口服L-精氨酸对腹主动脉缩窄后大鼠血压、心肌肥厚和血管舒张功能的影响

本文利用缩窄大鼠腹主动脉的方法制备高血压模型，观察了正常大鼠，未服和口服Ｌ－精氨酸两周的腹主动脉狭窄的大鼠的血压，心肌肥厚及血管舒张功能的改变，旨在了解Ｌ－精氨酸对腹计劝缩窄性高血压大鼠的作用，研究发现腹主动脉狭窄后大鼠发生了肥厚，且血管环对１０＾－８￣１０＾－５ｍｏｌ／Ｌ乙酰胆碱诱导的舒张反应明显减低，而Ｌ－精氨到口服治疗两周舒张功能，但两组大鼠腹主动脉缩窄后的血压均升高，两者相比较差别无统计学     

内皮源舒张因子合成抑制剂致大鼠心血管变化及意义

目的：探讨内皮源舒张因子（ＥＤＲＦ）合成受抑制时的心血管病理生理的变化及意义。方法：实验组大鼠（ｎ＝６）长期应用ＥＤＲＦ抑制剂──Ｌ－硝基精氨酸１５ｍｇ，ｋｇ~（－１）／ｄ，腹腔注射，共２８天），对照组（ｎ＝６）给予注射用水。结果：与对照组比较，Ｌ－硝基精氨酸使大鼠血压明显增高、心率减慢、心功能增强，主动脉环对去甲肾上腺素（１０~（１１）～１０~（－５）ｍｏｌ／Ｌ）和内皮素（１０~（－１０）～１０~（－６）ｍｏｌ／Ｌ）的收缩反应增强（Ｐ＜０．０５），对乙酰胆碱（１０~（－９）～１０~（－５）ｍｏｌ／Ｌ）和降钙素基因相关肽（１０~（－１０）～１０~（－８）ｍｏｌ／Ｌ）舒张反应减弱（Ｐ均＜０．０５），血浆和组织内皮素增高，主动脉组织环磷酸鸟苷活性减低，血浆血管紧张素Ⅱ和肾素活性减低，血浆丙二醛增高。肾入球小动脉内膜增厚。结论：ＥＤＲＦ对心血管有重要调控功能，ＥＤＲＦ减少可导致心血管一系列病理生理变化。     

L—精氨酸及其N衍生物对高血压大鼠离体血管的舒张作用

用Ｌ－精氨酸及Ｌ－精氨酸Ｎ端ａ衍生物Ｎ－乙酰精氨酸、Ｎ－苯甲酰精氨酸，对原发性高血压大鼠离体主动脉血管平滑肌的舒张作用进行研究，并与正常血压大鼠的主动脉血管平滑肌做比较。     

卡托普利对大鼠肥厚心肌受缺血再灌注损伤的保护作用及其机制探讨

腹主动脉缩窄致大鼠心肌肥厚模型作离体工作心脏灌流，观察卡托普利对大鼠肥厚心肌受缺血再灌注损伤的保护作用及血管紧张素Ⅱ（ＡｎｇⅡ）的影响。结果表明：在心脏停跳液及再灌注Ｋ－Ｈ液中加入卡托普利（２３．０μｍｏｌ／Ｌ）可明显改善肥厚心肌缺血再灌注后心功能的恢复，增加冠状动脉血流量，降低心肌组织乳酸、Ｎａ＋、Ｃａ２＋及ＭＤＡ的含量，并使心肌组织ＣＫ酶峰前移；而ＡｎｇⅡ（１０ｎｍｏｌ／Ｌ）可减弱卡托普利对肥厚心肌受缺血再灌注损伤的保护作用。我们认为，卡托普利对肥厚心肌受缺血再灌注损伤有保护作用，其机制可能与抑制心脏肾素－血管紧张素系统有关     

潜阳合剂对腹主动脉缩窄致高血压左室肥厚的影响

目的研究中药复方潜阳合剂对腹主动脉缩窄致高血压左室肥厚的影响,并探讨其作用机制。方法使用腹主动脉缩窄致高血压左室肥厚模型,Wistar大鼠随机分成假手术组和模型组,将高血压造模成功的大鼠随机分成模型组、培哚普利组和潜阳合剂组,每组10只,并开始灌胃,各组药物干预8周。使用心脏超声评价左室肥厚水平,尾动脉仪测量大鼠左前肢血压,天狼猩红染色观察心肌胶原含量,免疫组化法测定心肌组织Ⅰ型、Ⅲ型胶原纤维的含量。结果腹主动脉缩窄后12周,与假手术组相比,模型组血压升高,左室后壁及室间隔厚度增厚(P<0.001),左室舒张末内径和收缩末内径缩小(P<0.001);与模型组相比,培哚普利组和潜阳合剂组血压降低,左室后壁和室间隔厚度降低(P<0.001),舒张末内径(P<0.001)和收缩末内径(P<0.05)改善;与模型组相比,培哚普利组、潜阳合剂组大鼠心肌组织胶原较少,Ⅰ型和Ⅲ型胶原纤维表达减少。结论潜阳合剂可以改善腹主动脉缩窄致高血压大鼠的左室肥厚,其机制与降压、抑制心肌胶原纤维增生相关。     

血管紧张素-(1-7)对腹主动脉缩窄大鼠的抗心肌肥厚效应

目的　探讨血管紧张素 (1 7)能否预防和减轻腹主动脉缩窄所诱导的大鼠心肌肥厚。方法　 45只大鼠随机分为假手术组、腹主动脉缩窄组、腹主动脉缩窄 +血管紧张素 (1 7)治疗组 ,每组 15只。在腹主动脉缩窄术后 1d开始 ,腹主动脉缩窄血管紧张素 (1 7)治疗组大鼠经置入式微量泵持续颈静脉给予血管紧张素 (1 7) ,给药剂量 2 5μg·kg- 1 ·h- 1 ,假手术组及腹主动脉缩窄组经微量泵只给予同量的生理盐水 ,4周后检测颈动脉血压、心率、血浆和心肌血管紧张素Ⅱ浓度、左心室重量指数和心肌胶原容积分数。结果　腹主动脉缩窄可导致颈动脉血压升高、心率加快、心肌血管紧张素Ⅱ浓度升高、左心室重量指数和心肌胶原容积分数增加 ;血管紧张素 (1 7)不改变腹主动脉缩窄所诱导增高的血压、心率和心肌血管紧张素Ⅱ浓度 ,但能明显减轻腹主动脉缩窄所诱导增高的左心室重量指数和心肌胶原容积分数。结论　外源性血管紧张素 (1 7)能减轻腹主动脉缩窄所诱导的大鼠心肌肥厚。其机制不是通过改变血流动力学或心肌血管紧张素Ⅱ浓度所致 ,可能与它抑制血管紧张素Ⅱ的细胞内信号转导有关。     

内皮素和内皮衍化的松弛因子在高血压发病上的作用

给予Ｗｉｓｔａｒ大鼠腹腔注射ＥＤＲＦ合成抑制剂（ＬＮＮＡ）２８ｄ，可诱发大鼠产生持续性高血压伴ＥＴ水平增高，ＥＴ／ｃＧＭＰ比值增大，主动脉环对ＥＴ的收缩反应明显增高，对乙酰胆碱（Ａｃｈ）舒张反应明显减低。然而同时给于Ｌ－精氨酸或ＥＴ抗血清可使血压降至正常，ＥＴ水平明显降低ＥＴ／ｃＧＭＰ比值缩小，使主动脉环对ＥＴ收缩反应减低，对Ａｃｈ舒张反应增加。     

慢性缺氧对大鼠肺动脉舒张反应的影响

目的：探讨大鼠缺氧性肺动脉高压发生过程中肺动脉舒张反应的改变。方法：本实验比较了正常（ｎ＝１１）与慢性缺氧４天（ｎ＝１１）、间断缺氧３周（ｎ＝１１）大鼠离体肺动脉环对几种作用机制不同的血管舒张药物的反应。结果：慢性缺氧显著抑制了大鼠肺动脉环对乙酰胆碱的舒张反应（Ｐ＜０．０５），而对硝普钠（１０－７～１０－１１ｍｏｌ／Ｌ）和硝苯地平（１０－４～１０－８ｍｏｌ／Ｌ）诱发的舒张反应无明显影响；克罗卡林（１０－７～１０－１１ｍｏｌ／Ｌ）在缺氧４天大鼠肺动脉环的舒张作用显著增强（Ｐ＜０．０５）。结论：慢性缺氧显著抑制大鼠肺动脉内皮依赖性舒张反应，而对非内皮依赖性及钙通道依赖性舒张反应无明显影响；钾通道依赖性舒张反应在缺氧早期是增强的     

氯沙坦与赖诺普利对大鼠压力负荷性心血管重构的影响

目的探讨心血管重构的结构、功能改变以及氯沙坦和赖诺普利的干预作用.方法膈下腹主动脉缩窄法建立大鼠心肌肥厚模型.检测各实验组平均动脉压(mean avterial pressure,MAP)、心肌肥厚程度、胸主动脉内皮功能. 结果与假手术组相比,模型组MAP、左室重量(left ventricular weight,LVW)、左室重量指数(left venticuler mess index,LVMI)、心肌细胞横径(transverse diameter of myoeardium,TDM)分别提高28.6%、20.5%、26.9%、17.9%(P＜0.01),胸主动脉环对乙酰胆碱(ACh)血管舒张反应明显降低(P＜0.01);降压剂量氯沙坦与赖诺普利和非降压剂量氯沙坦干预后,能完全预防心肌肥厚,使胸主动脉环对ACh血管舒张反应正常化,以降压剂量氯沙坦作用最为明显;非降压剂量赖诺普利能改善心肌肥厚程度,但与假手术组有差异(P＜0.01),胸主动脉环对ACh血管舒张反应无改善.六组动物胸主动脉环对硝普钠(SNP)最大舒张反应均无差别,模型组反应曲线右移.结论氯沙坦与赖诺普利能预防心肌肥厚,改善内皮功能,与剂量有一定关系.     

解除大鼠腹主动脉缩窄逆转左心室肥厚的形态学观察

目的通过解除大鼠腹主动脉缩窄逆转左心室肥厚,并比较逆转后大鼠心脏和左心室肥厚心脏及正常大鼠心脏的形态学、胶原容积分数和凋亡指数的差别。方法雄性SD大鼠75只,随机分为正常组(n=15)、缩窄组(n=30)和解除缩窄组(n=30)。缩窄组和解除缩窄组行第1次手术通过缩窄腹主动脉方法建立左心室肥厚模型。术后第5周确认动物模型成功后,解除缩窄组大鼠行第2次手术解除腹主动脉狭窄。采用心脏超声、常规病理和定量病理等多种技术方法,对各组大鼠在第1次手术(腹主动脉缩窄)后第5周、第2次手术(解除缩窄)后第4周行形态学观察及形态学定量分析。结果腹主动脉缩窄后第5周,大鼠室间隔舒张期末厚度、左心室后壁舒张期末厚度显著增厚;心脏质量指数、左心室质量指数、心肌胶原容积分数、心肌凋亡指数显著增加;解除缩窄后的第4周,解除缩窄组大鼠上述指标显著下降,但仍高于正常组。结论通过解除大鼠腹主动脉缩窄可以部分逆转左心室肥厚,大鼠心脏形态、心肌胶原容积分数、凋亡指数有明显改善,但与正常大鼠仍有差异。     

Increased resistance and impaired maximal vasodilation in normotensive vascular beds of rats with coarctation hypertension

To study the resistance of normotensive vascular beds in coarctation hypertension, we measured perfusion pressures of pump-perfused (blood), innervated, isolated hindlimbs of 12 rats (Group A) with 4 weeks of hypertension due to partial contriction of the abdominal aorta above the renal arteries, and of three control groups: 11 normotensive rats (Group B) with aorta sham-constricted, nine normotensive rats (Group C) with slight (5%) hindquarters atrophy due to partial constriction of the abdominal aorta below the renal arteries, and six rats with two-kidney, one clip Goldblatt hypertension (Group D). After aortic constriction, measured femoral arterial pressures in Group A rats remained normotensive. In hypertensive rats of Groups A and D, compared to normotensive Group B or C rats, hindlimb pressure-flow curves were displaced toward the pressure axis (p < 0.05). Compared to normotensive rats, drop in hindlimb resistance after acute local nerve section was increased in rats with coarctation hypertension. Residual resistance after maximal vasodilation with intraarterial sodium nitroprusside remained elevated in hypertensive rats of Groups A and D (p < 0.05), as compared to normotensive Group B or C rats; compared to Group B rats, this residual resistance in the coarcted rats of Group A was increased by 9%. Thus, in normotensive vascular beds of rats with chronic hypertension caused by aortic coarctation, resistance is elevated. The neurogenic component contributes to this high resistance, and structural vascular changes, indicated by impaired maximal vasodilation, may also contribute to the elevated resistance. It is most unlikely that these resistance changes are attributable to elevated hindlimb intravascular pressures.     

Role of endothelium-derived prostanoid in angiotensin-induced vasoconstriction

To test the hypothesis that prostanoids contribute to angiotensin II-induced vascular contraction, we compared the effect of angiotensin II on isometric tension development by rings of descending thoracic aorta bathed in Krebs' bicarbonate buffer with and without indomethacin (10 microM) to inhibit cyclooxygenase, CGS13080 (10 microM) to inhibit thromboxane A2 synthesis, or SQ29548 (1 microM) to block thromboxane A2/prostaglandin endoperoxide receptors. The comparisons were made in rings of aorta taken from normotensive rats and from rats with aortic coarctation-induced hypertension at 12 days and 90-113 days after coarctation. These rings released thromboxane B2, which was found to be endothelium dependent, increased in hypertensive rats, and stimulated by angiotensin II (10(-6) M) in normotensive rats and in hypertensive rats at 12 days after coarctation. The angiotensin II (10(-6) to 10(-5)M)-induced contraction of aortic rings was increased by about 30% at 12 days after coarctation and decreased at 90-113 days after coarctation. Removal of the endothelium increased the contractile effect of angiotensin II (10(-6) M) in aortic rings of normotensive rats and hypertensive rats at 90-113 days after coarctation but decreased the effect in aortic rings of hypertensive rats at 12 days after coarctation. In rats at 12 days after coarctation, the angiotensin II (10(-6) M)-induced contraction of aortic rings with endothelium was attenuated by indomethacin and SQ29548 but not by CGS13080. These data suggest that a prostanoid-mediated and endothelium-dependent mechanism of vasoconstriction contributes to the constrictor effect of angiotensin II in aortic rings of rats in the early phase of aortic coarctation-induced hypertension.     

Impaired endothelium-dependent relaxations in rabbits subjected to aortic coarctation hypertension

Rabbits were rendered hypertensive by suprarenal coarctation of the abdominal aorta. Seven days later, endothelium-dependent and endothelium-independent vascular relaxations were examined in vascular rings taken from hypertensive (thoracic aorta, carotid artery) and normotensive (abdominal aorta) regions. Relaxation of phenylephrine-contracted rings in response to endothelium-dependent agonists (acetylcholine, A23187) was impaired, compared with that in sham-operated and intact controls, in regions exposed to the elevated blood pressure (i.e., above the coarctation). Responses to acetylcholine and A23187 in the abdominal aorta, below the coarctation, were not altered. The diminished endothelium-dependent responses in the thoracic aorta were not affected by pretreatment with the cyclooxygenase inhibitor indomethacin. In contrast to acetylcholine and A23187, responses to the endothelium-independent agonist nitroprusside were not attenuated in vessels from hypertensive regions, indicating that the defect occurred in the endothelium. The EC50 for acetylcholine-induced relaxations of thoracic aorta correlated significantly with mean arterial pressure above the coarctation, indicating that the extent to which endothelium-dependent relaxation is impaired is in proportion to the degree of blood pressure elevation. This study suggests that the diminished relaxations by endothelium-dependent agonists is a local response to the elevation of blood pressure and is not due to a circulating factor.     

Prostaglandin I2 does not contribute to the hypotensive effect of the superoxide dismutase mimetic Tempo in rats with aortic coarctation-induced hypertension

This study was designed to investigate the contribution of prostaglandins to the vasodepressor effect of the superoxide dismutase mimetic Tempo in rats made hypertensive by ligation of the abdominal aorta at a point between the left and right renal arteries. Rings of thoracic aorta taken from rats with aortic coarctation released more 6-keto-PGF1alpha (a non-enzymatic product of PGI2 degradation) in the presence than in the absence of Tempo (1 mmol/L; 35.3 +/- 10.1 versus 13.6 +/- 2.6 pg/mg tissue). However, Tempo administered intravenously (2 mg/kg bolus injection plus infusion at 3 mg/kg/h) to rats with aortic coarctation did not increase significantly the concentration of 6-keto-PGF1alpha in vena cava blood. Treatment with Tempo did not affect the arterial pressure of un-operated normotensive rats but promptly decreased the arterial pressure of rats with aortic coarctation-induced hypertension (from 178 +/- 2 to 125 +/- 6 mmHg). The vasodepressor effect of Tempo in hypertensive animals was not affected by pretreatment with indomethacin to inhibit prostaglandin synthesis. These data argue against the hypothesis that PGI2 contributes to the acute hypotensive effect of Tempo in rats with aortic coarctation.     

Abnormal ion and water composition of veins and normotensive arteries in coarctation hypertension in rats.

We examined the water, sodium, and potassium composition of the thoracic aorta, abdominal aorta (plus iliac arteries), and veins (vena cava and portal vein) from rats with aortic coarctation. The aortas of 10 rats (group A) were coarcted above the renal arteries to produce hypertension. Control groups consisted of 10 rats sham-coarcted above and 10 rats coarcted below the renal arteries. In group A rats heart weights and carotid artery pressures were elevated over controls (P less than 0.01), whereas there were no significant differences in femoral arterial pressures. In group A rats both the hypertensive thoracic aorta and the normotensive abdominal aorta contained about 20% more water per unit of wet weight, and about 35% and 60% more sodium and potassium, respectively, per unit of dry weight than did the corresponding portions of aorta from control rats (P less than 0.01). In group A rats water (P less than 0.01), sodium (P less than 0.02), and potassium (P less than 0.05) contents of veins also were increased. There were no significant correlations between level of carotid arterial pressure and magnitude of changes in arterial and venous composition, nor were there significant differences between the magnitude of changes in the normotensive and hypertensive portions of the aorta. These results indicate that in rats abnormalities in vascular wall salt and water content are not necessarily a direct effect of the elevated pressure in hypertension.     

Treatment with the arginase inhibitor N(omega)-hydroxy-nor-L-arginine improves vascular function and lowers blood pressure in adult spontaneously hypertensive rat

OBJECTIVE: High vascular arginase activity and subsequent reduction in vascular nitric oxide production were recently reported in animal models of hypertension. The present study investigated the effects of in-vivo arginase inhibition on blood pressure and vascular function in adult spontaneously hypertensive rats. METHODS: Ten-week-old spontaneously hypertensive rats and normotensive age-matched Wistar-Kyoto rats were treated with or without the selective arginase inhibitor N-hydroxy-nor-L-arginine for 3 weeks (10 or 40 mg/kg per day, intraperitoneally). Systolic blood pressure and cardiac rate were measured before and during treatment. Flow and pressure-dependent reactivity as well as remodeling of mesenteric arteries, acetylcholine-dependent vasodilation of aortic rings, cardiac hypertrophy, arginase activity and nitric oxide production were investigated in 13-week-old spontaneously hypertensive rats. RESULTS: In spontaneously hypertensive rats, N-hydroxy-nor-L-arginine treatment decreased arginase activity (30-40%), reduced blood pressure ( approximately 35 mmHg) and improved the reactivity of mesenteric vessels. However, vascular and cardiac remodeling was not different between treated and untreated spontaneously hypertensive rats. In Wistar-Kyoto rats, N-hydroxy-nor-L-arginine did not affect blood pressure. Finally, arginase inhibition was associated with increased nitric oxide production. Consistent with this, the response of aortic rings to acetylcholine was fully restored by N-hydroxy-nor-L-arginine, and the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester significantly reduced the effect of N-hydroxy-nor-L-arginine on flow-dependent vasodilation. CONCLUSION: Pharmacological inhibition of arginase in adult spontaneously hypertensive rats decreases blood pressure and improves the reactivity of resistance vessels. These data represent in-vivo argument in favor of selective arginase inhibition as a new therapeutic strategy against hypertension.     

Functional and morphological pattern of vascular responses in two models of experimental hypertension

OBJECTIVES:

To determine the reactivity and accompanying structural changes in thoracic aorta and carotid artery from nitric oxide (NO)-deficient hypertensive and spontaneously hypertensive rats (SHR).

ANIMALS AND METHODS:

For the functional study, isolated rat arterial rings were precontracted with a submaximal concentration of phenylephrine (1 μM) and relaxant responses to cumulative concentrations of acetylcholine were obtained. For the morphological study, arteries were processed by a standard method for electron microscopy. The geometry of the arteries – the inner diameter and the wall thickness (tunica intima plus tunica media) – was evaluated by light microscopy.

RESULTS:

Increased systolic blood pressure was accompanied by increased heart weight to body weight ratio in both NO-deficient and SHR compared with normotensive controls, indicating cardiac hypertrophy. Morphometry of the thoracic aorta and carotid artery in both models of hypertension showed increased wall thickness, cross-sectional area and wall to diameter ratio. The inner diameter increased in aorta but not in carotid artery. In isolated arteries from normotensive rats, the addition of acetylcholine to precontracted vessels resulted in dose-dependent relaxation. The relaxing effect was more prominent in thoracic aorta than in carotid artery. Endothelium-dependent relaxation of arteries from NO-deficient hypertensive rats was markedly reduced. On the other hand, in aorta and carotid artery from SHR, the endothelium-dependent relaxation in response to acetylcholine was not significantly attenuated. The relaxation of arteries from SHRs, as well as the residual relaxation of arteries from NO-deficient hypertensive rats, was abolished by addition of N^G-nitro-l-arginine methyl ester, an inhibitor of NO synthase, to the incubation medium.

CONCLUSIONS:

These results suggest that increased systolic blood pressure and accompanying structural changes are not primarily responsible for impairment of endothelium-dependent relaxation in experimental hypertension.     

Ultrastructure of hypertensive rat aorta. Increased basement membrane-like material

To determine the effect of elevated blood pressure on the ultrastructure of rat aorta, hypertension (average mean pressure 163 +/- 17 mm Hg) was produced by suprarenal aortic coarctation. After 3 weeks, the subendothelium of the hypertensive thoracic aorta showed significantly increased volume measurements for mononuclear leukocytes and basement membrane-like material compared with the sham-operated control group. Focal areas of rarefaction of the subendothelial extracellular material were associated with the nearby presence of mononuclear leukocytes. None of these alterations were found in the normotensive abdominal aorta. The tunica media of hypertensive thoracic aorta also contained significantly increased basement membrane-like material. This new finding in an animal hypertension model is the direct result of the quantitative morphological approach employed in this study. In some rats, the partially constricting aortic ligature compromised the right renal artery leading to ischemic atrophy of the right kidney and hyperreninemia in addition to hypertension. In this group, excluded from the previous analysis and evaluated separately, subendothelial thickening and accumulation of basement membrane-like material in the thoracic aorta were greatly increased compared with the control group and other hypertensive rats. This result could not be attributed to an effect of blood pressure alone and might have been caused in part by humoral factors. Basement membrane accumulation appears to be an important early response of the arterial wall to hypertension or other factors in this rat model.     

Effects of chronic aortic coarctation on atherosclerosis and arterial lipid accumulation in the Watanabe hereditary hyperlipidemic (WHHL) rabbit.

The effects of high blood pressure on atherosclerosis were examined in the Watanabe heritable hyperlipidemic (WHHL) rabbit. For this purpose, the subdiaphragmatic aorta of rabbits was partially ligated (coarctation) to increase blood pressure. Atherosclerosis was assessed 4 months later by morphometric analyses and quantitation of arterial lipids. Results were compared to control WHHL rabbits with matched plasma triglycerides and cholesterol levels. A marked increase in atherosclerotic lesions was observed in the thoracic aorta of the hypertensive rabbits without qualitative changes in its morphometric features. The cross sectional area of the atherosclerotic plaques of the ascending and descending aorta in the hypertensive rabbits was two- and six-times larger than in normotensive rabbits, respectively. Lesions represented 12.0% +/- 3.5% of the total medial cross sectional area of the descending aorta of normotensive rabbits, versus 45.0% +/- 5.7% in hypertensive rabbits. No lesions were observed downstream of the coarctation in hypertensive rabbits, nor in the normotensive rabbits. Accumulation of cholesterol and choline-containing phospholipids in the descending aorta of hypertensive rabbits was increased 3.2- and 1.5-fold, respectively, when compared to normotensive rabbits. Hypertension did not change the unesterified cholesterol/total cholesterol and sphingomyelin/lecithin + lysolecithin molar ratios. In conclusion, chronic coarctation enhances the atherosclerotic response in WHHL rabbits in the high blood pressure compartment, and reduces the variability of this response.