The balance of the vascular tone between afferent and efferent arterioles (AAs and EAs, respectively) is a crucial determinant of glomerular hemodynamics. Thus, it is important to study the mechanisms that control their vascular tone to understand renal physiology and pathophysiology. In order to directly study the mechanisms that regulate their vascular tone, we have developed several in vitro microperfusion preparations of these arterioles, which have the advantage of allowing us to observe the arteriolar diameter directly in the absence of systemic hemodynamic and hormonal influences. In the AA but not EA, we have directly demonstrated the presence of two intrinsic mechanisms, namely the myogenic response and macula densa-mediated tubuloglomerular feedback, that play an important role in the control of vascular tone. We also found that both mechanism-induced constrictions of AAs can be modulated by endogenous nitric oxide. In addition, several humoral factors (such as angiotensin II or prostaglandins) play an important role in the control of AA tone. On the other hand, angiotensin II is one major factor that controls the vascular tone of the EA. We have found that the vasoconstrictor effect of angiotensin II on EAs is modulated by prostaglandins produced by the upstream glomerulus. Thus, this may be a mechanism whereby the glomerulus controls its own capillary pressure by releasing prostaglandins and thereby adjusting the resistance of the downstream EA. These varying mechanisms regulating AA and EA tone play an important role in the precise control of glomerular hemodynamics.