Renal autoregulation maintains a stable glomerular filtration rate (GFR) and renal blood flow (RBF) despite fluctuations in systemic arterial pressure. For example, even when a person’s blood pressure rises or falls within a certain range, the kidneys are able to maintain a consistent filtering of waste products and fluid balance. This stability is achieved through two intrinsic mechanisms: the myogenic response and tubuloglomerular feedback. The myogenic response involves the constriction or dilation of afferent arterioles in response to changes in arterial pressure. Tubuloglomerular feedback, on the other hand, involves a feedback loop within the nephron that adjusts GFR based on the concentration of sodium chloride in the distal tubule.
The maintenance of a constant GFR is essential for consistent removal of metabolic waste products and maintenance of electrolyte balance, contributing to overall homeostasis. Historically, the understanding of these mechanisms has evolved significantly, progressing from early observations of relatively constant renal function despite changes in perfusion pressure to a detailed understanding of the cellular and molecular mechanisms that mediate the myogenic response and tubuloglomerular feedback. This knowledge is critical for understanding the pathophysiology of kidney diseases where autoregulation is compromised, and informs the development of targeted therapies.
