The JGA regulates blood pressure and GFR through the renin-angiotensin-aldosterone system (RAAS). When the macula densa senses low sodium chloride levels, it signals the juxtaglomerular cells to release renin. Renin then converts angiotensinogen into angiotensin I, which is subsequently converted into angiotensin II. Angiotensin II causes vasoconstriction and stimulates aldosterone release, leading to increased sodium and water reabsorption, and ultimately, an increase in blood pressure and GFR.
