Reduced sodium chloride, dilates arterioles, increases Renin release.
The renin released from these cells then functions as an enzyme to increase the formation of angiotensin I, which is converted into angiotensin II.
Macula densa cells sense changes in volume to the distal tubule by means of a signal that is not fully understood. Experimental studies show that the glomerular filtration rate slows down the flow rate in the loop of Henle, causing an increased percentage of reabsorption of the proportion of sodium ions and chloride delivered to the loop of Henle, thereby reducing sodium concentration chlorides in macula densa cells.
This reduction in sodium chloride initiates a signal from densa macula that has two effects: (1) It reduces the resistance to blood flow in the incoming arterioles, which increases glomerular hydrostatic pressure and helps the glomerular filtration level returns to normal, and (2) it increases the release of renin from the granulosa cells of the incoming and outgoing arterioles, which is the major store of renin.
The renin released from these cells then functions as an enzyme to increase the formation of angiotensin I, which is converted into angiotensin II. Eventually, Angiotensin II contracts the divertic arteries, thereby increasing glomerular hydrostatic pressure and returning glomerular filtration levels to normal.
Figure. Structure of the glomerular apparatus, demonstrating its possible feedback role in controlling nephron function.
The two components of the bridge-tubular feedback mechanism, working together by the special anatomical structure of the granulocyte machinery, provide feedback signals to the arterioles both to and from, to self-regulate. effective glomerular filtration rate in blood pressure changes. When both functional mechanisms are working together, the glomerular filtration rate changes only a few percent, even with large variations in arterial pressure between limits of 75- and 160-mm Hg.
Angiotensin II blockers form a decrease in glomerular filtration rate in reducing renal perfusion. Angiotensin II prioritizes contraction of the arterioles to prevent a serious reduction in glomerular hydrostatic pressure and glomerular filtration rate when renal perfusion pressure falls below normal. drugs that block the formation of angiotensin II (angiotensin-converting enzyme inhibitors) or block the action of angiotensin II (angiotensin II receptor antagonists) may cause a greater decrease in glomerular filtration than normal when applied Renal artery force fell below normal. Therefore, an important complication of the use of drugs to treat patients with hypertension caused by renal artery stenosis (partial obstruction of the renal artery) is the possible significant reduction in glomerular filtration rate, In some cases, acute renal failure. However,
Figure. Macula densa feedback mechanism to self-regulate glomerular hydrostatic pressure and glomerular filtration rate (GFR) when renal artery pressure is reduced.