Bernier N J, Perry S F
Department of Biology, University of Ottawa, Ontario, Canada.
Am J Physiol. 1997 Jul;273(1 Pt 2):R49-57. doi: 10.1152/ajpregu.1997.273.1.R49.
Immunohistochemical and pharmacological techniques were utilized to investigate the relationships between angiotensins and catecholamine release from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss). Double labeling with [Asp1, Ile5]angiotensin II-fluorescein isothiocyanate (ANG II-FITC) and anti-dopamine beta-hydroxylase revealed specific ANG II binding sites on chromaffin cells. Injection (1 nmol/kg body wt) of either ANG II-FITC, [Asn1, Val5, Asn9]ANG I, [Asp1, Ile5, His9]ANG I, [Asn1, Val5]ANG II, [Asp1, Val5]ANG II, or [Asp1, Ile5]ANG II elicited catecholamine release from in situ perfusion preparations of the head kidney. Catecholamine release elicited by [Asn1, Val5]ANG II (10(-13) to 10(-7) mol/kg body wt) was dose dependent, and the secretion of epinephrine (Epi) was greater than that of norepinephrine (NE). Relative to the results obtained with the [Asn1, Val5]ANG II treatment (1 nmol/kg body wt), Epi release was 72 and 82% lower in response to injections (1 nmol/kg body wt) of [Asn1, Val5]ANG I [amino acid (AA) positions 1-7] and [Asn1, Val5]ANG I (AA 1-6), respectively. Pretreatment with either losartan (10(-5) M), PD-123319 (10(-5) M), or hexamethonium (10(-3) M) had no effect on [Asn1, Val5]ANG II-elicited catecholamine release. Pretreatment with captopril (10(-4) M) significantly reduced [Asn1, Val5, Asn9]ANG I-elicited Epi and NE release and decreased basal catecholamine release. These results provide direct evidence that angiotensins can elicit catecholamine release from the chromaffin tissue via specific ANG II binding sites and indicate that the synthesis of ANG II may be either local or systemic.
利用免疫组织化学和药理学技术研究了血管紧张素与虹鳟（Oncorhynchus mykiss）嗜铬组织中儿茶酚胺释放之间的关系。用[天冬酰胺1，异亮氨酸5]血管紧张素II-异硫氰酸荧光素（ANG II-FITC）和抗多巴胺β-羟化酶进行双重标记，揭示了嗜铬细胞上特定的ANG II结合位点。注射（1 nmol/kg体重）ANG II-FITC、[天冬酰胺1，缬氨酸5，天冬酰胺9]ANG I、[天冬酰胺1，异亮氨酸5，组氨酸9]ANG I、[天冬酰胺1，缬氨酸5]ANG II、[天冬酰胺1，缬氨酸5]ANG II或[天冬酰胺1，异亮氨酸5]ANG II可引起头肾原位灌注制剂中儿茶酚胺的释放。[天冬酰胺1，缬氨酸5]ANG II（10(-13)至10(-7) mol/kg体重）引起的儿茶酚胺释放呈剂量依赖性，肾上腺素（Epi）的分泌大于去甲肾上腺素（NE）。相对于[天冬酰胺1，缬氨酸5]ANG II处理（1 nmol/kg体重）的结果，注射[天冬酰胺1，缬氨酸5]ANG I [氨基酸（AA）位置1-7]和[天冬酰胺1，缬氨酸5]ANG I（AA 1-6）（1 nmol/kg体重）后，Epi释放分别降低了72%和82%。用氯沙坦（1×10(-5) M）、PD-123319（1×10(-5) M）或六甲铵（1×10(-3) M）预处理对[天冬酰胺1，缬氨酸5]ANG II引起的儿茶酚胺释放没有影响。用卡托普利（1×10(-4) M）预处理可显著降低[天冬酰胺1，缬氨酸5，天冬酰胺9]ANG I引起的Epi和NE释放，并降低基础儿茶酚胺释放。这些结果提供了直接证据，表明血管紧张素可通过特定的ANG II结合位点引起嗜铬组织中儿茶酚胺的释放，并表明ANG II的合成可能是局部性的或全身性的。
