Angiotensin. II. Important role in the maintenance of arterial blood pressure

An angiotensin II antagonist, [1-sarcosine, 8-alanine]-angiotensin II, was given intravenously to anesthetized dogs with thoracic caval constriction and ascites to investigate the role of angiotensin II in the control of arterial pressure. The antagonist produced a striking fall in arterial pressure and in aldosterone secretion and an accompanying increase in plasma renin activity. In a control experiment, normal anesthetized dogs were given the angiotensin analog, but it failed to reduce arterial pressure or to influence plasma renin activity. In conscious dogs with caval constriction, the antagonist produced essentially the same drop in arterial pressure as observed in anesthetized animals. These results suggest an important role for angiotensin II in the maintenance of arterial pressure by its action on specific receptor sites in arteriolar smooth muscle and in the adrenal cortex.     

Inhibition of angiotensin conversion in experimental renovascular hypertension

Constriction of the renal artery and controlled reduction of renal perfusion pressure is followed by a prompt increase in systemic renin activity and a concomitant rise in blood pressure in trained, unanesthetized dogs. The elevated blood pressure induced by the renal artery stenosis can be prevented by prior treatment with the nonapeptide Pyr-Trp-Pro-Arg-Pro-Gln-Ile-Pro-Pro, which blocks conversion of angiotensin I to angiotensin II. Further, the nonapeptide can restore systemic pressure to normnal in the early phase of renovascular hypertension. These results offer strong evidence that the renin-angiotensin system is responsible for the initiation of hypertension in the unilaterally nephrectomized dog with renal artery constriction.     

Neurogenic Component of Chronic Renal Hypertension

Infusion of angiotensin or renin in small quantities affects the sympathetic nervous system so that responses are increased to either drugs or reflexes that cause release of norepinephrine at nerve endings. Response to injected norepinephrine is relatively unchanged. This action of angiotensin is dependent upon an intact sympathetic nervous system. The direct vasoconstrictor action of angiotensin is not an essential part of the enhanced response. The phenomenon was shown to have relevance to acute and chronic experimental renal hypertension in dogs by the fact that in both the pressor response to tyramine was enhanced. We believe that the ability of angiotensin to intensify the effect of normal neurogenic vasomotor activity, along with an upward reset of the carotid sinus buffer mechanism, might account importantly for the neurogenic component of renal hypertension.     

A new, long-lasting competitive inhibitor of angiotensin

An analog of angiotensin II, [Sar(1), Ile(8)]-angiotensin II, has a potent and long-lasting competitive antagonistic effect against angiotensin II when tested for its myotropic action on the isolated rabbit aorta and for its effect on blood pressure in anesthetized cats and dogs. Compared to [Ile(8)]-angiotensin II, the new analog has equal antagonistic potency on the isolated system but a much greater potency in vivo. It is assumed that sarcosine in position 1 protects the peptide against enzymatic degradation and enhances its half-life. This study demonstrates that the modification in both positions 1 and 8 are important for the in vivo antagonistic potencies of angiotensin analogs.     

安氟醚对犬心血管和呼吸系统的影响

研究了不同浓度的安氟醚对12只健康犬心血管、呼吸系统等的影响。结果显示,随着吸入浓度的升高,血压明显下降;平均动脉压与吸入浓度有高度相关性(r=0.7790)。只有在深麻醉时(1.5MAC),心率才趋于减慢。随吸入浓度增加,呼吸频率减慢,从而导致每分通气量显著减少和 PaCO_2升高。实验表明,安氟醚麻醉平稳,苏醒期短,各项生理值恢复快。作者认为,吸入1.0MAC 安氟醚为手术麻醉的理想浓度。     

Hypertension of renal origin: evidence for two different mechanisms

Antibody to angiotensin 11, or a specific peptide competitive inhibitor of angiolensin II, was used to investigate the role of the renin-angiotensin system in two types of renal hypertension in rats. The data indicate that angiotensin II is in fact critically involved in the pathogenesis of the form of renal hypertension in which one renal artery is clamped and the contralateral kidney is left in place, but that it probably plays no significant role in the maintenance of experimental renal hypertension in which the opposite kidney has been removed.     

BRADYKININ: VASCULAR RELAXANT, CARDIAC STIMULANT

Bradykinin infusion causes an increase in cardiac output in rats whether the autonomic nervous system is blocked or not. After autonomic blockade, bradykinin causes a lesser decrease in the total peripheral resistance but a greater increase in cardiac output, resulting in an elevation of arterial pressure. The increase in cardiac output is caused by a small increase in heart rate and a substantial increase in stroke volume. The fact that these increases are observed after autonomic blockade suggests that bradykinin increases cardiac output by direct stimulation of the heart.     

Intrarenal formation of angiotensin I

In 5 patients and 16 dogs the mean concentration of angiotensin I, but not II, was higher in the plasma of the renal vein than in the plasma of the renal artery. The fact that I was higher in the vein than in the artery supports the concept that I is formed in the renal vasculature. In the vein the mean concentration of I was 45 times higher than that of II. The probable formation of angiotensin I within the kidney and its high concentration in the renal vein suggest that if the renin angiotensin system plays a role in the regulation of intrarenal blood flow, then angiotensin I may be the major effector hormone in this process.     

Adaptation of cardiac output to peripheral runoff studied in intact dogs

A pump with sinusoidal piston movement was connected to the abdominal aorta of intact anesthetized dogs, causing slow oscillations of arterial blood pressure. Evidence was found for the existence of a mechanism which enables the heart to adjust its output immediately to changes of peripheral outflow.     

Physiological role of silent receptors of atrial natriuretic factor

A ring-deleted analog of atrial natriuretic factor--des[Gln18, Ser19, Gly20, Leu21, Gly22] ANF4-23-NH2 (C-ANF4-23)--binds with high affinity to approximately 99% of ANF receptors in the isolated perfused rat kidney. In this preparation, C-ANF4-23 is devoid of detectable renal effects and does not antagonize any of the known renal hemodynamic and natriuretic actions of biologically active ANF1-28. In contrast, both C-ANF4-23 and ANF1-28 increase sodium excretion and decrease blood pressure in intact anesthetized rats. This apparent contradiction is resolved by the finding that the ring-deleted analog markedly increases plasma levels of endogenous immunoreactive ANF in the rat. The results show that the majority of the renal receptors of ANF are biologically silent. This new class of receptors may serve as specific peripheral storage-clearance binding sites, acting as a hormonal buffer system to modulate plasma levels of ANF.     

Mechanism and prevention of fixed high vascular resistance in autografted and allografted lungs

The fixed vascular resistance observed in tranisplanted Ilunlgs and attriblted to denervation can be avoided by angioplastic wideniing of the pulmonary artery anastotosis. With distenisible arterial anrastomoses, aultografted an, d allografted Ilunzgs vasodilate niormzally with inicreased flow and cani sutstaini dogs whose contralateral pulmonary artery is ligated imumediately after lutng transplanitation.     

Angiotensin-sodium interaction in blood pressure maintenance of renal hypertensive and normotensive rats

A specific inhibitor of angiotensin II was used in rats to investigate whether angiotensin is involved in the maintenance of blood pressure in one-kidney Goldblatt hypertension, in which plasma renin levels are not usually increased. The inhibitor produced marked falls in blood pressure, often down to normal levels in the hypertensive animals only when they were depleted in sodium and not after sodium repletion. Much lesser but still significant falls in blood pressure were also produced in normotensive sodium-depleted rats but not in repleted rats. We conclude that the importance of angiotensin for maintaining blood pressure is largely determined by its relation to available sodium or fluid volume, since the renin component in maintenance of either the hypertensive or the normotensive state could be exposed only by sodium deprivation. Therefore, volume expansion per se or other pressor factors may be involved in maintaining blood pressure of these sodium-replete normotensive or hypertensive animals.     

高钠饲料引起的肉鸡腹水、右心衰竭、肺动脉高压和肺小动脉肌型化研究

随机抽取30羽饲料钠离子过量所致的腹水综合征(AS)自然患鸡和30羽同种、同龄健康AA肉鸡,用生理学和组织形态学方法对患AS肉鸡和健康肉鸡肺动脉压和肺微细动脉结构变化进行定量检测和比较分析,结果显示:饲料钠离子过量显著增加了肉鸡AS的发病率、右心室与全心室重量比(RV/TV)、平均肺动脉压(mPAP)、肺末梢厚壁血管百分率(%TWPV)和肺微细动脉管壁平均中膜厚度(mMTPA)(P<0.05).从而揭示了饲料钠离子过量性AS患鸡发生了以肺微细动脉管壁增生肥厚为主要特征的肌型化和肺动脉高压.     

Hypertension in the recently weaned Dahl salt-sensitive rat despite a diet deficient in sodium chloride

The Dahl rat is used as a model of hypertension that is "sensitive" to dietary salt (sodium chloride, NaCl). When dietary salt is supplemented in the Dahl rat, the arterial blood pressure of the "salt-sensitive" strain (S) becomes much greater than that of the "salt-resistant" strain (R). It has been widely reported that arterial blood pressure of the young Dahl S rat is not greater than that of the young Dahl R rat before dietary salt is supplemented. In the present study, however, mean arterial pressure directly measured in unanesthetized, unrestrained S rats was greater than in R rats, both when they had been recently weaned and for at least 10 weeks thereafter, despite their having been fed a diet frankly deficient in salt. In weanling S rats, the ratio of heart weight to body weight was also significantly greater than that in weanling R rats, suggesting that the greater blood pressure in the S rat causes cardiac hypertrophy. Thus, biologic differences demonstrated between the S rat and the R rat after weaning, including the phenomenon of salt-sensitivity, could be a consequence of, or be dependent on, an already extant difference in arterial blood pressure between the two strains.     

Blood pressure control--special role of the kidneys and body fluids

The arterial pressure of the adult human rarely deviates from normal by more than 10 to 15 percent during each day. To achieve such constancy, the body has a network of pressure control systems. Several are based on neural receptors that respond within seconds to help correct any abnormal pressure. The activities of these systems are followed within minutes by activation of hormonal controllers. Within hours or days, a kidney pressure control system is induced that increases body fluid volume when the pressure falls (or decreases the volume when the pressure rises). This kidney-fluid system is the dominant method of establishing long-term pressure control.     

Angiotensin pressor inhibition by aldosterone in the rabbit

Rabbits pretreated with aldosterone exhibited lessened response to the pressor agent angiotensin. This observation may help to explain the absence of hypertension in certain instances in which both the formation of angiotensin and the secretion of aldosterone are above normal.     

基于灰色神经网络的换热器污垢预测研究

由于影响换热器污垢热阻的因素较为复杂,对其预测比较困难.针对这种情况,提出了利用灰色神经网络预测方法对污垢热阻进行预测.本文用一种灰色理论算法改进模型和RBF神经网络分别对换热器污垢热阻值进行预测,并对预测结果进行最优组合,同时给出了预测曲线.结果表明与GM（1,1）模型相比较,灰色神经网络组合模型（GMNN）预测精度更高,可以较准确地预测污垢热阻随时间的变化趋势.     

Generation of unidirectionally propagated action potentials in a peripheral nerve by brief stimuli

Single, unidirectionally propagated action potentials can be elicited in peripheral nerves by electrical stimuli of short duration. Propagation in one direction is blocked anodically by means of a quasi-trapezoidal stimulus wave form and a modified tripolar electrode configuration. Propagation in the other direction proceeds unhindered. This technique may be applicable to collision blocking of motor nerves for neural prostheses.     

Hypertensive action of 18-hydroxydeoxycorticosterone

18-Hydroxydeoxycorticosterone is an adrenal steroid hormone causing salt and water retention and is secreted in greatly increased amounts in response to the pituitary hormone adrenocorticotropic hormone. Its production is abnormally high in some forms of hypertension in man and rat. Direct proof that 18-hydroxydeoxycorticosterone is capable of causing hypertension is present. Daily subcutaneous injections of 200 micrograms, a low physiological dose, significantly increase the blood pressure of unilaterally nephrectomized saline-treated rats after 2 weeks. This strengthens the hypothesis that 18-hydroxydeoxycorticosterone contributes to the etiology of hypertension, possibly by a mechanism involving stressinduced release of adrenocorticotropic hormone.     

彩色多普勒超声对早期高血压患者心脏及血管改变的诊断意义

目的评价彩色多普勒超声对早期高血压患者心脏及血管改变的诊断意义。方法应用彩色多普勒超声探测82例高血压患者及65例健康自愿者的心脏、颈动脉、肾动脉及大脑中动脉血流变化。结果高血压组心室间隔与左室后壁均增厚52例、左房扩大42例、二尖瓣口血流频谱E/A〈1者有72例、颈动脉内膜-中层增厚47例、颈动脉粥样硬化斑36例、肾段动脉阻力指数RI〉0.70者50例、大脑中动脉峰值流速〉106 cm/s者67例,而对照组分别为5、17、12、11、14、15、22例,两组差异均有统计学意义（P〈0.01）。高血压组心脏、颈动脉、肾动脉及大脑中动脉血流均出现异常表现者43例（52.4%）,对照组均无异常。结论彩色多普勒超声可了解早期高血压患者心脏结构、颈动脉内膜情况及肾动脉、脑动脉血流改变。