Intrarenal control of renal function is by tubuloglomerular feedback and by glomerulotubular balance. In tubu- loglomerular feedback, Na/Cl delivery to the distal tubule serves as a signal to provide negative feedback control of GFR. In glomerulotubular balance, filtration at the glomerulus alters the oncotic pressure of the plasma that exits the glomerulus and flows into the peritubular capillaries. This consequently alters the balance of transcapillary fluid exchange in the peritubular capillary bed.

Distal tubule NaCl delivery is proportionate to glomerular filtration rate. Tubuloglomerular feedback adjusts GFR to maintain a relatively constant rate of distal tubule NaCl delivery. A drop in the delivery of Na+ or Cl to the distal tubule is sensed at the macula densa. This signal is transmitted to the afferent arteriole. The afferent arteriole dilates, which increases glomerular capillary pressure. The afferent arteriole cells release renin, leading to intrarenal angiotensin II formation. Angiotensin II constricts preferentially the efferent arterioles, as the efferent arterioles are much more sensitive to angiotensin II. Efferent arteriolar constriction increases glomerular capillary pressure. Both vascular changes combine to cause an increase in GFR, which restores distal tubule Na+ or Cl delivery.

Tubuloglomerular feedback results in the regulation of GFR. A drop in arterial blood pressure causes both a decrease in GFR and a decrease in renal blood flow. The drop in GFR causes a tubuloglomerular feedback-mediated arteriolar dilation, restoring GFR and also increasing renal blood flow. Consequently, the regulation of GFR also results in the autoregulation of renal blood flow.

Glomerulotubular balance ties peritubular capillary filtrate reabsorption to glomerular filtration rate. An increase in filtration at the glomerulus enhances filtrate reabsorption at the peritubular capillaries. Increased GFR increases the oncotic pressure of the blood exiting the glomerulus. When that blood enters the peritubular capillaries, the higher oncotic pressure increases reabsorption of filtrate from the renal tubules. An increase in GFR causes a proportionate increase in fluid reabsorption from the proximal tubules and loop of Henle. This balance is not perfect, so increase in GFR does increase fluid delivery to the late tubule segments