Analysis of changes in reactivity of rabbit arteries and veins two weeks after induction of hypertension by coarctation of the abdominal aorta.

Vessel dimensions and characteristic responses to norepinephrine were measured in various arteries and veins of the rabbit made hypertensive by partial constriction of the upper abdominal aorta. The ear, radial, and basilar arteries taken from the circulation proximal to the ligature (the hypertensive arteries) were thickened in proportion to the rise is arterial blood pressure. The water, sodium, and potassium contents of these and all other vessels were not significantly changed in the hypertensive rabbits. The maximum response to norepinephrine in the ear artery, a representative vessel from the hypertensive part of the rabbit, was increased, whhereas the sensitivity of this vessel to norepinephrine expressed as the ED50 did not alter with changes in the arterial blood pressure. In contrast, the thickness and the maximum response to norepinephrine of the saphenous artery, representative of vessels distal to the ligature (normotensive vessels) and of the saphenous and cephalic veins were unaltered. The sensitivity as indicated by the norepinephrine ED50 of the veins, but not of the saphenous artery, increased with a rise in carotid artery blood pressure. These results suggest that the increased responsiveness to norepinephrine of arteries proximal to the ligature is due to changes in muscle mass and that the increased responsiveness of the veins is due to increased sensitivity to norepinephrine.     

脉压差对高血压病患者颈动脉粥样硬化的作用

目的 :高血压病是冠状动脉粥样硬化的危险因素 ,人们普遍关心收缩压与舒张压和动脉粥样硬化与冠心病的关系 ,而对于脉压尚未进行广泛的研究。方法 :本文通过多普勒超声检查高血压病患者颈动脉粥样硬化的方法 ,观察了 64例高血压病患者脉压差与颈动脉粥样硬化斑块的发生率及内中膜厚度的相互关系。结果 :脉压差高的患者其颈动脉粥样硬化斑块的发生率及内中膜厚度也高 (P <0 0 5 ,P <0 0 1)。结论 :脉压差与颈动脉粥样硬化斑块和内中膜厚度相关 ,脉压差可能参与动脉粥样硬化的形成和发展。     

Morphometric evidence for non-pressure-related arterial wall thickening in hypertension

To investigate the relation of pressure and vascular wall thickening in hypertension, we coarcted the abdominal aorta upstream to the renal arteries in 14 rats. Sham-coarcted (n = 16) and two-kidney, one-clip (Goldblatt) hypertensive rats (n = 13) served as controls. Tail, femoral, and carotid arterial pressures rose (p less than 0.01) in the two-kidney, one-clip hypertensives; only carotid pressure rose (p less than 0.01) in the coarcted rats, tail and femoral pressures remaining normal (p greater than 0.25). Thus, the hindquarters of the coarcted rats remained normotensive. Four to six weeks after surgery we perfusion-fixed vascular tissues of the hindquarters, including kidneys, with formalin at in vivo levels of pressure. Glycol methacrylate-embedded tissues were sectioned at 1 micron thickness and vessels quantitatively evaluated. The outer medial and lumen perimeters of abdominal aorta, femoral artery, and renal arterioles were measured; from these measurements, vessel outer and lumen diameters, medial thickness, medial area, and medial thickness-to-lumen radius ratios were calculated. Compared with sham-coarcted rats, abdominal aorta, femoral arteries, and renal arterioles less than 61 microns outer diameter in rats with coarctation and Goldblatt hypertension had significantly increased (up to +100%) medial area, medial thickness, and medial thickness-to-lumen radius ratios. In general, magnitudes of abnormalities were similar in Goldblatt and coarcted rats. Renal arterioles greater than 60 microns outside diameter in Goldblatt hypertensive, but not coarcted, rats also were thickened. These results indicate that vascular wall thickening occurs in conduit arteries and smaller renal arterioles in the normotensive hindquarters of coarcted rats, providing morphometric evidence for non-pressure-related mechanisms involved in vascular growth in this form of hypertension.     

Regression of Radial Artery Wall Hypertrophy and Improvement of Carotid Artery Compliance After Long-Term Antihypertensive Treatment in Elderly Patients

Objectives. The present study was designed to assess whether a diuretic- or an angiotensin-converting enzyme inhibitor–based treatment can reduce arterial wall hypertrophy of a distal muscular medium-sized artery—the radial artery—and the stiffness of a proximal large elastic artery—the common carotid artery.Background. Large-artery wall thickness and stiffness are increased during sustained essential hypertension and contribute to the increased risk of complications. Whether antihypertensive treatment can normalize the wall hypertrophy of conducting arteries has not yet been determined.Methods. Seventy-seven elderly hypertensive patients were randomized to receive 9 months of double-blind treatment with perindopril (2 to 8 mg/day) or the diuretic combination of hydrochlorothiazide (12.5 to 50 mg/day) plus amiloride (1.25 to 5 mg/day) after a 1-month placebo washout period. If systolic blood pressure remained at >160 mm Hg after 5 months, chlorthalidone or atenolol was added, respectively. Arterial variables, including radial artery mass and common carotid artery compliance, were calculated from noninvasive measurements of internal diameter and wall thickness with the use of high resolution echo-tracking systems at baseline and after 5 and 9 months.Results. During treatment, blood pressure and arterial variables changed to the same extent in both groups. After a 9-month treatment, systolic, diastolic and pulse pressures and radial artery wall thickness, mass and thickness/radius ratio decreased significantly (p < 0.01), whereas carotid compliance increased (p < 0.001). The decrease in radial artery thickness/radius ratio after a 9-month treatment was significantly related to the reduction in pulse pressure (p < 0.01), whereas the improvement in carotid compliance was related to the reduction in mean arterial pressure (p < 0.01). In healthy subjects and untreated hypertensive patients, radial artery diameter, wall thickness and thickness/radius ratio and carotid artery compliance did not change significantly during a 9-month observation period.Conclusions. These results indicate that in elderly hypertensive patients, both angiotensin-converting enzyme inhibitor– and diuretic combination–based treatments can reduce radial artery wall hypertrophy and improve carotid artery compliance.     

Structural Changes in the Cardiovascular System of Untreated Essential Hypertensives

Arterial hypertension is associated with structural changes in the cardiovascular system. This study has examined the effect of hypertension on the carotid artery wall and examined the relation between changes in the structure of carotid artery wall and left ventricle in untreated hypertensives. The carotid artery wall was visualized using a high resolution ultrasound technique in 37 untreated hypertensive patients (25 males, 12 females) and 37 age and sex matched normotensive individuals and carotid intima-media thickness (IMT) and carotid artery diameter measured. IMT and intima-media cross sectional area was significantly greater in the hypertensive group compared with the normotensive group, though the carotid artery diameter did not differ significantly. There was a significant association between age and IMT in both groups. In the hypertensive group there was also a significant association between left ventricular mass index, ventricular septal or posterior wall thickness and IMT. This study indicates that there is an association between cardiac and carotid arterial structure in hypertension. Such a relationship may be important in understanding the associated risks of high blood pressure.     

高血压病对颈动脉及桡动脉结构及功能变化的影响

目的　探讨高血压病时同为导管动脉的大动脉和中动脉结构及功能变化的异同。方法　筛选 6 3例 1～ 2级高血压患者和性别年龄与之匹配的正常人 31例作为对照组。用高分辨率超声血管探头检测颈总动脉和桡动脉的内膜中层厚度 ,管腔内径 ,并用相应公式计算动脉内膜中层厚度 /腔径比值、动脉内膜中层横截面积、动脉管腔横截面积、动脉壁 /腔横截面积比值、动脉扩张性以及动脉横截面积顺应性。用协方差校正除血压以外的其它影响因素后比较上述指标。结果　与对照组相比 ,高血压组颈总动脉和桡动脉动脉内膜中层厚度及与管腔内径的比值、内膜中层面积及与管腔面积的比值均显著增加 ,颈总动脉扩张性及横截面积顺应性降低 ,但桡动脉扩张性及横截面积顺应性无改变。即使校正除血压以外的影响因素后 ,结果仍不变。结论　高血压病对导管动脉的损伤呈不均一性。     

Hemodynamics of the carotid artery after vasodilation in essential hypertension

We performed simultaneous noninvasive measurements of common carotid artery and brachial artery hemodynamics in nine normal subjects and 10 subjects with sustained essential hypertension. In hypertensive subjects, brachial artery blood flow and forearm vascular resistance were in the normal range while carotid artery blood flow and carotid artery resistance were decreased and increased, respectively. The most important findings were the changes in the internal caliber of large arteries. Although the brachial and carotid artery diameters of hypertensive subjects were measured for the same level of mean arterial pressure, brachial artery diameter was significantly increased and carotid artery diameter was strictly normal as compared with values found in normal subjects. To assess whether carotid artery circulation could influence the baroreceptor reflex response to arteriolar vasodilation, carotid artery and brachial artery hemodynamics were measured in immediate succession in normotensive and hypertensive subjects before and after oral administration of cadralazine, a dihydralazine derivative. After cadralazine treatment, carotid artery tangential tension decreased in hypertensive subjects, and the changes were significantly correlated to the increase in heart rate. A similar correlation was found in normal subjects, but it was reset toward higher heart rates. These results indicate that the carotid artery does not behave like the brachial artery in response to a chronic increase in blood pressure. This behavior indicates intrinsic alterations of the arterial wall and might be involved in the resetting of the carotid baroreceptor reflex. Carotid artery circulation could play a role in hypertension by modulating the carotid baroreceptor mechanisms involved in the response to drug-induced arteriolar vasodilation.(ABSTRACT TRUNCATED AT 250 WORDS)     

Removal of heparan sulfate by heparinase treatment inhibits FGF-2-dependent smooth muscle cell proliferation in injured rat carotid arteries

Smooth muscle cells (SMC) of the rat carotid arterial media proliferate and migrate in response to injury during the formation of a neointima. The interaction of fibroblast growth factor (FGF-2), which is released at the site of injury, with heparan sulfate proteoglycans (HSPGs) is necessary to induce signaling, which elicits an FGF-dependent mitogenic response by arterial smooth muscle cells, and also serves as a mechanism for storage of the growth factor within the extracellular matrix. However, whether these interactions are critical during neointimal formation has not been directly tested. In this study, a model of FGF-2-dependent medial SMC mitogenic response in balloon-injured rat carotid artery was used to test the effect of degradation of vessel wall heparan sulfate on subsequent SMC proliferation. Treatment of balloon-catheterized rat carotid arteries with chondroitin ABC lyase and/or heparin lyases eliminated heparan sulfates in the vessel wall, as determined by immunoperoxidase staining. In contrast, the distribution in the carotid vessel wall of the large core protein of perlecan, a major vessel wall HSPG that binds FGF-2, is not decreased. The effect of glycosaminoglycan digestion in situ on medial SMC proliferation in response to a bolus injection of FGF-2 after injury was determined by measuring the percentage of SMC nuclei that incorporated 5-bromo-2'-deoxyuridine (BrdU) 48 h after injury. Enzymatic removal of heparan sulfate reduced BrdU incorporation into medial SMC by 60-70% (P < 0.001) at 48 h after injury. Moreover, pre-incubation of FGF-2 with heparin prior to injection restored SMC replication to the levels present in injured vessels treated with buffer alone (P < 0.01). These experiments indicate that endogenous HSPGs are essential to promote FGF-2-driven medial SMC proliferation following injury, and that heparinase treatment can abrogate FGF-2-dependent responses in vivo.     

Vascular remodeling of the carotid artery in patients with untreated essential hypertension increases with age.

We examined whether hypertrophy of the carotid artery in patients with untreated essential hypertension is associated with compensatory carotid artery enlargement as these patients age. Carotid ultrasonography was evaluated in 163 patients with untreated essential hypertension (74 males and 89 females) and in 76 normotensive subjects. Intima-media end-diastolic thickness (IMT) and outer vessel diameter (VD) were measured, and relative wall thickness (IMT/R, R=VD/2) and vascular mass (VM) were calculated. Determinants of vascular hypertrophy in patients with untreated essential hypertension were also investigated. VD, VM, and IMT were significantly correlated with age in both the normotensive and hypertensive groups. Additionally, IMT was significantly correlated with VD in both groups. There was no correlation between increasing age and IMT/R in either group. IMT, VD and VM were significantly higher in the hypertensive group >50 years than in age-matched normotensive controls. However, IMT/R was significantly higher in the 50-59 years hypertensive group than in normotensive controls of the same age group. In addition to age, VM was related to systolic blood pressure, pulse pressure, fasting blood sugar, IMT, VD, and IMT/R in the hypertensive group. Multivariate regression analysis in the hypertensive group indicated that IMT/R was the strongest predictor of carotid vascular mass. Age and pulse pressure were also independently related to vascular mass. These results indicate that, as patients with untreated hypertension age, carotid arteries undergo remodeling. This should add further impetus to the implementation of appropriate hypertension treatment for such patients.     

肥胖对高血压病患者颈动脉粥样硬化的作用

目的肥胖是心脑血管疾病的危险因素,而关于肥胖与颈动脉粥样硬化的关系尚不清楚。方法通过多普勒超声检查高血压病患者颈动脉粥样硬化的方法,观察了82例高血压病患者体重指数与颈动脉粥样硬化斑块的发生率及内中膜厚度的相互关系。结果体重指数高的患者其颈动脉粥样硬化斑块的发生率及内中膜的厚度也高(P<005,P<001)。结论体重指数与颈动脉粥样硬化斑块和内中膜厚度相关,肥胖可能参与动脉粥样硬化的形成和发展。     

Evidence for an increase in adrenergic nerve function in blood vessels from experimental hypertensive rabbits.

The possibility of changes in the adrenergic innervation of blood vessels in experimental hypertension was investigated by measuring arterial norepinephrine content, neuronal uptake of norepinephrine, and the neurogenic contractile response in rabbits made hypertensive by partial constriction of the abdominal aorta proximal to the kidneys. Two to 3 weeks after surgery, norepinephrine content was increased in the arteries above the ligature, where arterial blood pressure was increased, but not in the arteries below the ligature, where arterial blood pressure was normal, in the heart, or in the veins. Neuronal norepinephrine uptake per unit length of vessel and the neurogenic contractile response increased with the rise in arterial blood pressure. The neurogenic contractile response can be taken as an indication of an increase in transmitter release. The results taken together suggest an increase in the function and possibly the amount of the adrenergic neuroneal terminal in hypertension. Since the distributions of the changes in the adrenergic innervation and the increases in smooth muscle cell proliferation in hypertension are similar, these two processes may be interrelated.     

Morphometric study of structural changes in the mesenteric blood vessels of spontaneously hypertensive rats

Structural changes of three categories of mesenteric arteries (representing elastic, muscular and arteriolar vessels) from 10- to 12-week-old and 28-week-old spontaneously hypertensive rats (SHR) were studied morphometrically at the light microscope level, and the results compared with age-matched Wistar-Kyoto normotensive rats. In 10- to 12-week-old SHR, hypertrophy of the vessel wall occurred only in the muscular and arteriolar vessels. At 28 weeks, further thickening of the vessel wall occurred in the muscular and arteriolar vessels, and the superior mesenteric artery (elastic vessel) was also thickened in the SHR. There was no evidence that the wall of the relaxed hypertrophied vessels encroached upon the lumen of the vessel. The structural basis for the increase in the vessel wall thickness varied with vessel type. In the superior mesenteric artery, increase in the media at 28 weeks of age would be consistent with hypertrophy of the smooth muscle cells. In the large muscular arteries, at 10-12 weeks of age, increase in medial mass occurred with increase in the number of the smooth muscle cell layers whereas at 28 weeks further increase in media could be due to hypertrophy of the smooth muscle cells. In the small arteriolar vessels, medial enlargement was due at all ages to an increase in the number of smooth muscle layers. Our results show that in the SHR hypertrophy of the media occurs not only in the small arteriolar vessels, but also in large elastic and muscular arteries.     

Association of common carotid intima-media thickness and lipoprotein(a) with coronary artery disease

BACKGROUND: Carotid artery intimal medial thickness is a simple, non-invasive and reproducible clinical tool to evaluate atherosclerosis and predict coronary artery disease. Lipoprotein(a) levels are related to both atherogenesis and thrombogenesis and may be a key link between lipid and coronary artery disease. This study evaluated the association of carotid intimal medial thickness and lipoprotein(a) with coronary artery disease. METHODS AND RESULTS: We studied 185 randomly selected patients hospitalized for coronary angiogram in our institute. There were 110 angiographically proven patients of coronary artery disease with mean age of 55.8 +/- 9 years (range 34-72 years) and 75 subjects with normal coronary artery anatomy with mean age of 54.8 +/- 8 years (range 34-68 years). The mean carotid intimal medial thickness of subjects with coronary artery disease was significantly higher than in subjects without coronary artery disease (0.84 +/- 0.16 mm v. 0.65 +/- 0.15 mm, p<0.001). The mean carotid intimal medial thicknesses in patients with triple vessel, double vessel and single vessel disease were 0.96 +/- 0.12 mm, 0.84 +/- 0.11 mm and 0.78 +/- 0.13 mm, respectively (p=0.05). The mean lipoprotein(a) of subjects with coronary artery disease was significantly higher than in subjects without coronary artery disease (35.9 +/- 22.3 mg/dl v. 19.1 +/- 21.2 mg/dl, p<0.001). Mean lipoprotein(a) levels in subjects with carotid intimal medial thickness <0.80 was 26.4 +/- 24.2 mg/dl and in subjects with carotid intimal medial thickness > or = 0.80 was 32.1 +/- 22.1 mg/dl (p=0.05). CONCLUSIONS: There is a strong correlation between carotid and coronary atherosclerosis and carotid intimal medial thickness is a good predictor of presence and extent of coronary artery disease. Lipoprotein(a) level is a powerful independent risk factor for atherosclerosis. Carotid intimal medial thickness and lipoprotein(a) in conjoint can predict coronary artery disease reliably.     

美国黑人青年长期应用可卡因对颈内动脉管径的影响(英文)

目的观察美国黑人青年长期应用可卡因对其颈内动脉管径变化的影响。方法对美国巴尔地摩市57名可能有应用可卡因历史的黑人青年进行问卷调查,同时抽血检测血常规、血脂、C反应蛋白（CRP）,并行颈内动脉核磁共振检查（MRI）以了解颈内动脉结构的变化情况。应用多元回归模型分析颈内动脉管径变化与应用可卡因的关系。结果在应用可卡因的患者（n=40）CRP及白细胞总数WBC（1×109/L）较未应用过可卡因的患者（n=17）均略有升高[（5.14±12.31）vs（1.29±0.92）μg/L,P=0.059及（5.03±1.70）vs（4.12±1.22）,P=0.059],而平均红细胞容积（MCH）和平均红血球浓度（MCHC）稍低于未用过可卡因的患者[（29.34±2.18）vs（31.77±4.50）pg,P=0.055及（33.23±0.75）vs（33.67±0.49）g/dl,P=0.38],但均无显著差别。平均颈内动脉壁厚度（MTICV）可卡因组与无可卡因组未见显著差别[（0.952±0.244）vs（0.968±0.275）cm,P=0.822],颈内动脉壁增厚者（MTICV>1.0 cm）比例两组无显著差别（25.0%vs29.4%,P=0.729）;应用单变量线性回归模型分析,可见颈内动脉水平测量外径（HOD）、垂直内径（VID）、外轮廓面积（OA）、颈内动脉内轮廓面积（ILA）、外轮廓体积（OV）、内径轮廓体积（LV）与应用可卡因呈显著负相关。应用多变量回归模型分析,可见颈内动脉的HOD,VID,OA,ILA,OV,LV仅与应用可卡因呈现显著负相关,而颈内动脉的管径变化与年龄、性别、身高体质量指数（BMI）、CRP、HIV感染无相关性。结论长期慢性应用可卡因可造成颈内动脉的缩窄。由于动脉长期缩窄可引起动脉缺血和动脉粥样硬化,由此或可推论长期慢性应用可卡因引起的颈内动脉收缩也许是动脉粥样硬化最初表现的形式。     

Echographic assessment of carotid and femoral arterial structure in men with essential hypertension

Extracoronary in vivo structural arterial changes were studied in asymptomatic essential hypertension. Carotid and femoral arteries were examined with B-mode echography for the presence or absence of plaque (the whole vascular segments of each vessel in the both sides) and for automated measurement of the far wall intima-media thickness (the vascular segment of each vessel proximal to the bifurcation in the right side) in 53 never treated hypertensive men and 133 normotensive men similar with regard to age, serum cholesterol levels, and smoking history. In the hypertensive group carotid plaque was more frequent (P < .05) and carotid and femoral intima-media thicknesses were greater (P < .001) than in the normotensive group. In the overall normotensive and hypertensive population intima-media thickness was independently associated with age and systolic pressure in both arteries (P < .001) and with cholesterol in the femoral artery (P < .05) while plaque was associated with systolic pressure (P < .01), and cholesterol (P < .01) in the carotid arteries and with age (P < .01), cholesterol (P < .05), and smoking (P < .001) in the femoral arteries. No significant difference in intima-media thickness in both arteries existed between hypertensive subjects with plaque and those without.Wall thickening and plaque were more frequent in hypertensive patients. Thickening was distributed homogeneously to both arteries, while plaque affected preferentially the femoral bed. The influence of age and pressure was more marked on intima-media thickness than on plaque. The lack of association between wall thickening and plaque suggested that vascular hypertrophy and early atherosis might be two different structural changes.     

高血压患者动态血压负荷参数与颈动脉粥样硬化关系的探讨

目的探讨高血压患者动态血压负荷参数与颈动脉粥样硬化的关系。方法采用B型超声测定颈动脉内膜中层厚度和硬化斑块指数。检测105例患者,高血压伴颈动脉硬化患者95例。分为4组,0期组23例,Ⅰ期组23例,Ⅱ期组28例,Ⅲ期组21例。正常血压(对照组)16例。分别测定24 h、白昼、夜间血压负荷及分级血压负荷(分为1~3级)。结果高血压颈动脉硬化0期组的血压负荷与对照组比较有显著差异(P<0.001);0期、Ⅰ期组昼夜血压负荷差大,Ⅱ、Ⅲ期组夜间血压负荷明显上升。0期、Ⅰ期组分级血压负荷主要集中在1级血压负荷,Ⅱ、Ⅲ期组中的2、3级血压负荷依次递增,负荷脉压差增大。结论夜间血压负荷的增加致昼夜节律异常,分级血压负荷的升高,负荷压差的增加均对高血压颈动脉硬化的综合评价起重要作用。     

Arterial hypertrophy in the fetal and neonatal spontaneously hypertensive rat

Large artery dimensions in prenatal and postnatal normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) were evaluated to determine whether increased medial thickness is evident during early development. Microscopic cross-sections from perfusion-fixed aortas and carotid arteries of fetal (22-day gestation) and neonatal (5-day-old) animals were examined for numbers of laminae, luminal diameter and area, and medial thickness and area. SHR had a smaller mean body weight, and luminal diameters were the same in both strains. However, medial thickness and the numbers of laminae were significantly greater in SHR at both stages. Normalized ratios of medial thickness/luminal diameter and medial area/luminal area were also greater in SHR, indicating a disproportionate size of the arterial wall relative to the luminal space. Medial area/body weight ratios were also larger for SHR, suggesting the presence of greater medial mass per unit of body weight. The data support the view that the increased mass of the hypertensive arterial system is established in SHR as early as the fetal stage.     

Parallel cardiac and vascular adaptation in hypertension.

BACKGROUND. Although vascular damage in the noncoronary circulation is a major cause of complications in hypertension, relatively little is known of the in vivo geometry and function of the arterial circulation in patients with uncomplicated hypertension or of their relation to left ventricular hypertrophy, a marker of enhanced risk of cardiovascular complications. METHODS AND RESULTS. Wall thickness and internal diameter of the common carotid artery and the presence of atherosclerosis within the extracranial carotid arteries were determined by ultrasound in 43 asymptomatic hypertensive patients and 43 normotensive subjects matched for sex, age, and body size. Vascular stiffness was estimated from simultaneous superimposed carotid pressure waveforms obtained with an external solid-state transducer. Left ventricular size and function were determined echocardiographically. Compared with normal subjects, hypertensive patients had greater left ventricular absolute and relative wall thicknesses, left ventricular mass, and carotid absolute and relative wall thicknesses (p < 0.005). Carotid intimal-medial thickness exceeded the 95th percentile of normal values in 28% of hypertensive patients (p < 0.01). Carotid atherosclerosis was equally prevalent within the two blood pressure groups and was associated with older age, larger left ventricular and carotid wall thicknesses, and carotid diameter. Despite similar carotid pulse pressures, vascular stiffness was significantly increased in the hypertensive patients. Among the population as a whole, significant relations existed between cardiac and vascular wall thicknesses and internal dimensions. In multivariate analyses, these relations were statistically independent of age and blood pressure. CONCLUSIONS. The present study documents the presence of geometric and functional changes within the common carotid artery in uncomplicated hypertension that parallel findings within the left ventricle. The potential contribution of these changes to the cardiovascular complications of hypertension, particularly in the setting of left ventricular hypertrophy, is unknown.     

Vascular remodeling in the growth hormone transgenic mouse

Using mice transgenic for the growth hormone gene (TGHM), we have studied the effects of a systemic elevation of growth hormone on vascular growth with the aim of investigating the role of vascular mass changes in producing hypertension. In contrast to human acromegaly or gigantism, there was no elevation of blood pressure in TGHM, but there were significant increases in vascular wall mass. In accordance with a presumably increased perfusion of larger organs, the medial cross-sectional areas of thoracic aorta and mesenteric resistance vessels were greater in the TGHM. These differences could be normalized in the aorta by body weight and in the mesenteric vessel by small intestine weight. Furthermore, the brain was not significantly heavier in the TGHM, and their carotid and cerebral vessels also were not larger. Wall-to-lumen ratios were similar in the aorta, carotid, and middle cerebral arteries suggesting that wall stress was the controlling factor in wall thickness. Surprisingly, the mesenteric vessels had increased wall-to-lumen ratio, which was similar to that seen in hypertensive vascular remodeling but in a normotensive animal. In an attempt to explain this finding it was noted that the pattern of mesenteric vascular networks and even organized structure within the vessel wall itself appeared to be fixed, perhaps by genetic mechanisms. Thus, vascular network structure may be a potentially limiting factor in the ability of the vessel wall to remodel and may have been responsible for the greater wall-to-lumen ratio in TGHM mesenteric vessels. A similar situation in human acromegaly or gigantism could result in a circulation marginally able to correct for other demands on blood flow resulting in about one third of cases being hypertensive.