Short-term effect and the mechanism of radix Angelicae on pulmonary hypertension in chronic obstructive pulmonary disease]

The changes of hemodynamics, hemorheology and blood gas were investigated in 28 stable COPD patients with pulmonary hypertension after short-term treatment by Radix Angelicae. The level of TXA2, PGI2 were measured in 10 of the 28 patients before and after treatment. The results show that Radix Angelicae produced significant improvement on pulmonary hypertension, blood viscosity, hematocrit and the level of TXA2 decreased significantly. But the blood gas, blood pressure and the level of PGI2 remained unchanged in all of the patients.     

Changes in plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha in bronchial asthma

We measured the plasma levels of TXB2, a stable metabolite of TXA2, and 6-K-PGF1 alpha, a stable metabolite of PGI2, in 28 asthmatics (16 of extrinsic type, 12 of intrinsic type) during symptomatic period and asymptomatic period respectively with radioimmunoassay. At the same time, plasma TXB2 and 6-K-PGF1 alpha were measured in 30 normal subjects for control. The results were as follows: (1) In the extrinsic asthmatics: The plasma TXB2 level measured during symptomatic period was significantly higher than that during asymptomatic period (P less than 0.05), while the plasma level of 6-K-PGF1 alpha measured during symptomatic period was significantly lower than that of normal subjects (P less than 0.01). The ratio of TXB2/6-K-PGF1 alpha measured during symptomatic period was significantly higher than that measured during asymptomatic period and that measured in the normal subjects (P less than 0.05). (2) In intrinsic asthmatics: The plasma 6-K-PGF1 alpha level measured during symptomatic period was significantly lower than that of normal subjects. There was no significantly difference between either plasma TXB2 level or ratio of TXB2/6-K-PGF1 alpha measured during symptomatic period and that measured during asymptomatic period as well as that of normal subjects. From these results it is suggested that (1) The TXA2 and PGI2 may play a different role in different types of asthma, (2) The imbalance between TXA2-PGI2 may be one of the important factors that take part in the pathogenesis of extrinsic asthma.     

花生四烯酸细胞色素p450表氧化酶基因对肺动脉高压大鼠血浆和组织中ET-1、NO、TXA2和PGI2变化的影响

目的观察野百合碱(MCT)诱导的肺动脉高压大鼠中花生四烯酸色素p450表氧化酶CYP2J2基因过表达时血浆和肺组织中内皮素-l(ET-1)、一氧化氮(NO)血栓素A2(TXA2)和前列腺素I2(PGI2)的水平及肺组织中一氧化氮合酶(NOS)活性的变化。方法成年雄性SD大鼠60只随机分为正常对照组(n=30)和MCT模型组(n=30),皮下注射MCT(60mg/kg)建立肺动脉高压模型。三周后尾静脉分别注射生理盐水和质粒分为6组:NS组,pCDNA3.1(n=10),pcDNA3.1-CYP2J2(n=10),MCT+NS(n=10),MCT+pCDNA3.1(n=10),MCT+pCDNA3.1-CYP2J2(n=10)。三周后,检测大鼠肺动脉压(mPAP),测定血浆和肺组织中ET-1和NO水平,检测肺组织中NOS和eNOS的活性,检测血浆和肺组织TXA2代谢产物TXB2和PGI2代谢产物6-酮-前列腺素1α(6-keto-PGF1α)水平及TXB2/6-keto-PGF1α的比值。结果 MCT模型组mPAP,血浆和肺组织中ET-1水平和TXB2含量和TXB2/6-keto-PGF1α比值均明显高于正常对照组(P<0.05),而pCDNA3.1-CYP2J2治疗组与MCT模型组比均显著降低(P<0.05),但仍高于正常对照组(P<0.05);MCT模型组血浆和肺组织中NO和6-keto-PGF1α含量,肺组织eNOS和NOS活性,TXB2/6-keto-PGF1α比值均明显低于正常对照组(P<0.05),而pCDNA3.1-CYP2J2治疗组均明显增高(P<0.05),但仍低于正常对照组(P<0.05)。结论花生四烯酸色素p450表氧化酶基因CYP2J2可逆转MCT诱导的肺动脉高压,其机制可能与降低肺组织和血浆中的ET-1和TXA2含量,升高PGI2含量,上调TXA2/PGI2比值,上调机体内eNOS和总NOS活性,增加体内NO水平有关。CYP2J2基因治疗对肺动脉高压有积极的治疗作用。     

Plasma renin activity, angiotensin II, angiotensin converting enzyme, thromboxane A2 and prostacyclin I2 levels in pigs with severe hypoxia and hypercapnea and acidosis shock]

To evaluate the role of certain plasma biosubstances on the development of pulmonary hypertension and shock during severe hypoxia, hypercapnia and acidosis, plasma renin activity (PRA), angiotensin II (ATII), angiotensin converting enzyme (ACE), TXB2 and 6-Keto-PGF1 alpha (the stable metabolites of TXA2 and PGI2) were assayed in blood from pulmonary artery and aorta in seven pigs. Pulmonary arterial pressure (PAP) was monitored via Swan-Ganz catheter. During hypoxic and hypercapnic ventilation, PaO2 dropped to 4.7 kPa, PaCO2 rose to 21.1 kPa, pH dropped to 6.82, PAP increased from 2.43 +/- 0.06 to 4.46 +/- 0.45 kPa when acidotic shock developed (all P less than 0.05). Meanwhile ATII levels rose (all P less than 0.05). PRA significantly increased during acidotic shock as compared with normal ventilation (P less than 0.02). ACE dropped significantly (P less than 0.05), TXB2 and 6-keto-PGF1 alpha showed no significant change before and after hypoxic and hypercapnic ventilation.     

The clinical investigation of the pulmonary arterial pressure in stable-stage chronic obstructive pulmonary disease with cor pulmonale]

We measured pulmonary arterial pressure with Swan-Ganz catheters both at rest and after exercise in 21 patients with stable-stage chronic obstructive pulmonary disease (COPD). The results were as follows: pulmonary arterial mean pressure cases (PAPm) increased at rest in 11 cases (PAPm greater than or equal to 2.66kPa); in 6 cases PAPm was normal at rest (PAPm less than 2.66kPa) but increased above the normal level after exercise (PAPm greater than or equal to 3.99 kPa); in 4 cases PAPm was within the normal limit both at rest and after exercise. These results suggest that (1) pulmonary arterial pressure in some patients with COPD and cor pulmonale can return to the normal level; (2) exercise load test can detect early-stage or latent pulmonary hypertension; (3) attention should be paid to the patient selection when long-term vasodilators are administered.     

Prostanoid production in varicose veins: evidence for decreased prostacyclin with increased thromboxane A2 and prostaglandin E2 formation

In this study, formation of arachidonic acid-derived prostanoids was investigated in saphenous veins of varicosed and nonvaricosed patients, all undergoing saphenectomy respectively for varicosis or in preparation for coronary bypass operation. Venous production of prostacyclin (PGI2), thromboxane A2 (TXA2) and prostaglandin E2 (PGE2) was assessed by bioassay and/or radioimmunologic assays as appropriate. Fragments of saphenous veins from varicosed patients produced significantly less PGI2 and more TXA2 and PGE2 than those from the control patients. Addition of arachidonic acid to incubation mixtures dose dependently increased release of these prostanoids, but the levels of PGI2 produced were consistently lower in veins from varicosed patients. No differences were found in varicosed patients between various segments of the same vein, no matter whether macroscopically affected or unaffected. These results demonstrate that the cyclooxygenase pathway in the venous wall of subjects with varicosis is shifted toward lesser formation of PGI2 and higher production of proaggregatory and proinflammatory prostanoids such as PGE2 and TXA2. These biochemical changes may be relevant to inflammation and thrombogenesis in varicosis.     

Increased levels of prostaglandin D(2) suggest macrophage activation in patients with primary pulmonary hypertension.

STUDY OBJECTIVE: TXA(2) (thromboxane A(2)) is a lipid mediator believed to be produced primarily by platelets in normal subjects, although macrophages are capable of synthesis. There is increased production of TXA(2) in patients with primary pulmonary hypertension (PPH), which may reflect augmented production by macrophages. The objective of this study was to determine if macrophages are activated in PPH and whether they contribute to the increased production of TXA(2). STUDY TYPE: Case control. SETTING: University hospital. METHODS: We measured the urinary metabolites of three mediators that predominantly derive from different cell types in vivo: (1) TX-M (platelets and macrophages), a TXA(2) metabolite; (2) prostaglandin D(2) (PGD(2)) metabolite (PGD-M); and (3) N-methylhistamine (mast cells), a histamine metabolite, in 12 patients with PPH and 11 normal subjects. RESULTS: The mean (+/- SEM) excretion of both TX-M and PGD-M at baseline was increased in PPH patients, compared to normal subjects (460 +/- 50 pg/mg creatinine vs 236 +/- 16 pg/mg creatinine [p = 0.0006], and 1,390 +/- 221 pg/mg creatinine vs 637 +/- 65 pg/mg creatinine [p = 0.005], respectively). N-methylhistamine excretion was not increased compared to normal subjects. There was a poor correlation between excretion of TX-M and PGD-M (r = 0.36) and between excretion of PGD-M and methylhistamine (r = 0.09) in individual patients. CONCLUSION: In patients with PPH, increased levels of PGD-M, without increased synthesis of N-methylhistamine, suggest that macrophages are activated. The lack of correlation between urinary metabolite levels of TXA(2) and PGD(2) implies that macrophages do not contribute substantially to elevated TXA(2) production in patients with PPH. They may, however, have a role in the pathogenesis and/or maintenance of PPH, which warrants further investigation.     

非洛地平对高血压患者内皮功能的影响

目的　探讨高血压患者内皮血管活性物质的变化及非洛地平对其影响。方法　对 30例高血压患者和 2 4例正常对照组的血浆采用化学比色法测定 NO、NOS及采用射放免疫分析法测定 ET、Ang- 、TXA2 及 PGI2 ,并进行对照研究 ;对高血压组给予非洛地平治疗 ,并进行治疗前后的对照研究。结果　高血压组 ET、Ang- 及 TXA2 明显高于正常对照组 ,而 NO、NOS及 PGI2 明显低于正常对照组 ;非洛地平治疗组治疗后 ET、Ang- 及 TXA2 明显低于治疗前 ,NO、NOS及 PGI2 较治疗前无明显变化 ;非洛地平治疗高血压有效率 83.3%。结论　非洛地平抗高血压作用除主要通过拮抗钙通道以外 ,尚可通过降低 ET、Ang- 及 TXA2 起作用 ,而 NO通路不是其主要的作用机制。     

钙通道阻断剂与阿斯匹林对肺高压时肺小动脉壁增生的影响

本实验将新西兰大白兔的左肺动脉与降主动脉进行吻合,环束吻合口近端的左肺动脉,建立单侧动力性肺动脉高压模型。术后用药组兔给饮用大剂量心痛定与小剂量阿斯匹林,并定期测定血中内皮素、血栓素A2／PGI2的浓度变化。观察2－3个月后测肺动脉压及行肺组织病检,发现在形成左→右分流的肺高压兔中,用药组兔虽也行成了肺高压,但肺小动脉壁增生程度明显较肺高压对照组轻,用药组血浆中内皮素的峰值及血栓素A2／PGI2比值也较肺高压对照组低。提示钙阻滞剂＋阿斯匹林对肺高压时肺小动脉壁的增生有一定的抑制作用,此种作用可能与药物抑制内皮素及血栓素A2的生成及促进PGI2的形成有一定关系。     

Effect of intracardiac repair on biosynthesis of thromboxane A2 and prostacyclin in children with a left to right shunt.

OBJECTIVE--To investigate the effect of intracardiac repair on the abnormal biosynthesis of prostacyclin (PGI2) and thromboxane A2 (TXA2) in children with congenital heart disease and increased pulmonary blood flow. DESIGN--A prospective study with immunoaffinity chromatography and gas chromatography-mass spectrometry to measure the urinary excretion products of PGI2 (2,3-dinor-6-oxo-prostaglandin (PG) F1 alpha (2,3-dinor-6-oxo-PGF1 alpha)) and TXA2 (2,3-dinor-TXB2) before operation, in the first 12-24 h after operation, and at discharge from hospital. SETTING--A supraregional referral centre for patients with congenital heart disease. PATIENTS--15 patients aged 2 to 60 months (median 7 months) with a left to right shunt who underwent intracardiac repair. RESULTS--The preoperative 2,3-dinor-TXB2 excretion rate was greater than that found previously in a control group of 16 healthy children with a median (range) age of 24 (6-36) months (1159(201) v 592(122) ng/g creatinine in controls, P = 0.006). The excretion rate rose after operation to 9600(3832) ng/g creatinine (P = 0.01) and decreased before discharge to 1071(191) ng/g creatinine (NS), but remained greater than that of the control group (P = 0.014). Before operation 2,3-dinor-6-oxo-PGF1 alpha excretion rates were similar to those of the healthy children (482(68) v 589(95) ng/g creatinine in controls) but increased after operation to 19,668(11,162) ng/creatinine (P = 0.002) and fell at discharge to 1621(245) ng/g creatinine although this was higher than both preoperative and control rates (P = 0.005 and P = 0.0002 respectively). The preoperative ratio of 2,3-dinor-TXB2 to 2,3-dinor-6-oxo-PGF1 alpha excretion was greater than that of the control group (3.2(0.8) v 1.3(0.22) in controls, (P = 0.005)), decreased significantly after operation to 0.9(0.13) (P = 0.016), and changed little, to 0.7(0.12), before discharge. The last two ratios were similar to those in normal children and significantly lower than those before operation (P = 0.004). CONCLUSION--In children with a left to right shunt the ratio of the excretion rates of the metabolites of TXA2 and PGI2 was abnormal before operation, which favoured vasoconstriction and platelet aggregation, but had decreased at discharge from hospital. The increase in excretion of PGI2 metabolites over TXA2 metabolite after intracardiac repair augurs well for pulmonary vascular recovery.     

Ⅰ型肝肾综合征患者前列腺素I2和血栓素A2水平分析

目的 通过分析肝硬化腹水伴Ⅰ型肝肾综合征(HRS)患者的临床资料、实验室指标、前列腺素I2(PGI2)和血栓素A2(TXA2),探讨花生四烯酸代谢与Ⅰ型HRS发生的关系.方法 纳入肝硬化腹水伴Ⅰ型HRS患者38例(HRS组)及肝硬化腹水且肾功能正常患者50例(非HRS组),收集两组患者的一般资料和血液,分析肝肾功能、电解质、PGI2和TXA2水平.结果 HRS组和非HRS组的PGI2、TXA2、PGI2/TXA2水平分别为(32517±6023) pg/ml、(7432±2186) pg/ml、4.79 ±1.58和(29 597±3343) pg/ml、(5032 ±2104)pg/ml、7.50±2.38,HRS组TXA2水平高于非HRS组(t=2.385,P=0.027),而PGI2/ TXA2水平低于非HRS组(t=2.29,P=0.035),两组PGI2水平差异无统计学意义(t=1.233,P=0.23).结论 Ⅰ型肝肾综合征患者PGI2/TXA2比例失调,花生四烯酸代谢异常可能和Ⅰ型HRS发生有关.     

Relation of arachidonate metabolites to abnormal control of the pulmonary circulation in a child

To evaluate the role of arachidonate metabolites in regulating pulmonary vascular tone, we performed multiple studies on a 17-month-old girl with idiopathic pulmonary hypertension, systemic arterial hypoxemia (due to ventilation-perfusion mismatching), and an elevated thromboxane A2 (TXA2) to prostacyclin (PGI2) ratio due to increased TXA2 (measured as their stable metabolites, TXB2 and 6-keto-PGF1 alpha, respectively). Intravenous infusions of PGI2 reduced mean pulmonary arterial pressure (from 80 to 47 mmHg), increased cardiac output (from 3.43 to 3.97 L/min), increased systemic arterial oxygen saturation (from 60 to 72 percent), and decreased the TXB2 to 6-keto-PGF1 alpha ratio (from 5.9 to 0.2); mean systemic arterial pressure was unchanged. Pharmacologically decreasing the TXB2 to 6-keto-PGF1 alpha ratio with administration of nifedipine or diltiazem also reduced pulmonary hypertension and increased systemic arterial oxygen saturation in this patient. Nifedipine and diltiazem decreased the ratio by decreasing TXB2. Prostacyclin decreased the ratio by increasing 6-keto-PGF1 alpha. These studies support the hypothesis that the balance between TXA2 and PGI2 is an important influence on pulmonary vascular tone.     

Increased prostacyclin and thromboxane A2 biosynthesis in atherosclerosis.

It has been proposed that atherosclerotic arteries produce less prostacyclin (PGI2) than nonatherosclerotic arteries do, thereby predisposing arteries to vasospasm and thrombosis in vivo. We reexamined this concept by measuring spontaneous as well as arachidonate-induced PGI2 biosynthesis in aortic segments from nonatherosclerotic and cholesterol-fed atherosclerotic New Zealand White rabbits. Thromboxane A2 (TXA2) generation was also measured. Formation of PGI2, as well as TXA2, as measured by radioimmunoassay (RIA) of their metabolites, was increased in atherosclerotic aortic segments relative to nonatherosclerotic segments (P less than or equal to 0.05) at 0, 5, 10, 15, and 30 min of incubation with arachidonate. Pretreatment of arterial segments with indomethacin inhibited PGI2 as well as TXA2 formation, whereas pretreatment with the selective TXA2 inhibitor OKY-046 inhibited only TXA2 release, thus confirming the identity of icosanoids. To confirm the RIA data, aortic segments were incubated with [14C]arachidonate prior to stimulation with unlabeled arachidonate. The uptake of arachidonate was similar, but the release of incorporated [14C]arachidonate was significantly (P less than or equal to 0.05) greater in atherosclerotic segments than in nonatherosclerotic ones. Conversions of released [14C]arachidonate to 6-keto[14C]prostaglandin F1 alpha and [14C]thromboxane B2 were similar in the two types of aortic segments. Thus, synthesis of PGI2 as well as TXA2 is increased in atherosclerosis, and this alteration in arachidonate metabolism is related to increased release of arachidonate.     

Effects of a selective thromboxane synthetase inhibitor (OKY-046) in patients with coronary artery disease during exercise

We studied the levels of thromboxane B2 (TXB2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), platelet aggregability, beta-thromboglobulin and platelet factor 4 in 30 coronary artery disease (CAD) patients and 21 normal subjects during exercise. During treadmill exercise, 13 of 30 CAD patients reported chest pain. We administered a selective thromboxane synthetase inhibitor (OKY-046) for 2 weeks to 10 CAD patients with exercise-induced chest pain and studied its effects. At rest, the plasma TXB2 levels and platelet aggregation were significantly lower in normal subjects than in CAD patients, and there was no difference between CAD patients with and without exercise-induced chest pain. On treadmill testing, plasma TXB2 levels and platelet aggregation increased significantly only in the CAD patients with exercise-induced chest pain. Plasma 6-keto-PGF1 alpha levels in normal subjects were significantly higher than those in CAD patients both at rest and during exercise. After administration of OKY-046, mean exercise time increased significantly from 7.5 to 8.6 min (p less than 0.001). Plasma TXB2 level and platelet aggregation decreased significantly after OKY-046 administration both at rest and during exercise. These results suggest that a marked increase in TXA2, with only a minimal change in PGI2, during exercise may contribute to exercise-induced myocardial ischemia, and that OKY-046 is useful in the treatment of CAD patients.     

重症急性胰腺炎患者早期血液流变学及血管活性指标血栓素A2、前例环素I2水平变化

目的：观察重症急性胰腺炎（SAP）患者早期血液流变学指标及血栓素A2（TXA2）、前列环素I2（PGI2）的变化。方法2012年1月至2013年9月住院的32例SAP患者为SAP组,30例体检健康人为NC组。于患者入院后治疗前即静脉采血,平行检测血液流变学指标及血浆TXA2、PGI2水平,并计算TXA2、PGI2比值。结果比较进行t检验。结果 SAP组血液流变学中除红细胞变形指数低于NC组（t＝2．185,P＜0．05）外,全血高、中、低切黏度、血浆黏度高于NC 组（t＝2．820、2．755、2．700、3．622,P＜0.05）,全血高切还原黏度、全血低切还原黏度高于NC组（t＝3．391、2．018,P＜0．05）,红细胞压积、红细胞刚性指数、红细胞聚集指数高于NC组（t＝2．980、2.209、2.004,P＜0．05）、全血高切相对指数、全血低切相对指数高于NC组（t＝2.630、2．440,P＜0．05）;SAP组TXA2、PGI2、TXA2、PGI2比值高于NC组（t＝3．256、2.589、2.640,P＜0．05）。结论 SAP患者早期即存在血液流变性异常及血管内皮细胞活性增高。     

Drug modulation of thromboxane A2/prostacyclin balance and lipid peroxidation in patients with coronary artery disease

Sixty patients with coronary artery disease (CAD) were investigated in a randomized, placebo-controlled study. Therapeutic dose of diltiazem markedly inhibited the production of whole blood thromboxane A2(TXA2), but had no effect on the production of prostacyclin(PGI2). Both aspirin 20mg/d and diltiazem plus aspirin had marked inhibitive effects on both TXA2 and PGI2. The order of potency of the three regimens in decreasing TXA2/PGI2 ratio was diltiazem plus aspirin greater than diltiazem greater than aspirin. Diltiazem, aspirin and combination of both all decreased significantly serum lipid peroxides level, but had no effect on serum superoxide dismutase concentration. The results indicate that both therapeutic dose of diltiazem and low-dose of aspirin may modulate TXA2/PGI2 balance and inhibit lipid peroxidation in CAD and that the combination of both drugs may result in best therapeutic effect.     

急性心肌梗死患者血脂与前列环素、血栓素相关性的研究

目的 本试验观察了140例正常人及80例急性心肌梗死(AMI)患者的血脂水平和PGI2(前列环素)、TXA2(血栓素)的稳定代谢产物6-Keto-PGFla、TXB2及T/P水平的变化,并对AMI患者中血脂各项和6-Keto-PGFla、TXB2及T/P进行相关分析,结果显示:AMI患者的TC、TG、LDL、APOB、6-Keto-PGFla、TXB2水平高于正常人,而HDL、APOAI、T/P水平低于正常人(P<0.05),单因素相关分析表明:AMI患者的6-Keto-PGFla与TC、LDL显著相关(P<0.05)、6-Keto-PGFla、TXB2与LP(a)显著相关(P<0.05)。提示:AMI患者的血脂、PGI2、TXB2之间有一定的相关关系,表明冠心病、急性心梗的发病机制的两大学说——血脂沉积学说和血小板聚集血栓形成学说之间可能有些内在联系。     

Protective action of endogenous prostacyclin (PGI2) and prostaglandin E2 (PGE2) in endoscopic polypectomy-induced human ulcers

To assess how endogenous prostaglandin (PG) in gastric mucosa acts against ulcer formation, we determined the mucosal prostacyclin (PGI2), PGE2, PGF2 alpha, and thromboxane A2(TXA2) concentrations before and after polypectomy in 6 patients in whom gastric ulcers were produced by electric burning resection of gastric polyps. These artificially induced ulcers all healed within short periods (25.7 +/- 7.4 days, mean +/- SE). Of the PGs assayed, the level of PGI2 was highest. The pG levels were increased at 4 and 7 days post-polypectomy; the most remarkable increase took place in the mucosa along the ulcer margin rather than the mucosa far from the ulcer site. We suggest that the observed increase in endogenous PGs represents a physiological response against polypectomy-induced ulcer formation.     

Allergic sensitization in elderly patients with chronic obstructive pulmonary disease

To study whether allergic sensitization occurs in elderly patients with chronic pulmonary obstructive disease (COPD), we examined serum IgE and skin test reactivity to allergens in three age-matched groups of normal subjects, and in patients with COPD and bronchial asthma (BA). Serum IgE was significantly higher in patients with COPD and BA than in normal subjects (p less than 0.05), and patients with COPD showed serum IgE levels as high as those of patients with BA. However, the skin test scores were significantly higher in patients with BA than in normal subjects and patients with COPD (p less than 0.05). Neither serum IgE nor skin test score significantly correlated with FEV1%, PaO2, PaCO2 or Brinkman's Index in any group (p greater than 0.20). These results suggest that allergic sensitization occurs in elderly patients with COPD and that symptoms associated with COPD may be partly due to allergic inflammation.     

Plasma calcitonin gene-related peptide (CGRP) level in patients with essential hypertension

Calcitonin gene-related peptide (CGRP) is a 37-amine acid bioactive polypeptide and known to be a powerful vascular relaxant. CGRP was measured in 45 cases with essential hypertension (EH). The results suggested that plasma CGRP level in patients with EH was lower than that in normal subjects (P less than 0.001). It was found that decrease of plasma CGRP was closely related with the severity of hypertension. However, the level of plasma atrial natriuretic factor (ANF) in EH patients was significantly increased as compared with normal subjects (P less than 0.01). A negative correlation between plasma CGRP and ANF (r = -0.3615, P less than 0.02) was found. These data suggested that decrease of plasma CGRP may play an important role in the pathogenesis of hypertension.