Page created on November 11, 2019. Last updated on January 24, 2022 at 16:17
Regulation of renal blood flow
The GFR is proportional to the renal blood flow. If the renal blood flow were not autoregulated a 25% increase in blood pressure would increase the GFR by the same amount. This would increase the amount of urine produced 30-fold. To prevent this, the renal blood flow is autoregulated.
The renal blood flow is autoregulated as long as the MAP is between 80 and 200 mmHg. This ensures that the RBF and therefore the GFR is constant independent of the blood pressure. This autoregulation is maintained by the Bayliss effect and by the tubuloglomerular feedback.
The macula densa is a structure in the wall of the distal tubule of the nephron, at the junction between the thick ascending limb of Henle and the distal convoluted tubule. It consists of a group of specialized epithelial cells.
The function of the macula densa is to regulate the GFR and RBF. These cells sense changes in the GFR by sensing changes in the volume of the filtrate at the level of the distal tubule. If the GFR is decreased less filtrate reaches the macula densa. It will then increase the GFR back to normal by two mechanisms:
- It vasodilates the afferent arteriole
- It increases the secretion of renin from the juxtaglomerular apparatus (see later)
This mechanism is called the tubuloglomerular feedback.
Factors which decrease RBF:
- Sympathetic activation
- Angiotensin II
These factors vasoconstrict renal arterioles, leading to a decrease in RBF. Sympathetic activation during exercise redirects renal blood flow to other organs such as the muscles.
Factors which increase RBF:
- Nitric oxide (NO)
- Atrial natriuretic peptide (ANP)
The renal vessels are not innervated by parasympathetic nerves.
The renin-angiotensin-aldosterone system (RAAS) is the most important system for long-term regulation of the blood pressure. It’s a slow system which controls the level of two important hormones, angiotensin II and aldosterone.
The most important function of RAAS is to regulate long-term blood pressure, but it has other effects as well. It also regulates the blood volume and the salt and water balance of the body. It is what allows us to drink large amounts of water or eat large amounts of salt without there being large changes in plasma volume or blood pressure.
Steps of RAAS:
- The juxtaglomerular apparatus senses a decrease in blood pressure
- The juxtaglomerular apparatus produces renin
- Renin converts angiotensinogen into angiotensin I
- Angiotensin-converting enzyme (ACE) converts angiotensin I into angiotensin II
- Angiotensin causes the adrenal cortex to secrete aldosterone
If the juxtaglomerular apparatus senses an increase in blood pressure it will reduce its production of renin, thereby decreasing the level of angiotensin II and aldosterone, reducing the blood pressure.
Juxtaglomerular cells and renin:
So-called juxtaglomerular cells are in the walls of the afferent arterioles of nephrons. These are specialized smooth muscle cells which sense changes in the blood pressure in the afferent arterioles, which is proportional to the systemic blood pressure.
When the juxtaglomerular cells sense a decrease in blood pressure, they release renin. Renin is an enzyme whose function is to convert angiotensinogen into angiotensin.
The so-called juxtaglomerular apparatus consists of the juxtaglomerular cells and the macula densa.
Angiotensinogen, angiotensin I and angiotensin-converting enzyme:
Angiotensin is the substrate for renin. It’s produced by the liver and is always present in the plasma, but it is inactive before it is activated by renin. Renin converts angiotensinogen into angiotensin I.
Angiotensin I is also inactive, but like renin it is activated by an enzyme. Angiotensin I is activated by angiotensin-converting enzyme (ACE). ACE is abundant in vessels in the lung but is also found in other vessels in the body. ACE converts angiotensin I into angiotensin II.
Angiotensin II is active. It has many effects on the body:
- It stimulates the release of aldosterone from the adrenal cortex
- It vasoconstricts arteries and arterioles in the whole body
- It vasoconstricts the efferent arterioles in the kidney (but not the afferent)
- It increases Na+ and water reabsorption in the distal tubules
- It stimulates thirst and craving for salt
By vasoconstricting arteries and arterioles in the body angiotensin II increases the total peripheral resistance, increasing the blood pressure. It also vasoconstricts the renal artery, reducing renal blood flow. This would reduce the GFR, but angiotensin II also vasoconstricts the efferent arteriole, which raises the GFR back to normal despite the decreased RBF.
By increasing Na+ and water reabsorption the kidney will retain more fluid, which will enter the plasma. When the plasma volume increases the blood pressure increases. The same occurs when someone ingests more salt and water.
Aldosterone is released from the adrenal cortex in response to angiotensin II. Aldosterone is a steroid hormone and the most important mineralocorticoid hormone. It acts on mineralocorticoid receptors in the distal tubule of the nephron.
After binding to its receptor aldosterone:
- Increases Na+ and Cl– reabsorption
- Increases water reabsorption
- Increases K+ secretion
- Increases H+ secretion
The result is that the plasma volume increases and so the blood pressure increases.