BACKGROUND/AIMS: Pendrin (SLC26A4), a transporter accomplishing anion exchange, 
is expressed in inner ear, thyroid gland, kidneys, lung, liver and heart. Loss 
or reduction of function mutations of SLC26A4 underlie Pendred syndrome, a 
disorder invariably leading to hearing loss with enlarged vestibular aqueducts 
and in some patients to hypothyroidism and goiter. Renal pendrin expression is 
up-regulated by mineralocorticoids such as aldosterone or deoxycorticosterone 
(DOCA). Little is known about the impact of mineralocorticoids on pendrin 
expression in extrarenal tissues.
METHODS: The present study utilized RT-qPCR and Western blotting to quantify the 
transcript levels and protein abundance of Slc26a4 in murine kidney, thyroid, 
heart and lung prior to and following subcutaneous administration of 100 mg/kg 
DOCA.
RESULTS: Slc26a4 transcript levels as compared to Gapdh transcript levels were 
significantly increased by DOCA treatment in kidney, heart, lung and thyroid. 
Accordingly pendrin protein expression was again significantly increased by DOCA 
treatment in kidney, heart, lung and thyroid.
CONCLUSION: The observations reveal mineralocorticoid sensitivity of pendrin 
expression in kidney, heart, thyroid and lung.