Jin J G, Murthy K S, Grider J R, Makhlouf G M
Department of Medicine and Physiology, Medical College of Virginia, Richmond 23298-0711, USA.
Am J Physiol. 1996 Aug;271(2 Pt 1):G357-69. doi: 10.1152/ajpgi.1996.271.2.G357.
Vasoactive intestinal peptide (VIP) release, nitric oxide (NO) formation, and relaxation induced by nerve stimulation were examined in rabbit and rat gastric muscle. VIP stimulated NO formation in muscle strips, whereas NO stimulated VIP release. Nerve stimulation (0.025-16 Hz or 2-940 pulses) elicited frequency-dependent stimulation of VIP release, NO formation, and relaxation, all significant at two to three pulses. NG-nitro-L-arginine (L-NMA) abolished NO formation, abolished VIP release and relaxation at low frequencies, and partly inhibited them at higher frequencies. Oxyhemoglobin (oxy-Hb) inhibited VIP release and relaxation by 80% at low frequencies and 20-30% at higher frequencies. VIP-(10-28) abolished NO formation and relaxation at lower frequencies and partly inhibited them at higher frequencies; in contrast, VIP-(10-28) augmented VIP release in both species. The pattern of inhibition was similar in both species. Inhibition of maximal NO formation by VIP-(10-28) (82% in rabbit; 48% in rat) implied that a major component of NO is formed in muscle cells by the action of VIP. Thus 1) inhibition of relaxation by L-NNA reflects suppression of NO and VIP release from nerve terminals and NO formation in muscle cells, 2) inhibition by VIP-(10-28) partly reflects suppression of NO formation in muscle cells, and 3) inhibition by oxy-Hb reflects neutralization of extracellular NO and suppression of VIP release. The study demonstrates the dual origin of NO from nerves and muscle and its interplay with VIP in regulating relaxation.
在兔和大鼠的胃肌中，研究了血管活性肠肽（VIP）释放、一氧化氮（NO）生成以及神经刺激诱导的舒张情况。VIP刺激肌条中的NO生成，而NO刺激VIP释放。神经刺激（0.025 - 16Hz或2 - 940个脉冲）引起频率依赖性的VIP释放、NO生成和舒张刺激，在两到三个脉冲时均有显著变化。NG - 硝基 - L - 精氨酸（L - NMA）消除NO生成，在低频时消除VIP释放和舒张，在高频时部分抑制它们。氧合血红蛋白（oxy - Hb）在低频时抑制VIP释放和舒张80%，在高频时抑制20 - 30%。VIP - (10 - 28)在低频时消除NO生成和舒张，在高频时部分抑制它们；相反，VIP - (10 - 28)在两种动物中均增强VIP释放。两种动物的抑制模式相似。VIP - (10 - 28)对最大NO生成的抑制（兔中为82%；大鼠中为48%）表明，NO的主要成分是由VIP作用于肌细胞形成的。因此，1）L - NNA对舒张的抑制反映了神经末梢NO和VIP释放以及肌细胞中NO生成的抑制，2）VIP - (10 - 28)的抑制部分反映了肌细胞中NO生成的抑制，3）oxy - Hb的抑制反映了细胞外NO的中和以及VIP释放的抑制。该研究证明了NO来源于神经和肌肉的双重起源及其在调节舒张中与VIP的相互作用。
