The balance of the vascular tone between afferent (Af-Arts) and efferent arterioles (Ef-Arts) is a crucial determinant of glomerular hemodynamics. In order to directly study the mechanisms that regulate their vascular tone, we have developed several in-vitro microperfusion preparations of these arterioles, which allow us to observe the arteriolar diameter in the absence of systemic hemodynamic and hormonal influences. In the Af-Art, but not Ef-Art, we have demonstrated the presence of two intrinsic mechanisms, myogenic response and macula densa-mediated tubuloglomerular feedback, both of which play an important role in the control of vascular tone. We also found that both of these mechanisms are modulated by endogenous nitric oxide (NO). In addition, several humoral factors (such as angiotensin II [Ang II] and prostaglandins [PGs]) play an important role in the control of the tone of these arterioles although their actions are not identical in Af- and Ef-Arts. We found that Ang II caused much stronger constriction in Ef- than in Af-Arts, and that this difference was mediated by the NO-induced modulation of Ang II action in the Af-Art. We have also found that the vasoconstrictor effect of Ang II on Ef-Arts is modulated by PGs produced by the upstream glomerulus. Thus, this may be a mechanism whereby the glomerulus controls its own capillary pressure by releasing PGs, thereby adjusting the resistance of the downstream Ef-Art. Such different mechanisms that regulate Af- and Ef-Art tone play an important role in the precise control of glomerular hemodynamics.
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