Aging

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Hypertension in mice lacking 11beta-hydroxysteroid dehydrogenase type 2.

Y Kotelevtsev¹, R W Brown, S Fleming

¹Centre for Genome Research, University of Edinburgh, Edinburgh EH9 3JQ, Scotland, United Kingdom. Yuri.Kotelevtsev@ed.ac.uk

The Journal of Clinical Investigation

|March 13, 1999

Summary

Mice lacking 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) develop apparent mineralocorticoid excess (SAME), showing hypertension and kidney abnormalities. This genetic model aids in understanding SAME

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Area of Science:

Endocrinology
Nephrology
Genetics

Background:

11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) deficiency causes apparent mineralocorticoid excess (SAME) in humans.
Cortisol inappropriately activates mineralocorticoid receptors, leading to hypertension and electrolyte imbalances.
Incomplete correction of SAME suggests additional, potentially irreversible, kidney changes.

Purpose of the Study:

To create and characterize a mouse model of 11beta-HSD2 deficiency.
To investigate the physiological and histological consequences of disrupted 11beta-HSD2 function.
To explore the role of kidney adaptations in the pathophysiology of SAME.

Main Methods:

Targeted gene disruption of the 11beta-HSD2 gene in mice.
Phenotypic analysis of homozygous mutant mice (11beta-HSD2(-/-)) including survival, fertility, and blood pressure measurements.
Histological examination of kidney tissues, specifically the distal tubule epithelium.
Assessment of mineralocorticoid receptor antagonism effects.

Main Results:

Homozygous 11beta-HSD2(-/-) mice exhibit high mortality in the first 48 hours post-birth.
Survivors display hypokalemia, polyuria, and hypertension (mean arterial pressure 146 mmHg).
Distal tubule epithelium shows significant hypertrophy and hyperplasia, which are resistant to reversal by receptor antagonism.

Conclusions:

11beta-HSD2(-/-) mice recapitulate key features of human SAME.
The model demonstrates that 11beta-HSD2 deficiency leads to persistent kidney structural changes.
This mouse model provides a valuable tool for studying the molecular mechanisms underlying kidney resetting in hypertension associated with SAME.