Final answer:
The tubuloglomerular feedback mechanism involves the JGA, where macula densa cells adjust the GFR by monitoring Na+ concentration and altering afferent arteriole constriction or dilation.
Step-by-step explanation:
The mechanism by which the glomerulus receives feedback on the status of downstream tubular fluid is called tubuloglomerular feedback. This involves the juxtaglomerular apparatus (JGA) and particularly, the macula densa cells which monitor the Na+ concentration in the terminal portion of the ascending loop of Henle. These cells can cause vasoconstriction or vasodilation of afferent arterioles in response to changes in Na+ concentration, thereby altering the glomerular filtration rate (GFR). The increased osmolarity of forming urine and the greater flow rate within the distal convoluted tubule (DCT) activates macula densa cells to release adenosine and ATP. These function as paracrine factors to regulate the afferent arteriole's smooth muscle cells, modulating blood flow and GFR in relation to the filtrate's Na+ content.
Key to this feedback mechanism is the balance between vasoconstriction and vasodilation effects caused by adenosine, ATP, and nitric oxide (NO). When GFR increases, resulting in less Na+ reabsorption and higher filtrate osmolarity, ATP and adenosine stimulate afferent arteriolar constriction, reducing GFR. Conversely, decreased GFR means less Na+ in forming urine and a decrease in ATP and adenosine, allowing for afferent arteriole dilation to increase GFR. NO can counteract this effect by causing relaxation, thus promoting the fine-tuning of GFR