Maternal high-sodium intake alters the responsiveness of the renin-angiotensin system in adult offspring

Aims: The goal of the current study was to evaluate the impact of maternal sodium intake during gestation on the systemic and renal renin-angiotensin-aldosterone-system (RAAS) of the adult offspring. Main methods: Female Wistar rats were fed high- (HSD-8.0% NaCl) or normal-sodium diets (NSD-1.3% NaCl) from 8 weeks of age until the delivery of their first litter. After birth, the offspring received NSD. Tail-cuff blood pressure (TcBP) was measured in the offspring between 6 and 12 weeks of age. At 12 weeks of age, the offspring were subjected to either one week of HSD or low sodium diet (LSD-0.1 6%NaCl) feeding to evaluate RAAS responsiveness or to acute saline overload to examine sodium excretory function. Plasma (PRA) and renal renin content (RRC), serum aldosterone (ALDO) levels, and renal cortical and medullary renin mRNA expression levels were evaluated at the end of the study. Key findings: TcBP was higher among dams fed HSD, but no TcBP differences were observed among the offspring. Male offspring, however, exhibited increased TcBP after one week of HSD feeding, and this effect was independent of maternal diet. Increased RAAS responsiveness to the HSD and LSD was also observed in male offspring. The baseline levels of PRA. ALDO, and cortical and medullary renin gene expression were lower but the RRC levels were higher among HSD-fed male offspring (HSDoff). Conversely, female HSDoff showed reduced sodium excretion 4 h after saline overload compared with female NSDoff. Significance: High maternal sodium intake is associated with gender-specific changes in RAAS responsiveness among adult offspring. (C) 2012 Elsevier Inc. All rights reserved.

Cognitive Training and Educational Intervention for Individuals with Hypertension: Effects on Cognition

Objectives: To evaluate the possibility of combining cognitive training to an educational intervention composed by eight sessions about hypertension for a better management of the disease among the elderly. Methods: 64 older adults who reported having hypertension, divided into experimental group (EG, n=35) and control group (CG, n=29) participated in the study. Control participants received training after the post-test. The protocol contained socio-demographic and clinical data, Mini-Mental State Examination (MMSE), Geriatric Depression Scale (GDS), Rivermead Behavioral Memory Test (RBMT), Verbal Fluency Animal Category (VF) and Short Cognitive Test (SKT). Results: The EG showed better cognitive performance when compared with the CG, at post-test. Conclusion: Cognitive gains may occur after psychoeducational interventions for older adults with hypertension.

AEROBIC EXERCISE TRAINING CORRECTS CAPILLARY RAREFACTION AND ALTERATIONS IN PROPORTIONS OF THE MUSCLE FIBERS TYPES IN SPONTANEOUSLY HYPERTENSIVE RATS

Aerobic exercise training (ET) has been established as an important non-pharmacological treatment of hypertension, since it decreases blood pressure. Studies show that the skeletal muscle abnormalities in hypertension are directly associated with capillary rarefaction, higher percentage of fast-twitch fibers (type II) with glycolytic metabolism predominance and increased muscular fatigue. However, little is known about these parameters in hypertension induced by ET. We hypothesized that ET corrects capillary rarefaction, potentially contributing to the restoration of the proportion of muscle fiber types and metabolic proprieties. Twelve-week old Spontaneously Hypertensive Rats (SHR, n=14) and Wistar Kyoto rats (WKY, n=14) were randomly assigned into 4 groups: SHR, trained SHR (SHR-T), WKY and trained WKY (WKY-T). As expected, ten weeks of ET was effective in reducing blood pressure in SHR-T group. In addition, we analyzed the main markers of ET. Resting bradycardia, increase of exercise tolerance, peak oxygen uptake and citrate synthase enzyme activity in trained groups (WKY-T and SHR-T) showed that the aerobic condition was achieved. ET also corrected the skeletal muscle capillary rarefaction in SHR-T. In parallel, we observed reduction in percentage of type IIA and IIX fibers and simultaneous augmented percentage of type I fibers induced by ET in hypertension. These data suggest that ET prevented changes in soleus fiber type composition in SHR, since angiogenesis and oxidative enzyme activity increased are important adaptations of ET, acting in the maintenance of muscle oxidative metabolism and fiber profile.

Effects of an adapted physical activity program on the physical condition of elderly women: an analysis of efficiency

Background: Specific research tools and designs can assist in identifying the efficiency of physical activity in elderly women. Objectives: To identify the effects of physical activity on the physical condition of older women. Method: A one-year-long physical activity program (123 sessions) was implemented for women aged 60 years or older. Four physical assessments were conducted, in which weight, height, BMI, blood pressure, heart rate, absences, grip strength, flexibility, VO2max, and static and dynamic balance were assessed. The statistical analyses included a repeated measures analysis, both inferential (analysis of variance - ANOVA) and effect size (Cohen's d coefficient), as well as identification of the participants' efficiency (Data Envelopment Analysis - DEA). Results: Despite the observation of differences that depended on the analysis used, the results were successful in the sense that they showed that physical activity adapted to older women can effectively change the decline in physical ability associated with aging, depending on the purpose of the study. The 60-65 yrs group was the most capable of converting physical activity into health benefits in both the short and long term. The >65 yrs group took less advantage of physical activity. Conclusions: Adherence to the program and actual time spent on each type of exercise are the factors that determine which population can benefit from physical activity programs. The DEA allows the assessment of the results related to time spent on physical activity in terms of health concerns. Article registered in Clinicaltrials.gov under number NCT01558401.

The role of AT1 receptor-mediated reproductive function in renovascular hypertension in male rats

There is an association between hypertension and reproductive dysfunction. Angiotensin II (Ang II) is involved in the pathogenesis of hypertension and the regulation of reproduction. The present study aimed to determine whether the angiotensinergic system mediates the effects of hypertension on ieproductive function in male rats subjected to a two-kidney, one-clip (2K1C) model. Sexual behavior parameters, gametogenesis and plasma concentrations of Ang II, testosterone, prolactin and corticosterone were evaluated in male rats 28 days after 2K1C or sham surgery and losartan (Los) treatment (a type 1 angiotensin II (All) receptor antagonist) or vehicle (V) treatment. The animals were divided into Sham + V, 2K1C + V. Sham + Los and 2K1C + Los groups. The 2KiC + V group showed a hypertensive response, inhibition of sexual behavior, spermatogenesis dysfunction, and increases in plasma Ang II and prolactin. Conversely, plasma testosterone decreased, and plasma corticosterone remained constant. Losartan treatment normalized blood pressure and prevented the changes in plasma testosterone and prolactin, sexual behavior and spermatogenesis in the 2KiC + Los group. In addition, losartan treatment caused an additional increase in circulating Ang II in both groups (She m + Los arid 2K1C + Los). Together, these results suggest that Ang II, acting through the All receptor, modulates behavioral and endocrine parameters of reproductive function during renovascular hypertension. In addition, the effects of circulating Ang II on plasma testosterone and prolactin seem to contribute to the spermatogenic and sexual dysfunctions in hypertensive rats. (C) 2012 Els.evier Inc. All rights reserved.

Glutathione Peroxidase 1 Pro198Leu Polymorphism in Brazilian Alzheimer's Disease Patients: Relations to the Enzyme Activity and to Selenium Status

Background/Aims: Oxidative stress plays a central role in Alzheimer's disease (AD). Pro198Leu cytosolic glutathione peroxidase (GPx1) polymorphism seems to be associated with a lower activity of this enzyme, but there are no studies with AD patients. Thus, the aim was to determine the frequency of the GPx1 Pro198Leu polymorphism in AD patients and to verify its relation to glutathione peroxidase (GPx) activity and selenium (Se) status. Methods:The study was carried out in a group of AD elderly (n = 28) compared to a control group (n = 29). Blood Se concentrations were measured through hydride generation atomic absorption spectroscopy. GPx activity was determined using a commercial kit, and the polymorphism using amplified DNA sequencing. Results:The distribution of genotypes was not different between groups. The variant allele frequency was 0.179 (AD group) and 0.207 (control group). Although no differences regarding GPx activity were found between individuals with different genotypes, lower blood Se levels were found in Pro/Pro AD patients compared to Pro/Pro control subjects, which was not found in the Pro/Leu groups. Moreover, the association between the erythrocyte Se concentration and GPx activity was affected by the Pro198Leu genotype. Conclusions: Results indicate that this polymorphism had apparently affected Se status in AD patients and that more studies in this field are necessary. Copyright (c) 2012 S. Karger AG, Basel

Aorta from angiotensin II hypertensive mice exhibit preserved nitroxyl anion mediated relaxation responses

Hypertension is a disorder affecting millions worldwide, and is a leading cause of death and debilitation in the United States. It is widely accepted that during hypertension and other cardiovascular diseases the vasculature exhibits endothelial dysfunction; a deficit in the relaxatory ability of the vessel, attributed to a lack of nitric oxide (NO) bioavailability. Recently, the one electron redox variant of NO, nitroxyl anion (NO-) has emerged as an endothelium-derived relaxing factor (EDRF) and a candidate for endothelium-derived hyperpolarizing factor (EDRF). NO- is thought to exist protonated (HNO) in vivo, which would make this species more resistant to scavenging. However, no studies have investigated the role of this redox species during hypertension, and whether the vasculature loses the ability to relax to HNO. Thus, we hypothesize that aorta from angiotensin II (AngII)-hypertensive mice will exhibit a preserved relaxation response to Angeli's Salt, an HNO donor. Male C57B16 mice, aged 12-14 weeks were implanted with mini-osmotic pumps containing AngII (90 ng/min, 14 days plus high salt chow) or sham surgery. Aorta were excised, cleaned and used to perform functional studies in a myograph. We found that aorta from AngII-hypertensive mice exhibited a significant endothelial dysfunction as demonstrated by a decrease in acetylcholine (ACh)-mediated relaxation. However, vessels from hypertensive mice exhibited a preserved response to Angeli's Salt (AS), the HNO donor. To confirm that relaxation responses to HNO were maintained, concentration response curves (CRCs) to ACh were performed in the presence of scavengers to both NO and HNO (carboxy-PTIO and L-cys, resp.). We found that ACh-mediated relaxation responses were significantly decreased in aorta from sham and almost completely abolished in aorta from AngII-treated mice. Vessels incubated with L-cys exhibited a modest decrease in ACh-mediated relaxations responses. These data demonstrate that aorta from AngII-treated hypertensive mice exhibit a preserved relaxation response to AS, an HNO donor, regardless of a significant endothelial dysfunction. (C) 2011 Elsevier Ltd. All rights reserved,

Effect of a single session of aerobic walking exercise on arterial pressure in community-living elderly individuals

Several studies have demonstrated that one exercise session (ES) on a cycloergometer or ergometric treadmill causes a reduction in blood pressure (BP). However, there are few similar studies on walking, which is the exercise modality most available to the elderly. We investigated the immediate and 24-h effects of walking on BP in independent, community-living elderly individuals. Volunteers participated in a single ES and resting control session (CS). Before and after each session, BP was measured by auscultatory and oscillometric methods. After each session, 24-h ambulatory blood pressure monitoring was conducted. An accelerometer was installed 48 h before the sessions and left in place for 5 days. The mean volunteer age was 67.7 +/- 3.5 years; 11 were hypertensive patients under treatment, and 12 were normotensive. In the total sample, there were immediate 14mm Hg and 12 mm Hg reductions in systolic BP (SBP) after the ES according to the auscultatory and oscillometric methods, respectively. Diastolic BP (DBP) was reduced by 4 mm Hg after the ES according to both methods. SBP during wakefulness and sleep and DBP during wakefulness were lower after the ES than after the CS (P<0.01), when wakefulness and sleep were determined individually (variable-time pattern) using data from the activity monitors and provided by the volunteers. The variable-time pattern was more effective in detecting reductions in BP than the fixed-time pattern. Hypertension Research (2012) 35, 457-462; doi: 10.1038/hr.2011.227; published online 9 February 2012

The relationship between training status, blood pressure and uric acid in adults and elderly

Abstract Background Hypertension can be generated by a great number of mechanisms including elevated uric acid (UA) that contribute to the anion superoxide production. However, physical exercise is recommended to prevent and/or control high blood pressure (BP). The purpose of this study was to investigate the relationship between BP and UA and whether this relationship may be mediated by the functional fitness index. Methods All participants (n = 123) performed the following tests: indirect maximal oxygen uptake (VO2max), AAHPERD Functional Fitness Battery Test to determine the general fitness functional index (GFFI), systolic and diastolic blood pressure (SBP and DBP), body mass index (BMI) and blood sample collection to evaluate the total-cholesterol (CHOL), LDL-cholesterol (LDL-c), HDL-cholesterol (HDL-c), triglycerides (TG), uric acid (UA), nitrite (NO2) and thiobarbituric acid reactive substances (T-BARS). After the physical, hemodynamic and metabolic evaluations, all participants were allocated into three groups according to their GFFI: G1 (regular), G2 (good) and G3 (very good). Results Baseline blood pressure was higher in G1 when compared to G3 (+12% and +11%, for SBP and DBP, respectively, p<0.05) and the subjects who had higher values of BP also presented higher values of UA. Although UA was not different among GFFI groups, it presented a significant correlation with GFFI and VO2max. Also, nitrite concentration was elevated in G3 compared to G1 (140±29 μM vs 111± 29 μM, for G3 and G1, respectively, p<0.0001). As far as the lipid profile, participants in G3 presented better values of CHOL and TG when compared to those in G1. Conclusions Taking together the findings that subjects with higher BP had elevated values of UA and lower values of nitrite, it can be suggested that the relationship between blood pressure and the oxidative stress produced by acid uric may be mediated by training status.

Mechanisms of endothelial dysfunction in obesity-associated hypertension

Obesity is strongly associated with high blood pressure, dyslipidemia, and type 2 diabetes. These conditions synergistically increase the risk of cardiovascular events. A number of central and peripheral abnormalities can explain the development or maintenance of high blood pressure in obesity. Of great interest is endothelial dysfunction, considered to be a primary risk factor in the development of hypertension. Additional mechanisms also related to endothelial dysfunction have been proposed to mediate the development of hypertension in obese individuals. These include: increase in both peripheral vasoconstriction and renal tubular sodium reabsorption, increased sympathetic activity and overactivation of both the renin-angiotensin system and the endocannabinoid system and insulin resistance. The discovery of new mechanisms regulating metabolic and vascular function and a better understanding of how vascular function can be influenced by these systems would facilitate the development of new therapies for treatment of obesity-associated hypertension.

Prevalence of overweight and obesity in elderly people from Vitória-ES, Brazil

The scope of this study was to estimate the prevalence of overweight and obesity and its association with socio-economic status in a sample of non-institutionalized elderly people from Vitória-ES, Brazil. This was a cross-sectional survey with a sample of 882 elderly people aged 60 and over. Obesity and overweight were assessed using the body mass index (BMI) and waist circumference (WC). All subjects answered a personal and socio-demographic questionnaire in relation to age, gender, marital status, physical activity, number of children, chronic diseases and smoking. Associations between categorical variables were tested using chi-square analysis with a 5% significance level. The prevalence of overweight and obesity was high (41.8% and 23.4%, respectively) and 50.7% of the elderly had a substantially increased waist circumference. About 4.3% of the individuals had diabetes, 50.4% had hypertension and 14.9% were found to have both diseases. It was observed that both the BMI and WC were significant associated (p<0.05) with sex, marital status, the presence of diseases and with cigarette smoking.

Hypertension, hypercholesterolemia, hyperaldosteronism: a genetic perspective for personalized therapy.

Essential, primary, or idiopathic hypertension is defined as high BP in which secondary causes such as renovascular disease, renal failure, pheochromocytoma, hyperaldosteronism, or other causes of secondary hypertension are not present. Essential hypertension accounts for 80-90% of all cases of hypertension; it is a heterogeneous disorder, with different patients having different causal factors that may lead to high BP. Life-style, diet, race, physical activity, smoke, cultural level, environmental factors, age, sex and genetic characteristics play a key role in the increasing risk. Conversely to the essential hypertension, secondary hypertension is often associated with the presence of other pathological conditions such as dyslipidaemia, hypercholesterolemia, diabetes mellitus, obesity and primary aldosteronism. Amongst them, primary aldosteronism represents one of the most common cause of secondary hypertension, with a prevalence of 5-15% depending on the severity of blood pressure. Besides high blood pressure values, a principal feature of primary aldosteronism is the hypersecretion of mineralcorticoid hormone, aldosterone, in a manner that is fairly autonomous of the renin-angiotensin system. Primary aldosteronism is a heterogeneous pathology that may be divided essentially in two groups, idiopathic and familial form. Despite all this knowledge, there are so many hypertensive cases that cannot be explained. These individuals apparently seem to be healthy, but they have a great risk to develop CVD. The lack of known risk factors makes difficult their classification in a scale of risk. Over the last three decades a good help has been given by the pharmacogenetics/pharmacogenomics, a new area of the traditional pharmacology that try to explain and find correlations between genetic variation, (rare variations, SNPs, mutations), and the risk to develop a particular disease.

Die Rolle der IFN-gamma Signalübertragung und von MyD88 in der Angiotensin-II-induzierten vaskulären Dysfunkion, Inflammation und arteriellen Hypertonie

Im Rahmen dieser Arbeit wurde die Rolle von myelomonozytären Zellen, IFN-gamma (Interferon gamma), MyD88 (myeloid differentiation factor 88) und zugrundeliegenden Signalwege in der Angiotensin II (ATII)-induzierten vaskulären Inflammation, Dysfunktion und arteriellen Hypertonie untersucht. Wie bereits veröffentlichte Vordaten aus meiner Arbeitsgruppe zeigten, schützt die Depletion von Lysozym M (LysM)+ myelomonozytären Zellen (Diphteriatoxin-vermittelt in Mäusen, die transgen für den humanen Diphtheriatoxin-Rezeptor sind, LysMiDTR Mäuse) vor der ATII-induzierten vaskulären Dysfunktion und arterieller Hypertonie, und kann durch adoptiven Zelltransfer von Wildtyp Monozyten wiederhergestellt werden. In meiner Arbeit konnte ich zeigen, dass die Rekonstitution von Monozyten-depletierten LysMiDTR Mäusen mit Wildtyp Monozyten den Phänotyp der vaskulären Dysfunktion wiederherstellen kann, die Rekonstitution mit gp91phox-/y oder Agtr1-/- Monozyten jedoch nicht. Die Hypertonus-mediierenden Effekte dieser infiltrierenden Monozyten scheinen demnach von der intakten ATII und NADPH Oxidase Signalübertragung in diesen Zellen abhängig zu sein. Vermutlich ebenfalls für die Aktivierung der Monozyten funktionell wichtig sind IFN-gamma, produziert durch NK-Zellen, und der Transkriptionsfaktor T-bet (T-box expressed in T cells), exprimiert von NK-Zellen und Monozyten. IFN-gamma-/- Mäuse waren partiell geschützt vor der ATII-induzierten vaskulären Dysfunktion und charakterisiert durch reduzierte Level an Superoxid im Gefäß im Vergleich zu ATII-infundierten Wildtyp Mäusen. IFN-gamma-/- und T-bet defiziente Tbx21-/- Mäuse zeichneten sich ferner durch eine reduzierte ATII-mediierte Rekrutierung von NK1.1+ NK-Zellen, als ein Hautproduzent von IFN-gamma, sowie CD11b+GR-1low Interleukin-12 (IL-12) kompetenten Monozyten aus. Durch Depletions- und adoptive Transferexperimente konnte ich in dieser Arbeit NK-Zellen als essentielle Mitstreiter in der vaskulären Dysfunktion identifizieren und stellte fest, dass T-bet+LysM+ myelomonozytäre Zellen für die NK-Zellrekrutierung in die Gefäßwand und lokale IFN-gamma Produktion benötigt werden. Damit wurde erstmals NK-Zellen eine essentielle Rolle in der ATII-induzierten vaskulären Dysfunktion zugeschrieben. Außerdem wurde der T-bet-IFN-gamma Signalweg und die gegenseitige Monozyten-NK-Zellaktivierung als ein potentielles therapeutisches Ziel in kardiovaskulären Erkrankungen aufgedeckt. Des Weiteren identifizierte ich in meiner Arbeit MyD88 als ein zentrales Signalmolekül in der ATII-getriebenen Inflammation und vaskulären Gefäßschädigung. MyD88 Defizienz reduzierte den ATII-induzierten Anstieg des systolischen Blutdrucks und die endotheliale und glattmuskuläre vaskuläre Dysfunktion. Zusätzlich waren die vaskuläre Superoxid-Bildung sowie die Expressionslevel der NADPH Oxidase, der wichtigsten Quelle für oxidativem Stress im Gefäß, in ATII-infundierten MyD88-/- Mäusen im Vergleich zum Wildtyp reduziert. Mit Hilfe von durchflusszytometrischen Analysen deckte ich zudem auf, dass die ATII-induzierte Einwanderung von CD45+ Leukozyten, insbesondere CD11b+Ly6G-Ly6Chigh inflammatorischen Monozyten in MyD88-/- Mäusen signifikant abgeschwächt war. Diese Resultate wurden durch immunhistochemische Untersuchung von Aortengewebe auf CD68+, F4/80+ und Nox2+ Makrophagen/Phagozyten sowie Expressionsanalysen von Inflammationsmarkern untermauert. Analysen der mRNA Expression in Aortengewebe zeigten ferner eine in Wildtyp Mäusen nach ATII Infusion tendenziell gesteigerte Expression von inflammatorischen Monozytenmakern sowie eine abnehmende Expression von reparativen Monozytenmarken, während dieser Shift zu einem proinflammatorsichen Phänotyp in MyD88-/- blockiert zu sein schien. Dies zeigt eine Rolle von MyD88 in der terminalen Differenzierung von myelomonozytären Zellen an. Um dies weitergehend zu untersuchen und aufzudecken, ob die MyD88 Effekte abhängig sind von Zellen der hämatopoetischen Linie oder Gewebszellen, wurden Knochenmarktransferexperimente durchgeführt. MyD88 Defizienz in Knochenmark-abstammende Zellen reduzierte die ATII-induzierte vaskuläre Dysfunktion und Infiltration der Gefäßwand mit CD45+ Leukozyten und inflammatorischen myelomonozytären Zellen. Die protektiven Effekte der MyD88 Defizienz in der Angiotensin II-induzierten Inflammation konnten nicht auf Signalwege über die Toll-like Rezeptoren TLR2, -7 oder -9 zurückgeführt werden, wie die Untersuchung der vaskulären Reaktivität entsprechender Knockout Mäuse zeigte. Zusammenfassend konnte ich in meiner Arbeit zeigen, dass die Infiltration der Gefäßwand mit Nox2+AT1R+T-bet+MyD88+ myelomonozytären Zellen und die Wechselwirkung und gegenseitige Aktivierung dieser Zellen mit IFN-gamma produzierenden NK-Zellen eine zentrale Bedeutung in der Pathogenese der Angiotensin II (ATII)-induzierten vaskulären Dysfunktion, Inflammation und arteriellen Hypertonie einnehmen.

Regulation of GPCR signaling in hypertension

Hypertension represents a complex, multifactorial disease and contributes to the major causes of morbidity and mortality in industrialized countries: ischemic and hypertensive heart disease, stroke, peripheral atherosclerosis and renal failure. Current pharmacological therapy of essential hypertension focuses on the regulation of vascular resistance by inhibition of hormones such as catecholamines and angiotensin II, blocking them from receptor activation. Interaction of G-protein coupled receptor kinases (GRKs) and regulator of G-protein signaling (RGS) proteins with activated G-protein coupled receptors (GPCRs) effect the phosphorylation state of the receptor leading to desensitization and can profoundly impair signaling. Defects in GPCR regulation via these modulators have severe consequences affecting GPCR-stimulated biological responses in pathological situations such as hypertension, since they fine-tune and balance the major transmitters of vessel constriction versus dilatation, thus representing valuable new targets for anti-hypertensive therapeutic strategies. Elevated levels of GRKs are associated with human hypertensive disease and are relevant modulators of blood pressure in animal models of hypertension. This implies therapeutic perspective in a disease that has a prevalence of 65million in the United States while being directly correlated with occurrence of major adverse cardiac and vascular events. Therefore, therapeutic approaches using the inhibition of GRKs to regulate GPCRs are intriguing novel targets for treatment of hypertension and heart failure.

Relationship between chronic stress and carotid intima-media thickness (IMT) in elderly Alzheimer's disease caregivers

The stress associated with providing care for a spouse diagnosed with Alzheimer's disease can have adverse effects on cardiovascular health. One potential explanation is that chronic caregiving stress may contribute to the development of atherosclerosis. The purpose of this study was to determine whether the duration that one has provided care is associated with the degree of atherosclerotic burden, as measured by carotid artery intima-media thickness (IMT). One hundred and ten Alzheimer caregivers [mean age 74 ± 8 (SD) years, 69% female] underwent in-home assessment of carotid artery IMT via B-mode ultrasonography. Data regarding medical history, blood pressure, and multiple indicators of caregiving stress were also collected. Multiple regression indicated that duration of care was positively associated with IMT measured in the internal/bifurcation segments of the carotid artery (β = 0.202, p = 0.044) independent of risk factors such as age, gender, body mass index, smoking history, sleep quality, hypertension status, and caregiving stressors. Duration of care was positively associated with IMT in the common carotid artery, but the relationship was not significant. These findings provide more evidence of the link between chronic caregiving stress and cardiovascular disease and indicate that enduring the experience of caregiving over a period of years might be associated with atherosclerotic burden.