Tseng C J, Ho W Y, Lin H C, Tung C S, Kuan C J
Department of Pharmacology, National Defense Medical Center, Taipei, Taiwan, Republic of China.
Hypertension. 1994 Dec;24(6):714-8. doi: 10.1161/01.hyp.24.6.714.
The purpose of this study was to examine (1) whether endogenous adenosine receptors inhibit the release of epinephrine and norepinephrine from adrenal medulla in response to physiological and pharmacological stimuli and (2) whether the renin-angiotensin system modulates this effect of endogenous adenosine. We used a conscious animal model to approximate normal physiological conditions. Male Sprague-Dawley rats were treated with a surface adenosine receptor antagonist, 1,3-dipropyl- 8-(p-sulfophenyl)xanthine (DPSPX) to explore the effect of endogenous adenosine. Plasma epinephrine and norepinephrine levels in response to hydralazine-induced hypotension were measured in these animals. The same protocol was repeated in rats pretreated with either adrenalectomy or captopril. The results showed that DPSPX treatment significantly increased plasma epinephrine and norepinephrine levels at both baseline conditions and after hydralazine-induced hypotension. The results from the adrenalectomized rats showed that the difference in plasma epinephrine level between the control and DPSPX groups originated from the adrenal medulla. Pretreatment with captopril attenuated the rise of plasma epinephrine and norepinephrine levels in DPSPX-treated animals. This result suggests that endogenous adenosine receptors inhibit epinephrine release from the adrenal medulla and suppress plasma norepinephrine levels. When catecholamine release was stimulated by physiological and pharmacological stimuli, this inhibitory function of adenosine receptors was augmented. The renin-angiotensin system is at least partially responsible for the modulatory function of endogenous adenosine on the catecholamine response as demonstrated in this study.
（1）内源性腺苷受体是否会抑制肾上腺髓质在生理和药理刺激下释放肾上腺素和去甲肾上腺素；（2）肾素 - 血管紧张素系统是否会调节内源性腺苷的这一作用。我们使用清醒动物模型来模拟正常生理状况。用表面腺苷受体拮抗剂1,3 - 二丙基 - 8 -（对 - 磺苯基）黄嘌呤（DPSPX）处理雄性Sprague - Dawley大鼠，以探究内源性腺苷的作用。测量这些动物在肼屈嗪诱导的低血压状态下血浆肾上腺素和去甲肾上腺素的水平。对肾上腺切除或卡托普利预处理的大鼠重复相同实验方案。结果显示，DPSPX处理显著提高了基线状态以及肼屈嗪诱导低血压后血浆肾上腺素和去甲肾上腺素的水平。肾上腺切除大鼠的结果表明，对照组和DPSPX组之间血浆肾上腺素水平的差异源于肾上腺髓质。卡托普利预处理减弱了DPSPX处理动物血浆肾上腺素和去甲肾上腺素水平的升高。这一结果表明，内源性腺苷受体抑制肾上腺髓质释放肾上腺素并抑制血浆去甲肾上腺素水平。当生理和药理刺激激发儿茶酚胺释放时，腺苷受体的这种抑制功能增强。如本研究所示，肾素 - 血管紧张素系统至少部分负责内源性腺苷对儿茶酚胺反应的调节功能。
