Role of the efferent arteriole in tubuloglomerular feedback

Tubuloglomerular feedback (TGF) is generally regarded as being mediated by a single, humoral vasoconstrictor acting on the afferent arteriole. Examination of the literature reveals, however, that acute activation or blockade of TGF may, under certain circumstances, be associated with vasomotion of the efferent arteriole, either in the same or in the opposite direction as the afferent arteriole. The former appears to be the case particularly when myogenic autoregulation is attenuated, for example, with application of calcium channel blockers. Experiments in which the TGF signal is chronically lost by preventing tubular fluid flow at the macula densa also suggest participation of the efferent arteriole. Under these circumstances, stop flow pressure and single nephron filtration rate increase and glomerular blood flow falls. TGF activity at this stage is modestly enhanced. Taken together, these findings suggest efferent vasoconstriction. After a delay of some hours, vasoconstriction is also apparent in the afferent arteriole. It is not clear whether the mechanism involved in this response is related to the "normal" TGF response. Together, these findings are hard to reconcile with the hypothesis of a single vasoconstrictor acting on the afferent arteriole.