Of Mice and Renin
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See related article, pp 119–128
Organisms tend to compensate for the need of a cellular function by increasing the amount or the size of the responsible cell type. Hypertrophy of all muscle types under increased workload is a prominent example. Also several hormone systems react by increasing the amount of hormone-producing cells, when the main effector of the system is missing. This has been shown for thyroid hormones, leptin, glucagon, and corticosteroids only to name a few. In most cases, negative feedback mechanisms controlling hormone synthesis and release are inactivated by the depletion of the effector hormone. An article in this issue of Hypertension1 confirms that the renin–angiotensin system is no exception. In adult animals and humans, the first and rate-limiting enzyme in the synthesis of its effector peptide angiotensin II (Ang II), renin, is only expressed in a small amount of kidney cells (0.01%–0.02% of all cells) in the juxtaglomerular apparatus of afferent arterioles, the renin-producing cells (RPCs). Already since 1939 it is known that a fall in renal perfusion pressure2 or salt depletion induces the recruitment of additional RPCs along the afferent arteriole and larger renal vessels upstream. In this way, and not by augmenting renin mRNA in already synthesizing cells, the organism increases its capacity to synthesize renin and respond to a physiological need of more Ang II. This recruitment of RPCs reverses the process of their development in embryogenesis, when first most renal vascular wall cells express renin, which is successively reduced to the few juxtaglomerular cells after birth. Oka et al1 use lineage tracing methods to show that the recruited RPCs are the same which produced renin in embryogenesis and gave it up after birth. Although these cells are not able to produce renin in this study using renin-deficient mice, they still …