Bryant H U, Malven P V, Yim G K
Pharmacol Biochem Behav. 1984 Oct;21(4):651-4. doi: 10.1016/s0091-3057(84)80052-0.
Opiate receptor blockade, or forced imbibition of 2% NaCl to deplete pituitary dynorphin decreases 2-deoxy-D-glucose (2-DG), but not insulin-induced hyperphagia, indicating a possible role for dynorphin in the eating associated with endogenous opiates. Beta-adrenergic receptor blockade decreases vasopressin release induced by 2-DG but not by insulin. Because vasopressin and dynorphin are sometimes co-localized, it was hypothesized that naloxone-sensitive feeding might be selectively inhibited by beta-adrenergic blockade with propranolol. Propranolol in doses as low as 2.5 mg/kg inhibited 4 hr feeding induced by 2-DG (400 mg/kg). Propranolol did not significantly affect feeding induced by ketocyclazocine administration (3.0 mg/kg) or by 24 hr food deprivation. Feeding stimulated by insulin (10 U/kg) was significantly inhibited by propranolol (2.5 mg/kg) only when the propranolol was reinjected during the period 2 hr after insulin injection, when the induced feeding was greatest. In summary, propranolol inhibited opiate-related (2-DG) as well as opiate-independent (insulin) hyperphagias. It also failed to inhibit food intake resulting from the opiate related stimulus of 24 hr food deprivation. Therefore, naloxone sensitive hyperphagias were not specifically inhibited by beta-adrenergic blockade, indicating that vasopressin-associated dynorphin is not involved in opiate related feeding.
阿片受体阻断，或强制摄入2%氯化钠以耗尽垂体强啡肽，可减少2-脱氧-D-葡萄糖（2-DG）诱导的摄食，但不影响胰岛素诱导的摄食亢进，这表明强啡肽可能在内源性阿片类物质相关的进食中发挥作用。β-肾上腺素能受体阻断可减少2-DG诱导的血管加压素释放，但不影响胰岛素诱导的释放。由于血管加压素和强啡肽有时共定位，因此推测纳洛酮敏感的摄食可能会被普萘洛尔的β-肾上腺素能阻断选择性抑制。低至2.5mg/kg的普萘洛尔可抑制2-DG（400mg/kg）诱导的4小时摄食。普萘洛尔对酮环唑辛给药（3.0mg/kg）或24小时食物剥夺诱导的摄食无显著影响。仅在胰岛素注射后2小时内再次注射普萘洛尔（2.5mg/kg），且此时诱导的摄食最为强烈时，胰岛素（10U/kg）刺激的摄食才会被显著抑制。总之，普萘洛尔抑制了与阿片类物质相关（2-DG）以及与阿片类物质无关（胰岛素）的摄食亢进。它也未能抑制24小时食物剥夺这一阿片类物质相关刺激导致的食物摄入。因此，β-肾上腺素能阻断并未特异性抑制纳洛酮敏感的摄食亢进，这表明与血管加压素相关的强啡肽不参与阿片类物质相关的进食。
