Processing and release of secretory granules involve water movement across granule membranes. It was hypothesized that the water channel aquaporin-1 (AQP-1) contributes directly to recruitment of renin-positive cells in the afferent arteriole. AQP1(-/-) and (+/+) mice were fed a low NaCl diet (LS, 0.004% w/w) for 7 days and given enalapril (ACEI, 0.1 mg/ml) in the drinking water for 3 days. There were no differences in plasma renin concentration at baseline. After LS-ACEI, plasma renin concentration increased markedly in both genotypes but was significantly lower in AQP1(-/-) compared to (+/+) mice. Tissue renin concentration was higher in AQP1(-/-) mice and renin mRNA level was not different between genotypes. Mean arterial blood pressure was not different at baseline and during low salt diet but decreased significantly in both genotypes after addition of ACEI; the response was faster in AQP1(-/-) but then stabilized at similar level. Renin release after 200 µL blood withdrawal was not different. Isoprenaline-stimulated renin release from isolated perfused kidneys did not differ between genotypes. Cortical tissue norepinephrine concentration was lower after LS-ACEI compared to baseline with no difference between genotypes. Plasma nitrite/nitrate concentration was unaffected by genotype and LS-ACEI. In AQP1(-/-) mice, the number of afferent arterioles with recruitment was significantly lower compared to (+/+) after LS-ACEI. It is concluded that aquaporin-1 is not necessary for acutely stimulated renin secretion in vivo and from isolated perfused kidney, whereas recruitment of renin-positive cells in response to chronic stimulation is attenuated or delayed in AQP1(-/-) mice.
American Journal of Physiology: Renal Physiology, 2014, Vol 307, Issue 11