Adenosine and angiotensin II likely use different signal transduction mechanisms to affect juxtaglomerular cell function and inhibit renin release.
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A1AR effects on juxtaglomerular cells are weaker than ANG II; leaves open distinct signaling for renin regulation in vivo.
Background:Renin is mainly secreted from the juxtaglomerular cells (JGC) in the kidney situated in the afferent arteriole close to the vessel pole. Angiotensin II (ANG II) and adenosine inhibit renin secretion and synergistically constrict the afferent arteriole. ANG II depolarises JGC and increases the cytoplasmic free Ca²⁺ concentration [Ca²⁺]i. The responses of JGC to adenosine are less known. Methods:Effects of adenosine on membrane potential and [Ca²⁺]i were studied in afferent arterioles from NaCl-depleted rats and mice. Result:Stimulation of A₁ adenosine receptors (A₁AR) by adenosine (10 µM) or cyclohexyladenosine (1 µM) increased the spiking frequency of JGC, slightly depolarised the cells and, in ≤50% of the cases, increased [Ca²⁺]i. These effects were much smaller than those of ANG II (3 nM). Simultaneous application of cyclohexyladenosine and ANG II gave only additive effects on [Ca²⁺]i; in addition, responses to ANG II in JGC from A₁AR knockout mice were similar to those from control mice. Conclusion: The small changes in membrane potential and [Ca²⁺]i in response to A₁AR stimulation as compared to those of ANG II may suggest that these 2 tissue hormones use different signal transduction mechanisms to affect JGC function, including the inhibition of renin release.
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Laske-Ernst et al. (2008) studied this question.
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