From the Guidelines
The main chemicals that signal the afferent arteriole to contract in tubuloglomerular feedback are adenosine and angiotensin II. When increased sodium chloride is detected by the macula densa cells in the distal tubule, they release adenosine, which acts on A1 receptors on the afferent arteriole, causing vasoconstriction. Simultaneously, the juxtaglomerular cells release renin, which converts angiotensinogen to angiotensin I, which is then converted to angiotensin II by angiotensin-converting enzyme (ACE) 1. Angiotensin II is a potent vasoconstrictor that further constricts the afferent arteriole. This vasoconstriction reduces glomerular filtration rate, allowing less sodium to be filtered, which helps maintain sodium balance and blood pressure homeostasis. Some studies suggest that ATP may also play a role as a vasoconstrictor in this process, being released by macula densa cells and acting directly on the afferent arteriole or being converted to adenosine. This feedback mechanism is crucial for autoregulation of renal blood flow and glomerular filtration rate in response to changes in tubular sodium concentration. Key points to consider in this process include:
- The role of adenosine and angiotensin II in afferent arteriole contraction
- The importance of the macula densa cells and juxtaglomerular cells in detecting changes in sodium chloride concentration and responding accordingly
- The potential role of ATP as a vasoconstrictor in this process
- The overall goal of maintaining sodium balance and blood pressure homeostasis through autoregulation of renal blood flow and glomerular filtration rate. It's worth noting that while the provided evidence does not directly address the question of tubuloglomerular feedback, the information from 1 provides insight into the role of angiotensin II in renal physiology, which is relevant to this topic.
From the Research
Chemicals Involved in Tubuloglomerular Feedback
The main chemicals that signal the afferent arteriole to contract in tubuloglomerular feedback are:
- Adenosine: Adenosine mediates tubuloglomerular feedback responses via activation of A(1)-receptors on the renal afferent arteriole 2, 3, 4.
- Angiotensin II: Angiotensin II enhances the afferent arteriolar response to adenosine through increases in cytosolic calcium 3 and has a contractile effect on afferent and efferent arterioles 5.
- Nitric oxide (NO): Reduced nitric oxide production can lead to increased preglomerular reactivity 2.
- Reactive oxygen species (ROS): Increased levels of ROS have been linked to hypertension 2.
Mechanism of Action
The mechanism of action of these chemicals involves:
- Activation of A(1)-receptors by adenosine, leading to an increase in cytosolic calcium and contraction of the afferent arteriole 3, 4.
- Enhancement of the afferent arteriolar response to adenosine by angiotensin II through increases in cytosolic calcium 3.
- Modulation of afferent arteriolar tone by extravasal protein concentration, which can contribute to body fluid volume control 6.