The activity of the circulating RAAS is governed by the amount of renin secreted by the granular cells of the jg (juxtaglomerular) apparatus. There are 3 major controllers of renin secretion.

PS: Look at the RAAS, plasma angiotensinogen is synthesized in the liver and plasma angiotensinogen levels are normally high therefore do not limit the production of AII. Furthermore, ACE is expressed on the endothelial surfaces of the vascular system, particularly the pulmonary vessels, and avidly converts most of the angiotensin I into AII. Therefore, the major determinant of circulating AII is the amount of renin available to form angiotensin I.

The first contoller is sympathetic input. Norepinephrine released from postganglionic sympathetic neurons acts on beta1-adrenergic receptors in the granular cells. This activates a c-AMP-mediated pathway that causes the release of renin. The granular cells are quite sensitive to norepinephrine and respond to low levels of sympathetic activity that may have minimal direct effect on the renal vasculature or sodium transport.

The second controller of renin secretion is pressure in the afferent arteriole. The granular cells not only respond to vascular pressures indirectly via adrenergic stimulation, they respond directly to changes in afferent arteriolar pressure. When pressure in the afferent arteriole decreases, renin production increases. Except in cases of major renal arterial blockage, pressure in the arteriolar lumen at the granular cells is close to systemic arterial pressure and changes in parallell with it. Because the granular cells respond to vascular pressure, they are acting as baroreceptors. In fact, the granular cells are the intrarenal baroreceptors. Even though they are not neurons and do not send afferent feedback, they are baroreceptors nevertheless. Consider what happens when arterial pressure drops. The intrarenal baroreceptors (the granular cells) sense the drop in pressure and increase their secretion of renin. Simultaneously, the drop in pressure is also sensed by the arterial baroreceptors in the carotid arteries and aorta. The fall in their afferent signaling allows the vasomotor center to increase sympathetic drive to the granular cells, resulting in a huge combined stimulation of renin secretion.

The third contoller of renin release originates from another component of the jg apparatus; namely the macula densa. The operation of the macula densa is somewhat complicated, but serves as a fascinating example of negative feedback in biological systems. The meacula densa is a detection system and initiator of feedback that helps regulate renin secretion and GFR (tubuloglomerular feedback/TG feedback). For the regulation of GFR please refer to thread "Factors That Affect GFR" at http://www.tomhsiung.com/wordpress/2014/04/factors-that-affect-gfr/. The macula densa is located at the end of the loop of Henle where the tubule passes between the afferent and efferent arterioles of Bowman's capsulre. It is able to sense flow and salt content in the tubular lumen that are the net result of filtration and reabsorption in tubular elements preceding it, that is, it sense "everything done so far." Flow is sensed by cilia that project into the tubular lumen from macula densa cells. Bending of the cilia initiates intracellular signaling that leads to release of paracrine mediators. Tubular sodium chloride is sensed by uptake via Na-K-2Cl multiporters whose action changes ionic concentrations within the macula densa cells and also causes release of paracrine mediators.

When tubular flow and sodium content are high it is as if "the body has too much sodium" and "GFR is too high." The mediators released by the macula densa reduce the secretion of renin (thereby allowing more sodium excretion) and decrease GFR (restoring GFR to an appropriate level). The immediate mediators is ATP, which is converted extracellularly to adenosine. One or both bind to purinergic receptors on the nearby granular cells. This has the effect of increasing intracellular calcium and reducing the release of renin. In turn, the reduction in renin secretion reduces the levels of AII and allows the kidneys to excrete more of the filtered sodium. Simultaneously, the adenosine binds to purinergic receptors on afferent arteriole smooth muscle. The subsequent rise in calcium in these cells stimulates contraction, thus reducing pressure and flow through the glomerular capillaries and reducing GFR.

What happens in the opposite case? Now "the body has too little sodium" and "GFR is too low." This initiates the release of different mediators, specifically prostaglandins and nitric oxide. In the granular cells the prostaglandins stimulate or prolong the lifetime of c-AMP, thereby stimulating the release of renin. In the afferent arterioles NO is a dilator of smooth muscle. The effect is to raise flow and pressure in the glomerular capillaries, and restore GFR to an appropirate level.