促红细胞生成素导致高血压的临床研究

通过对４０例不同年龄、不同病因的尿素症维持性血透患者，应用不同剂量的促红素治疗，观察血色素、血粘度、血浆肾素、血管紧张素、心排出量、外周血管阻力以及血变化等临床指标，发现促红素肾性贫血的疗效为９０％，但高血压的发生也达３７．５％。高血压的发生与促红素的剂量、患者的年龄，以往有无高血压等有关。高血压发生的时间大部分随着血色素的增加而增高，但少数与此无关。     

Lisinopril对老年原发性高血压的疗效及安全性

Lisinopril是一种新的长效血管紧张素转换酶抑制剂,已被证实治疗高血压病有效,预料将广泛用于老年高血压的治疗。老年原发性高血压患者总外周血管阻力常增加,血管内容量减小,血浆肾素浓度降低。上述因素常使医生采用利尿剂或钙拮抗剂治疗老年高血压。只有在肾素浓度正常或增高时,才考虑使用血管紧张素转换酶抑制剂。但最近的研究对这一概念提出了异议,已经证实,血管紧张素转换酶抑制剂如巯甲丙脯酸(Captopril)、羧苯丙丙脯酸(Enalapril)、Enalaprilat对老年高血压,包括血浆肾素浓度降低者的疗效。本文回顾性分析     

老年原发性高血压患者动态血压参数与部分体液因素的相关性研究

目的观察老年原发性高血压患者动态血压参数与血浆肾素、血管紧张素Ⅱ及醛固酮的相关性及其临床意义。方法将162例患者分为A纽82例（〉60岁）,B组80例（〈60岁）,采用放射免疫法检测162例原发性高血压患者的血浆肾素、血管紧张素Ⅱ及醛固酮水平,同时测定24h动态血压,进行相关分析。结果（1）老年高血压具有是脉压增大,波动性大,晨峰高血压现象及并发症多的特点;（2）A组血浆肾素、血管紧张素Ⅱ及醛固酮水平明显高于B组;（3）血浆肾素、血管紧张素Ⅱ及醛固酮与老年高血压的特点,特别是脉压增大、波动性大、晨峰高血压现象有关。结论老年原发性高血压患者血浆肾素和血管紧张素Ⅱ浓度升高,提示血浆肾素、血管紧张素一醛固酮系统对老年原发性高血压心血管系统有影响,导致老年原发性高血压患者血压特征性的变化,血浆肾素、血管紧张素Ⅱ和醛固酮的测定可作为老年原发性高血压患者病情监测及治疗指标之一。     

慢性心力衰竭时应用小剂量巯甲丙脯氨酸(Captopril)的即期血液动力学效应和长期治疗

心力衰竭时体循环血管阻力及血浆容量的增加与肾素-血管紧张素-醛固酮系统的活性有关。在心力衰竭患者,静脉给于 teprotide 或口服巯甲丙脯氨酸以抑制血管紧张素转换酶能增加心排出量及降低左室充盈压。长期应用巯甲丙脯氨酸似能对改善症状和血液动力学。但这些研究均系使用大剂量巯甲丙脯氨酸(25～150毫克),其血液动力学的改善常伴有体循环低血压。本文报道小剂量巯甲丙脯氨     

肾性高血压大鼠血浆中降钙素基因相关肽与血管紧张素Ⅱ浓度及肾素活性的变化

降钙素基因相关肽与肾素－血管紧张素系统均参与血压的调节。在两肾一夹型肾性高血压大鼠模型，观察大鼠血浆中的降钙素基因相关肽、血管紧张素Ⅱ浓度及肾素活性的水平，以及用氯沙坦或培哚普利干预后这些活性肽在血浆中的变化，进一步分析这些血管活性肽在该模型的变化机制。研究显示，高血压组血浆中降钙素基因相关肽的浓度高于对照组，而血管紧张素Ⅱ与对照组相比无显著差异。用氯沙坦和培哚普利治疗6周后，血浆中肾素活性和血管紧张素Ⅱ及降钙素基因相关肽水平均升高。本研究发现在肾性高血压中期，循环中肾素－血管紧张素系统对血压的影响已不是主要因素，降钙素基因相关肽的释放增加可能是血压升高的代偿作用。应用氯沙坦和培哚普利后可增加血浆中血管紧张素Ⅱ浓度和肾素活性，同时也增加降钙素基因相关肽的合成与释放，这可能对其降压起一定的作用。     

原发性高血压患者年龄与血浆肾素-血管紧张素-醛固酮系统的关系

目的：探讨原发性高血压（EH）患者年龄与血浆肾素－血管紧张素－醛固酮（RAS）系统的关系。方法i200例EH患者按年龄分为5组,测定其血浆RAS含量,并进行统计学分析。结果：随着年龄的增加,血浆肾素（PRA）、血管紧张素II（AngⅡ）含量降低（P均〈0．05）,醛固酮（ALD）含量无明显变化（P〉0．05）。直线相关分析表明年龄与PRA,AngⅡ含量呈负相关（r=－0．283,P〈0．001,r=－0．165,P〈0．05）,年龄与脉压呈正相关（r=0．293,P〈0．001）。结论：随着年龄的增加,肾素－血管紧张素分泌减少,醛固酮与肾素呈分离现象。     

肾性高血压大鼠血浆中降钙素基因相关肽与血管紧张素Ⅱ浓度及肾素活性的变化

降钙素基因相关肽与肾素-血管紧张素系统均参与血压的调节.在两肾一夹型肾性高血压大鼠模型,观察大鼠血浆中的降钙素基因相关肽、血管紧张素Ⅱ浓度及肾素活性的水平,以及用氯沙坦或培哚普利干预后这些活性肽在血浆中的变化,进一步分析这些血管活性肽在该模型的变化机制.研究显示,高血压组血浆中降钙素基因相关肽的浓度高于对照组,而血管紧张素Ⅱ与对照组相比无显著差异.用氯沙坦和培哚普利治疗6周后,血浆中肾素活性和血管紧张素Ⅱ及降钙素基因相关肽水平均升高.本研究发现在肾性高血压中期,循环中肾素-血管紧张素系统对血压的影响已不是主要因素,降钙素基因相关肽的释放增加可能是血压升高的代偿作用.应用氯沙坦和培哚普利后可增加血浆中血管紧张素Ⅱ浓度和肾素活性,同时也增加降钙素基因相关肽的合成与释放,这可能对其降压起一定的作用.     

心血管病患者血浆肾素、血管紧张素Ⅱ和醛固酮的变化

心血管病患者血浆肾素、血管紧张素Ⅱ和醛固酮的变化李智培采用放射免疫法测定２１６例心血管病患者血浆肾素活性（ＰＲＡ）、血管紧张素Ⅱ（ＡⅡ）和醛固酮（ＡＬＤ）浓度变化，并对其临床意义初步探讨。对象与方法２１６例住院心血管病患者，男１４１例，女７５例，年龄...     

血浆肾素-血管紧张素系统与原发性高血压病的关系评价

目的探究肾素-血管紧张素系统与原发性高血压病的关系。方法选取自2015年以来我院收治的原发性高血压患者50例,其中高血压1级患者18例,2级患者17例,3级患者15例,同时随机选取50例正常健康体检者作为对照,采用放射免疫方法测定所有患者立位、卧位的血浆肾素活性、醛固酮浓度以及血管紧张素浓度,记录并作出比较。结果原发性高血压患者的立位、卧位血浆肾素活性均低于对照组,而立位、卧位的血浆醛固酮浓度以及血管紧张素浓度要高于对照组,并且随着病情的发展,这种差距逐渐增大,差异具有统计学意义(P0.05)。结论肾素-血管紧张素系统与原发性高血压有很密切的关系,其中的指标如血浆肾素活性、血管紧张素浓度、醛固酮浓度等可以作为原发性高血压并诊断、分型及分级的有效指标,同时血浆中的血管紧张素及醛固酮含量的降低也应该作为治疗原发性高血压的重要因素受到临床的重视。     

口服血管紧张素转化酶抑制剂对慢性心力衰竭的即时与持续血液动力学和临床改善

在心力衰竭伴心排出量低下的患者,全身血管阻力常增高。血管扩张剂能降低全身血管阻力,从而改善急性或慢性心力衰竭病人的心功能。在低心排出量心力衰竭时,肾素-血管紧张素系统被激活,血     

Normal renin uremic hypertension. Study of cardiac hemodynamics, plasma volume, extracellular fluid volume, and the renin angiotensin system.

Studies were undertaken in 33 uremic patients with or without hypertension, 11 normal subjects, and 15 essential hypertensive patients to assess cardiac hemodynamics, plasma volume, extracellular fluid volume, and peripheral renin levels. Cardiac output and intraarterial blood pressure were measured and peripheral vascular resistance index calculated. These studies suggest that uremic hypertension with normal renin values and hypervolemia is hemodynamically sustained by an increase in peripheral resistance rather than by an increased cardiac output. The renin angiotensin system plays a secondary role as compared to overexpansion in the genesis of hypertension in normoreninemic uremic hypertension.     

Follow-up of Renin in Essential Hypertension

Summary: Follow-up of renin in essential hypertension.
In a prospective study of patients with essential hypertension, plasma renin levels showed a progressive increase with longer follow-up. This was associated with a parallel increase in renal vascular resistance. Arterial blood pressure and plasma volume did not change significantly during follow-up. In patients where the hypertension was complicated by myocardial infarction there was a comparatively greater increase in renin levels and renal vascular resistance which may be attributable to chronic reduction of cardiac output.     

Regional hemodynamics after chronic nitric oxide inhibition in spontaneously hypertensive rats

BACKGROUND: Inhibition of nitric oxide (NO) synthase by L-arginine analogs is associated with elevation of blood pressure in rats. Because endothelium-dependent vasomotion in different vascular beds is not homogenous, the aim of this study was to characterize and compare regional hemodynamic responses in carotid, femoral, and renal vascular beds after chronic NO inhibition in spontaneously hypertensive rats. The possible role of circulating endothelin and renin angiotensin systems in mediating the effects of chronic NO inhibition was also studied. METHODS: Systemic and regional hemodynamics, left ventricular mass, plasma renin activity, and plasma endothelin-1 were determined in control and Nomega-nitro-Larginine methyl ester (L-NAME)-treated (10 mg/kg/day, 4 weeks) spontaneously hypertensive rats. RESULTS: L-NAME treatment increased arterial pressure and total peripheral and regional vascular resistance and decreased cardiac output, stroke volume, and regional blood flow. An increase in blood flow ratio and a decrease in vascular resistance ratio between carotid and renal as well as femoral and renal vascular beds in rats treated with L-NAME was found. Blood flow and vascular resistance ratios between femoral and carotid vascular beds remained unchanged. L-NAME increased plasma renin activity and left ventricular weight/body weight ratio, whereas plasma endothelin-1 was not modified. CONCLUSIONS: The results of this study showed that the renal circulation seemed to be more sensitive to the effects of chronic NO inhibition than carotid and femoral vascular beds. Simultaneous activation of the renin angiotensin system may further potentiate cardiovascular effects of chronic NO inhibition. No evidence that circulating endothelin-1 plays a role in this model of hypertension was found.     

Relation of renin status to neurogenic vascular resistance in borderline hypertension.

The relation of renin-angiotensin status to general hemodynamics and to neurogenic vascular resistance was studied in patients with border-line hypertension. Plasma renin activity during standing was referred to a standard renin-urinary sodium nomogram derived from 18 normal subjects. Among 22 patients with borderline hypertension the renin level was high in 8, low in 4 and within normal limits in the remaining 10. In patients with borderline hypertension and high or normal levels of plasma renin activity, the blood pressure elevation was due to increased total peripheral vascular resistance. In contrast, in patients with low renin borderline hypertension, total peripheral resistance was not significantly elevated; the blood pressure elevation reflected a cardiac index 12 percent higher than that in normal subjects. The neurogenic contribution to total peripheral vascular resistance was assessed by studying the effects of alpha adrenergic blockade with phentolamine, after prior autonomic blockade of the heart with atropine (0.04 mg/kg body weight) and propranolol (0.2 mg/kg). Phentolamine (15 mg) produced an immediate reduction in total peripheral resistance of 12.0 +/- 6.7 percent in patients with high renin borderline hypertension (P less than 0.01) but no change in normal subjects or those with borderline hypertension and normal or low renin levels. Normalization of the blood pressure followed "total" autonomic blockade with atropine, propranolol or phentolamine only in patients with high renin borderline hypertension. It is concluded from these preliminary data that in high renin borderline hypertension the blood pressure elevation is sustained by neurogenic mechanisms. The elevated renin level in these patients is probably an expression of increased sympathetic nervous activity. Although the elevated plasma renin level may possibly be contributing to the generation of higher sympathetic tone, or data do not support a direct role of circulating angiotensin in the maintenance of the elevated vascular resistance.     

Renal and systemic effects of enalapril in chronic one-kidney hypertension

We have investigated the role of angiotensin II in the development of high blood pressure and in the maintenance of renal function during 2 weeks of one-kidney renal artery stenosis in conscious dogs. Responses to a fixed degree of inflation of a balloon cuff around the renal artery were compared in dogs with or without continuous enalapril (MK 421) treatment. In six untreated dogs, mean aortic pressure was increased by 17.1 +/- 2.0 mm Hg, due primarily to increases in total peripheral resistance with little change in cardiac output, while glomerular filtration rate, renal blood flow, renal artery pressure, and plasma renin activity were back to prestenosis levels. In seven enalapril-treated dogs mean aortic pressure was increased by 23.0 +/- 2.7 mm Hg and was not significantly different from that occurring in untreated dogs. This rise was due to increases in total peripheral resistance (10%) and cardiac output (12%). In the absence of angiotensin II, glomerular filtration rate remained low, at only 56 +/- 6% of prestenosis levels. Renal blood flow returned to normal, but the renal artery pressure remained 25% lower than control values. Thus, the main role of angiotensin II in chronic one-kidney Goldblatt hypertension does not appear to be through its pressor properties but rather through its actions in the kidney to preserve glomerular filtration. This effect on renal function persisted throughout the course of the hypertension, even when the plasma renin levels returned to normal.     

Effects of a single administration of captopril on hemodynamics and serum angiotensin converting enzyme activity, plasma renin activity and plasma aldosterone concentration in hypertensive patients

Hemodynamic responses and behaviors of the renin-angiotensin-aldosterone system to a single administration of captopril (50 mg) were studied in 16 hypertensive patients (essential hypertension, n = 10; renovascular hypertension, n = 3; primary aldosteronism, n = 2; Cushing's syndrome, n = 1). In 10 essential hypertensive patients, the immediate blood pressure reduction caused by decreased total peripheral resistance after the administration of captopril was observed without changes of cardiac output and heart rate. Serum angiotensin converting enzyme activity and plasma aldosterone concentration significantly decreased, whereas plasma renin activity significantly elevated 2 hours after the administration of captopril. The close relationship between the pretreatment value of plasma renin activity and the maximum decrease in mean blood pressure in 16 hypertensive patients suggests that the depressor response to a single administration of captopril could evaluate the degree of angiotensin II dependency in the maintenance of high blood pressure in various types of hypertension.     

Systemic and renal effects of a new angiotensin converting enzyme inhibitor, benazepril, in essential hypertension

Seventeen essential hypertensive patients with normal renal function were treated with a new non-sulphydryl orally active angiotensin converting enzyme (ACE) inhibitor, benazepril, 10 mg given once or twice daily, according to diastolic blood pressure levels, for 6 weeks. In all patients, changes in blood pressure, systemic and renal hemodynamics, plasma renin activity and urinary aldosterone and albumin excretions were assessed at the end of a 2-week placebo run-in period and at the end of the study. Benazepril monotherapy controlled blood pressure well. No changes in cardiac output, heart rate or stroke volume were observed, while peripheral vascular resistance was significantly decreased (-11%, P less than 0.05). Plasma volume was unaltered. The glomerular filtration rate was stable, but effective renal plasma flow was increased because of the marked reduction in renal vascular resistance (-35%) and, therefore, the filtration fraction was decreased. Urinary albumin excretion remained unchanged. A significant increase in plasma renin activity (P less than 0.001) and a decrease in urinary aldosterone excretion were seen. No side effects were observed during the treatment period. In conclusion, our results suggest that benazepril alone is an effective antihypertensive agent in patients with essential hypertension. The blood pressure lowering effect is due mainly to systemic vasodilation and is observed up to 24 h after administration of the drug. The vasodilation appears to be more consistent in the renal than in the systemic circulation.     

Systemic and coronary hemodynamic effects of pinacidil in awake normotensive and hypertensive dogs

We studied the systemic and coronary hemodynamic effects of a new antihypertensive agent, pinacidil, in nine morphine-sedated chronically instrumented dogs with one-kidney renal hypertension and eight similarly treated sham-operated normotensive dogs. The renal hypertensive dogs exhibited higher mean aortic blood pressure, total peripheral vascular resistance, and plasma renin activity before pinacidil administration than the sham-operated animals. The renal hypertensive dogs also had a lower left ventricular norepinephrine content, but the two groups did not differ significantly in plasma norepinephrine levels, cardiac output, or heart rate. Pinacidil decreased mean aortic pressure and total peripheral vascular resistance and increased cardiac output and heart rate in both groups. The changes in aortic pressure, total peripheral vascular resistance, and cardiac output were similar between the two groups, but the increase in heart rate was attenuated in renal hypertension. The peak rate of rise of left ventricular pressure (dP/dt), the ratio of left ventricular dP/dt and the developed pressure during isovolumic contraction (dP/dt/P), myocardial oxygen consumption, and plasma norepinephrine levels increased after pinacidil administration in the sham-operated dogs, but did not change in the renal hypertension group. The two groups did not differ in their responses of left ventricular dP/dt to intravenous isoproterenol. Pinacidil also caused coronary vasodilation in both groups, as evidenced by an increase in coronary blood flow and decreases in coronary vascular resistance and myocardial oxygen extraction. The decrease in myocardial oxygen extraction was similar in the two groups, but the increase in coronary blood flow was significantly less (p less than 0.05), probably because of the absence of an increase in myocardial oxygen consumption in the renal hypertensive dogs.(ABSTRACT TRUNCATED AT 250 WORDS)     

Disparate cardiovascular effects of obesity and arterial hypertension

Since obesity and essential hypertension frequently coexist, a study was designed to analyze some of their cardiovascular effects. Twenty-eight obese patients, half of whom were normotensive and half with established hypertension, were matched for mean arterial pressure with 28 corresponding lean subjects. Systemic and renal hemodynamics, intravascular volume, plasma renin activity, and circulating catecholamine levels were measured. Obese patients had increased cardiac output (p less than 0.001), stroke volume (p less than 0.001), central blood volume (p less than 0.02), plasma and total blood volume (p less than 0.01), and decreased total peripheral resistance (p less than 0.001). In contrast, cardiac output, central blood volume, and stroke volume of hypertensive patients were normal, but they had increased total peripheral (p less than 0.001) and renal vascular resistance (p less than 0.001) and a contracted intravascular volume. Left ventricular stroke work was elevated to a similar level in obesity (p less than 0.001) and hypertension (p less than 0.02), but the increase was caused by an expanded stroke volume in the former and by an increase in systolic pressure in the latter. It is concluded that the disparate effects of obesity and hypertension on total peripheral resistance and intravascular volume counteract and may even offset each other. Thus, obesity may mitigate the effects of chronically elevated total peripheral resistance (and therefore end-organ damage) in essential hypertension. Since both entities affect the heart through different mechanisms, their presence in the same patient results in a double burden to the left ventricle, thereby gently enhancing the long-term risk of congestive failure.     

Hemodynamic changes by recombinant erythropoietin therapy in hemodialyzed patients

Recombinant human erythropoietin therapy was given to 15 patients undergoing long-term hemodialysis with normal cardiac function. None of the patients had hypertension before the erythropoietin therapy and had received no antihypertensive agents. Before and after the erythropoietin therapy M-mode and pulsed Doppler echocardiographic studies, measurements of plasma volume by radioiodinated human serum albumin, and measurements of atrial natriuretic factor were carried out. After 6 weeks of erythropoietin therapy, hematocrit increased from 20.0 to 33.0%. Cardiac output, stroke volume, left ventricular diastolic dimensions, and left ventricular wall stress were all significantly decreased. Total peripheral resistance, interventricular septal thickness, and left ventricular posterior wall thickness were significantly increased. In Doppler echocardiographic studies, the mean velocity of aortic ejection flow and left ventricular acceleration time were decreased. The blood volume derived from plasma volume and hematocrit was not changed, whereas plasma atrial natriuretic factor concentration was significantly decreased. These data suggest that recombinant human erythropoietin administration suppressed the hyperdynamic cardiac state that was required to maintain oxygen delivery to the peripheral tissues in severe uremic anemia.