Supowit S C, Gururaj A, Ramana C V, Westlund K N, DiPette D J
Department of Internal Medicine, (Division of General Internal Medicine and Hypertension Section), University of Texas Medical Branch, Galveston 77555-1065, USA.
Hypertension. 1995 Jun;25(6):1333-8. doi: 10.1161/01.hyp.25.6.1333.
Dorsal root ganglia neuronal cell bodies synthesize the vasodilator neuropeptide calcitonin gene-related peptide and innervate the blood vessels and spinal cord sites (laminae I and II) involved in blood pressure regulation. We previously demonstrated that calcitonin gene-related peptide mRNA content is significantly decreased in dorsal root ganglia and that immunoreactive calcitonin gene-related peptide levels are reduced in laminae I and II of the dorsal horn of the spinal cord in the spontaneously hypertensive rat compared with Wistar-Kyoto control rats. To determine whether neuronal calcitonin gene-related peptide expression is also altered in mineralocorticoid-salt hypertension, we quantified calcitonin gene-related peptide mRNA levels in dorsal root ganglia and protein content in laminae I and II of the spinal cord in rats with mineralocorticoid-salt-induced hypertension. To control for pellet implantation, saline drinking water, and/or uninephrectomy, four normotensive groups were similarly studied. By Northern hybridization analysis, the ratio of calcitonin gene-related peptide mRNA to 18S rRNA was increased approximately fivefold in hypertensive rats (33 +/- 7) compared with each of the four normotensive control groups (average of the four groups, 6 +/- 0.5; P < .01, mineralocorticoid-salt group versus each group). The density of the peptide, quantified by computer-assisted image analysis, in laminae I and II in the hypertensive rats was also increased (66 +/- 1 versus average of the four groups, 46 +/- 2 arbitrary units; P < .001, mineralocorticoid-salt group versus each group). In conclusion, neuronal levels of calcitonin gene-related peptide mRNA and protein are increased in mineralocorticoid-salt hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
背根神经节神经元细胞体合成血管舒张神经肽降钙素基因相关肽，并支配参与血压调节的血管和脊髓部位（I层和II层）。我们之前证明，与Wistar-Kyoto对照大鼠相比，自发性高血压大鼠背根神经节中降钙素基因相关肽mRNA含量显著降低，脊髓背角I层和II层中免疫反应性降钙素基因相关肽水平也降低。为了确定在盐皮质激素性高血压中神经元降钙素基因相关肽的表达是否也发生改变，我们对盐皮质激素性高血压大鼠背根神经节中降钙素基因相关肽mRNA水平以及脊髓I层和II层中的蛋白质含量进行了定量。为了控制植入小球、饮用盐水和/或单侧肾切除的影响，对四个正常血压组进行了类似研究。通过Northern杂交分析，与四个正常血压对照组（四组平均值为6±0.5；盐皮质激素组与每组相比，P<0.01）中的每一组相比，高血压大鼠中降钙素基因相关肽mRNA与18S rRNA的比率增加了约五倍（33±7）。通过计算机辅助图像分析定量的高血压大鼠I层和II层中该肽的密度也增加了（66±1与四组平均值46±2任意单位相比；盐皮质激素组与每组相比，P<0.001）。总之，在盐皮质激素性高血压中，神经元中降钙素基因相关肽mRNA和蛋白质水平升高。（摘要截短于250字）
