Taddei S, Pedrinelli R, Salvetti A
I Clinica Medica, University of Pisa, Italy.
Circulation. 1990 Dec;82(6):2061-7. doi: 10.1161/01.cir.82.6.2061.
Purine compounds modulate sympathetic neurotransmission; this modulation decreases nervous discharge by stimulating presynaptic inhibitory adenosine receptors, an effect antagonized by theophylline, and causes vasoconstriction through the stimulation of postsynaptic ATP receptors. In humans we evaluated the effect of local theophylline, which was infused into the brachial artery at the rate of 100 micrograms/100 cc/min, on the arteriolar sympathetic vasoconstriction induced by applying a lower-body negative pressure. Forearm blood flow changes were measured by strain-gauge venous plethysmography. Theophylline, which at this dosage blunted the vasodilator effect of adenosine (the physiological agonist for the P1 purinoceptor), significantly increased lower-body negative pressure-mediated vasoconstriction. To evaluate whether neurotransmitters different from norepinephrine participate in the vasoconstrictor effect of theophylline, we repeated the previous experiment in the presence of phenoxybenzamine, which was infused at a dose (60 micrograms/100 cc/min) that abolished the vasoconstrictor effect of norepinephrine. Also, after alpha-adrenoceptor blockade, theophylline continued to increase sympathetic vasoconstriction. Our data confirm that purinergic receptors and neurotransmitters also participate in endogenous sympathetic vasoconstriction in humans.
嘌呤化合物可调节交感神经传递；这种调节通过刺激突触前抑制性腺苷受体来减少神经放电，茶碱可拮抗这一作用，并且嘌呤化合物通过刺激突触后ATP受体引起血管收缩。在人体中，我们评估了以100微克/100毫升/分钟的速率注入肱动脉的局部茶碱，对下体负压引起的小动脉交感神经血管收缩的影响。通过应变片静脉体积描记法测量前臂血流变化。在此剂量下，茶碱可减弱腺苷（P1嘌呤受体的生理性激动剂）的血管舒张作用，显著增强下体负压介导的血管收缩。为了评估与去甲肾上腺素不同的神经递质是否参与茶碱的血管收缩作用，我们在注入苯氧苄胺（剂量为60微克/100毫升/分钟，该剂量可消除去甲肾上腺素的血管收缩作用）的情况下重复了先前的实验。此外，在α-肾上腺素受体阻断后，茶碱仍继续增强交感神经血管收缩。我们的数据证实，嘌呤能受体和神经递质也参与人体的内源性交感神经血管收缩。
