The JGA plays a complex regulatory role. A fall in glomerular blood flow/glomerular blood pressure/GFR can activate the JG cells to release renin which converts angiotensinogen in the blood to angiotensin I and further to angiotensin II. Angiotensin II, being a powerful vasoconstrictor, increases the glomerular blood pressure and thereby GFR. Angiotensin II also activates the adrenal cortex to release Aldosterone. Aldosterone causes reabsorption of Na⁺ and water from the distal parts of the tubule. This also leads to an increase in blood pressure and  GFR. This complex mechanism is generally known as the Renin-Angiotensin mechanism.