Pancreatic polypeptide family (APP, BPP, NPY and PYY) in relation to sympathetic vasoconstriction resistant to alpha-adrenoceptor blockade.
Pancreatic polypeptide family (APP, BPP, NPY and PYY) in relation to sympathetic vasoconstriction resistant to alpha-adrenoceptor blockade.
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胰多肽家族（APP、BPP、NPY 和 PYY）与抵抗 α-肾上腺素受体阻断的交感血管收缩有关。
DOI：
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发表时间：
1982
期刊：
影响因子：
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通讯作者：
K. Tatemoto
中科院分区：
文献类型：
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作者：
J. Lundberg;K. Tatemoto
电刺激猫颈交感神经干引起颌下腺唾液分泌和血管收缩，同时引起瞬膜收缩。用酚妥拉明或酚苄明联合普萘洛尔阻断α和β肾上腺素能受体后，刺激交感神经引起的唾液反应和瞬膜收缩几乎消失。然而，相当大的血管收缩反应（高达对照组的40%）仍然存在于下颌下腺。这种yasoconstriction在α-肾上腺素受体阻断后持续存在，开始时相当缓慢，持续时间长，无任何刺激后充血。局部动脉灌注去甲肾上腺素引起颌下血管收缩、唾液分泌和瞬膜收缩。然而，对外源性去甲肾上腺素的血流反应并不能模拟交感神经刺激对血管逃逸的影响。而神经刺激后的血管逃逸，其次是一个长期的血管收缩逐渐下降，逃逸后去甲肾上腺素输注伴随着血流正常化。局部动脉灌注胰多肽（PP）相关肽引起缓慢发展的血管收缩，持续时间长，在下颌下腺，但没有唾液分泌或收缩的瞬膜。作为血管收缩剂的相对摩尔效力约为PYY：1，神经肽Y（NPY）：5，禽和牛胰多肽100。PP相关肽的血管收缩作用对α-肾上腺素能受体阻断具有抗性，并且也存在于交感神经切除动物中，表明对血管平滑肌的直接作用。联合局部输注去甲肾上腺素和神经肽Y引起的血管反应，这是类似的交感神经刺激后所看到的下颌下腺。PYY和NPY在全身给药后引起全身动脉血压升高，这表明全身血管收缩作用。这种效应伴随着短暂的心动过缓，这是由于交感神经紧张的抑制，因为它是在普萘洛尔治疗的动物中不存在。
总之，本研究结果说明了不同的敏感性α-肾上腺素受体拮抗剂的下颌下血管收缩和唾液分泌，以及由交感神经刺激引起的瞬膜平滑肌收缩。这种剩余的血管收缩可以通过释放非肾上腺素能的PP相关递质（如NPY）来解释，NPY可能与血管神经中的去甲肾上腺素一起存在。另外一种血管收缩因子的释放也可以解释去甲肾上腺素的输注不能模拟体内交感神经刺激的血管效应。
Electrical stimulation of the cat cervical sympathetic trunk caused submandibular salivary secretion and vasoconstriction simultaneously with a contraction of the nictitating membrane. Following α- and β-adrenoceptor blockade by phentolamine or phenoxybenzamine combined with propranolol, the salivary response and the nictitating membrane contraction upon sympathetic stimulation were almost abolished. A considerable vasoconstrictor response (up to 40% of control) however still remained in the submandibular gland. This yasoconstriction, which persisted after α-adrenoceptor blockade, was rather slow in onset and had a long duration without any poststimulatory hyperemia. Local intra-arterial infusions of noradrenaline caused submandibular vasoconstriction, salivary secretion and nictitating membrane contraction. The blood flow response to exogenous noradrenaline did, however, not mimic the effects of sympathetic nerve stimulation with regard to vascular escape. Whereas the vascular escape after nerve stimulation was followed by a prolonged vasoconstriction with a gradual decline, the escape after noradrenaline infusions was accompanied by a normalization of blood flow. Local intra-arterial infusions of pancreatic polypeptide (PP)-related peptides caused a slowly developing vasoconstriction with a long duration in the submandibular gland, but no salivary secretion or contraction of the nictitating membrane. The relative molar potencies as vasoconstrictory agents were about PYY: 1, neuropeptide Y (NPY): 5, avian and bovine pancreatic polypeptid 100. The vasoconstrictor effects of PP-related peptides were resistant to α-adrenoceptor blockade and present also in sympathectomized animals, suggesting a direct action on vascular smooth muscle. Combined local infusions of noradrenaline and NPY caused a vascular response in the submandibular salivary gland which was similar to that seen upon sympathetic nerve stimulation. PYY and NPY caused increase in systemic arterial blood pressure upon systemic administration which indicates general vasoconstrictor actions. This effect was accompanied by a transient bradycardia which was due to inhibition of sympathetic tone, since it was absent in animals treated with propranolol.
In conclusion, the present findings illustrate the differential sensitivity to α-adrenoceptor antagonists of the submandibular vasoconstriction and salivation as well as smooth muscle contraction of the nictitating membrane induced by sympathetic nerve stimulation. This remaining vasoconstriction may be explained by release of a nonadrenergic, PP-related transmitter such as NPY which may be present together with noradrenaline in the vascular nerves. Release of an additional vasoconstrictory factor may also account for the finding that infusions of noradrenaline do not mimic the vascular effects of sympathetic nerve stimulation in vivo.