During periods of dehydration and salt deprivation renal Mesenchymal Stromal Cells (MSCs) differentiate to JG cells undergo expansion, and smooth muscle cells along the afferent arteriole re-differentiate to express renin.
Age-associated neurohormonal changes particularly affecting the renin angiotensin aldosterone system (RAAS), alterations in thermoregulatory mechanisms, changes in renal function and body composition render older persons vulnerable to dehydration, renal failure, heat stroke and increased mortality.
Renin-angiotensin system (RAS) inhibitors carry a risk of normotensive ischemic acute kidney injury in dehydration and concurrent nonsteroidal anti-inflammatory drug (NSAID) use.
Using genetic gain- and loss-of-function experiments, we show that ITP signaling acts analogous to the human vasopressin and renin-angiotensin systems; expression of ITP is elevated by dehydration of the fly, and the peptide increases thirst while repressing excretion, promoting thus conservation of water resources.
Loss-of-function mutations of the MR are responsible for renal pseudohypoaldosteronism type 1 (PHA1), a rare disease of mineralocorticoid resistance presenting in the newborn with weight loss, failure to thrive, vomiting and dehydration, associated with hyperkalemia and metabolic acidosis, despite extremely elevated levels of plasma renin and aldosterone.