Vasoactive intestinal peptide and XXXX secretion.

@entity1 @entity3549 @entity548 @entity326 @entity1372 @entity916 @entity934
@entity3549 has now been shown to produce an increase in @entity916 release in a number of species, including @entity1 . Our work suggests that @entity3549 is capable of producing this effect by a direct action on the @entity916 -secreting juxtaglomerular cells of the kidney. We have found no evidence to support the possibility that @entity3549 produces this effect as a neurotransmitter in the kidney. In this regard, it should be noted that @entity3549 has been identified as a cotransmitter primarily in cholinergic neurons. The kidney is thought to lack cholinergic innervation, and @entity934 has no effect on @entity916 secretion. We have explored two conditions where @entity916 secretion is known to increase and found that circulating levels of @entity3549 did not increase along with the increase in PRA. Thus, at least in @entity548 and dietary @entity1372 restriction, @entity3549 does not appear to affect @entity916 secretion through a humoral mechanism. There could be other untested situations where a humoral effect of @entity3549 might come into play since we have shown that the whole animal is capable of increasing plasma @entity3549 to levels that affect @entity916 release. Studies employing recently developed @entity3549 antagonists have the potential to determine in which physiological or pathological situations @entity3549 contributes to the control of @entity916 secretion. For example, in @entity326 , plasma levels of both @entity3549 and PRA are significantly elevated. Could the increase in PRA be partly dependent on an action of circulating @entity3549 ?
