Open AccessLack of an effect of nephron‐specific deletion of adenylyl cyclase 3 on renal sodium and water excretion or arterial pressure
Author(s) -
Kittikulsuth Wararat,
Stuart Deborah,
Van Hoek Alfred N.,
Kohan Donald E.
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12316
Subject(s) - nephron , adenylyl cyclase , endocrinology , excretion , blood pressure , medicine , sodium , renal sodium reabsorption , kidney , renal physiology , urology , chemistry , reabsorption , stimulation , organic chemistry
Adenylyl cyclase ( AC )‐stimulated cAMP plays a key role in modulating transport and channel activity along the nephron. However, the role of individual adenylyl cyclase isoforms in such regulation is largely unknown. Since adenylyl cyclase 3 ( AC 3) is expressed throughout nephron, we investigated its role in the physiologic regulation of renal Na + and water transport. Mice were generated with inducible nephron knockout of AC 3 ( AC 3 KO ) by breeding mice with loxP‐flanked critical exons in the Adcy3 gene with mice expressing Pax8‐rt TA and LC ‐1 transgenes. After doxycycline treatment at 1 month of age, nephron AC 3 KO mice had 100% Adcy3 gene recombination in all renal tubule segments, but not in glomeruli. Sodium intake, urinary Na + excretion, glomerular filtration rate, and blood pressure were similar between nephron KO mice and the controls during normal, high, and low Na + diets. Plasma renin concentration was not different between the two groups during varied Na + intake. Moreover, there were no differences in urine volume and urine osmolality between the two genotypes during normal or restricted water intake. In conclusion, these data suggested that AC 3 is not involved in the physiological regulation of nephron Na + and water handling.