Suzuki H, Noda Y, Gao X P, Séjourné F, Alkan-Onyuksel H, Paul S, Rubinstein I
Department of Medicine, University of Illinois at Chicago 60612, USA.
Am J Physiol. 1996 Jul;271(1 Pt 2):H282-7. doi: 10.1152/ajpheart.1996.271.1.H282.
The purpose of this study was to determine whether vasoactive intestinal peptide (VIP) elicits vasodilation in the in situ peripheral microcirculation of hamsters with spontaneous hypertension and whether encapsulation of VIP into liposomes modulates this response. Using intravital microscopy, we found that suffusion of VIP (0.05 and 0.1 nmol) alone over cheek pouch resistance arterioles of normotensive hamsters elicited significant vasodilation that was potentiated and prolonged by encapsulation of the peptide into liposomes (P < 0.05). By contrast, VIP (0.5 and 0.1 nmol) had no significant effects on arteriolar diameter in hamsters with spontaneous hypertension. However, encapsulation of VIP into liposomes restored its vasorelaxant effects in hypertensive animals, although the duration of vasodilation was significantly shorter in comparison with controls (P < 0.05). Empty liposomes had no significant effects on arteriolar diameter in either group. These data indicate that VIP-induced vasodilation in the peripheral microcirculation in situ is impaired in essential hypertension and that encapsulation of VIP into liposomes restores, in part, this response.
本研究的目的是确定血管活性肠肽（VIP）是否能在自发性高血压仓鼠的原位外周微循环中引起血管舒张，以及将VIP包裹于脂质体中是否能调节这种反应。通过活体显微镜观察，我们发现，单独向正常血压仓鼠的颊囊阻力小动脉灌注VIP（0.05和0.1 nmol）可引起显著的血管舒张，将该肽包裹于脂质体中可增强并延长这种舒张作用（P < 0.05）。相比之下，VIP（0.5和0.1 nmol）对自发性高血压仓鼠的小动脉直径没有显著影响。然而，将VIP包裹于脂质体中可恢复其在高血压动物中的血管舒张作用，尽管与对照组相比，血管舒张的持续时间明显缩短（P < 0.05）。空脂质体对两组动物的小动脉直径均无显著影响。这些数据表明，原发性高血压会损害VIP在原位外周微循环中诱导的血管舒张，而将VIP包裹于脂质体中可部分恢复这种反应。
