Objective: 

The salt balance of the organism controls the number of renin producing cells in the kidney in an inverse fashion by yet undefined mechanisms. This study aimed to assess a possible mediator role of preglomerular blood pressure in the control of renin expression by oral salt intake. For our investigations we used mice lacking angiotensin II (ANGII) type 1a (AT1a) receptors, because these mice display an enhanced salt sensitivity of renin expression.

Methods: 

Immunohistochemistry, 3D-Reconstructions, Realtime PCR measurements, Blood pressure measurements

Results: 

Utilizing 3-dimensional tissue reconstructions of the kidneys we found renin expressing cells along the preglomerular vascular tree in a typical distal to proximal distribution gradient which was most prominent at high salt intake and which was obliterated at low salt intake by the appearance of renin expressing cells in proximal parts of the preglomerular vasculature. This disappearance of the distribution gradient from afferent arterioles to arcuate arteries during low salt intake was accompanied by reductions of systolic blood pressure. Unilateral renal artery stenosis in mice on normal salt intake produced a similar distribution pattern of renin expressing cells as did low salt intake. Conversely, increasing blood pressure by administration of the NOS-inhibitor L-NAME in mice kept on low salt intake produced a similar distribution pattern of renin producing cells as did high salt intake alone.

Conclusions: 

These findings suggest that the influence of salt intake on the number and distribution of renin producing cells in AT1a deficient mice may be mediated by changes of preglomerular blood pressure.