Key result
Life-long deletion of A1 receptors significantly attenuated renal vasoconstrictor responses to sympathetic nerve stimulation compared to wild-type mice, indicating adenosine enhances postjunctional effects of norepinephrine.
Absolute Event Rate: 36% vs 59%
p-value: p=0.0363
Adenosine formed during renal sympathetic nerve stimulation enhances the postjunctional effects of released norepinephrine by activating A1 receptors.
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A1 receptor deletion attenuates sympathetic renal vasoconstriction in mice; leaves open whether this mechanism informs human cardiorenal therapies.
Jackson et al. (2012) studied Renal sympathetic neurotransmission. A1 receptor knockout (A1AR-/-) vs. Wild-type littermates (A1AR+/+) was evaluated on Vasoconstrictor response to renal sympathetic nerve stimulation at 7 Hz (change in perfusion pressure in mmHg) (p=0.0363). Life-long deletion of A1 receptors significantly attenuated renal vasoconstrictor responses to sympathetic nerve stimulation compared to wild-type mice, indicating adenosine enhances postjunctional effects of norepinephrine.
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