Blood Pressure In Normotensive Individuals Research Articles

NON-INTERVENTIONAL WEIGHT CHANGES AFFECT SYSTOLIC BLOOD PRESSURE IN NORMOTENSIVE INDIVIDUALS

Objective: The association between obesity and hypertension is well established. Weight loss has been shown to reduce blood pressure (BP) among hypertensive patients. Nevertheless, the effect of weight changes on BP in normotensive individuals is less clear. We explored the association between non-interventional weight alterations and BP changes in a large cohort of normotensive adults. Design and method: a retrospective analysis of normotensive individuals, between 2010–2018. All weight changes were non-interventional. Body mass index (BMI) and BP were measured annually. Patients were divided according to the change in BMI between visits: reduction of more than 5% (’large reduction’), between 2.5–5% (’moderate reduction’), reduction of less than 2.5% or elevation of less than 2.5% (’unchanged’), elevation between 2.5–5% (’moderate increase’) and elevation of more than 5% (’large increase’). The primary outcome was the change in systolic BP (SBP) between the visits. Results: The final analysis included 8,723 individuals. 20% of the subjects reduced their BMI by at least 2.5% and 24.5% increased their BMI by more than 2.5%. ’High reduction’ inferred an absolute decrease of 3.6 mmHg in SBP, while ’large increase’ resulted in an absolute increase of 1.9 mmHg in SBP. The proportion of individuals with at least 10 mmHg decrease in SBP progressively declined according to the relative decrease in BMI, and the proportion of patients with at least 10 mmHg increase in SBP progressively increased. This effect was more pronounced in individuals with higher baseline SBP. Conclusions: Among normotensive adults, modest non-interventional weight changes may have significant effects on SBP.

Non-interventional weight changes affect systolic blood pressure in normotensive individuals.

The association between obesity and hypertension is well established. Weight loss has been shown to reduce blood pressure (BP) among hypertensive patients. Nevertheless, the effect of weight changes on BP in normotensive individuals is less clear. The author explored the association between non‐interventional weight alterations and BP changes in a large cohort of normotensive adults. This is a retrospective analysis of normotensive individuals, between 2010 and 2018. All weight changes were non‐interventional. Body mass index (BMI) and BP were measured annually. Patients were divided according to the change in BMI between visits: reduction of more than 5% ("large reduction"), between 2.5% and 5% ("moderate reduction"), reduction of <2.5% or elevation of <2.5% ("unchanged"), elevation between 2.5% and 5% ("moderate increase"), and elevation of more than 5% ("large increase"). The primary outcome was the change in systolic BP (SBP) between the visits. The final analysis included 8723 individuals. 20% of the patients reduced their BMI by at least 2.5% and 24.5% increased their BMI by more than 2.5%. "High reduction" inferred an absolute decrease of 3.6 mmHg in SBP, while "large increase" resulted in an absolute increase of 1.9 mmHg in SBP. The proportion of individuals with at least 10 mmHg decrease in SBP progressively declined according to the relative decrease in BMI, and the proportion of patients with at least 10 mmHg increase in SBP progressively increased. This effect was more pronounced in individuals with higher baseline SBP. Among normotensive adults, modest non‐interventional weight changes may have significant effects on SBP.

How important is blood pressure variability?

Arterial blood pressure (BP) is a continuous variable, with a physiology characterized by significant variability stemming from the complex interaction among haemodynamic factors, neuronal reflexes, as well as hormonal, behavioural, and environmental stimuli. The homoeostatic response accounts for the physiologic variability in BP in normotensive individuals, which is more evident in hypertensive patients. Blood pressure variability is a complex phenomenon, which could be classified in various types: very short term (beat to beat), short term (during 24 h), mid-term (day by day), long term (<5 years), and very long term (>5 years). Accurate measurement of BP variability represents a complex and often controversial endeavour, despite several methodological approaches are available. Albeit a prognostic significance has been demonstrated for some indicators of BP variability, the clinical significance of this measurement is still uncertain. In fact, none of the indicators presently available for BP variability, including early morning BP rise, substantially affects, and redefines, the cardiovascular risk of the hypertensive patient, over and beyond the mere BP values. Accordingly, in defining the cardiovascular risk, the focus should be on the absolute BP values, which remain the most relevant risk factor, and the one more susceptible to modification with both non-pharmacologic and pharmacologic treatment.

Negative Affectivity Is Associated with a Higher Systolic and Diastolic Blood Pressure in Normotensive Middle-Aged and Older Adults: A Cross-Sectional Study.

Background and objectives: Type D personality, characterized by two stable traits (social inhibition and negative affectivity), is associated with adverse cardiovascular events. A possible mediating factor for this association could be hypertension. Previous research has shown that individuals with Type D personality were associated with an increased risk of hypertension. However, the association of negative affectivity and social inhibition on blood pressure in normotensive individuals has not yet been reported. Therefore, the aim of this study was to investigate whether negative affectivity and social inhibition were associated with systolic and diastolic blood pressure in normotensive middle-aged and older Taiwanese adults. Materials and Methods: A cross-sectional study design was used. Individuals attending general health examination at a regional hospital in southern Taiwan who were 40 to 75 years old were recruited. Patients with self-reported hypertension or currently receiving antihypertensive medication were excluded. Negative affectivity and social inhibition were assessed with the 14-item Type D Scale-Taiwanese version. Multiple linear regression analyses were conducted to determine the association of Z-score transformed negative affectivity and social inhibition on blood pressure. Results: A total of 92 patients with a mean age of 51.5 years were included in the study, and 15 (16.3%) were defined as having a Type D personality. The Z-score transformed negative affectivity score (p = 0.035, effect size = 0.18) and Z-score transformed social inhibition score (p = 0.054, effect size = 0.17) were significantly associated with a higher systolic blood pressure. In addition, the Z-score transformed negative affectivity score (p = 0.036, effect size = 0.28) and Z-score transformed social inhibition score (p = 0.154, effect size = 0.24) were significantly associated with a higher diastolic blood pressure. Conclusions: Negative affectivity of the Type D personality was significantly associated with higher systolic and diastolic blood pressure, with a medium effect size, in apparently healthy middle-aged and older adults. Assessment of negative affectivity may be clinically useful in identifying individuals at risk of hypertension.

The association between morning blood pressure and subclinical target organ damage in the normotensive population.

To investigate whether isolatedly elevated morning blood pressure (BP) is associated with subclinical target organ damage in normotensive individuals. In all, 287 normotensive individuals were included in this cross-sectional study. Each participant underwent anthropometric measurements, serum biochemistry evaluation, 24-h ambulatory BP monitoring, echocardiography, and carotid ultrasonography. The morning BP and morning surge were defined as: the average BP within 2 h after waking up, and the difference between the mean systolic BP (SBP) within 2 h after waking up and the mean SBP during the hour that included the lowest BP reading during sleep, respectively. The prevalence of elevated morning BP was 37.3%. Individuals with elevated morning BP had higher left ventricular mass index and morning surge, and also mean 24-h, daytime, and night-time SBP and diastolic BP, BP variability (all P < 0.05). Left ventricular mass index was correlated with 24-h, daytime, night-time, and morning SBP, and morning surge (Pearson's correlation coefficients: 0.271, 0.262, 0.215, 0.368, and 0.415, respectively; all P < 0.05); and standard deviations of 24-h, daytime, and night-time SBP (Pearson's correlation coefficient: 0.303, 0.234, and 0.309, respectively), and coefficient of variations of 24-h and night-time SBP (Pearson's correlation coefficients: 0.253 and 0.271, respectively). Morning surge had the strongest correlation with left ventricular mass index in multiple regression analysis. Only daytime and morning SBP could discriminate elevated morning surge (≥35 mmHg), with an area under the curve of 0.744 and 0.864, respectively (both P < 0.01), and an optimal threshold of 121.5 mmHg for morning SBP. Our findings suggest that isolated elevation of morning BP in normotensive individuals is associated with left ventricular hypertrophy. Home monitoring of morning BP may be suitable for detecting abnormal morning surge.

Evidence to Consider Angiotensin II Receptor Blockers for the Treatment of Early Alzheimer's Disease.

Alzheimer's disease is the most frequent type of dementia and diagnosed late in the progression of the illness when irreversible brain tissue loss has already occurred. For this reason, treatments have been ineffective. It is imperative to find novel therapies ameliorating modifiable risk factors (hypertension, stroke, diabetes, chronic kidney disease, and traumatic brain injury) and effective against early pathogenic mechanisms including alterations in cerebral blood flow leading to poor oxygenation and decreased access to nutrients, impaired glucose metabolism, chronic inflammation, and glutamate excitotoxicity. Angiotensin II receptor blockers (ARBs) fulfill these requirements. ARBs are directly neuroprotective against early injury factors in neuronal, astrocyte, microglia, and cerebrovascular endothelial cell cultures. ARBs protect cerebral blood flow and reduce injury to the blood brain barrier and neurological and cognitive loss in animal models of brain ischemia, traumatic brain injury, and Alzheimer's disease. These compounds are clinically effective against major risk factors for Alzheimer's disease: hypertension, stroke, chronic kidney disease, diabetes and metabolic syndrome, and ameliorate age-dependent cognitive loss. Controlled studies on hypertensive patients, open trials, case reports, and database meta-analysis indicate significant therapeutic effects of ARBs in Alzheimer's disease. ARBs are safe compounds, widely used to treat cardiovascular and metabolic disorders in humans, and although they reduce hypertension, they do not affect blood pressure in normotensive individuals. Overall, there is sufficient evidence to consider long-term controlled clinical studies with ARBs in patients suffering from established risk factors, in patients with early cognitive loss, or in normal individuals when reliable biomarkers of Alzheimer's disease risk are identified.

Interventricular Septum and Posterior Wall Thickness Are Associated With Higher Systolic Blood Pressure.

Elevated blood pressure (BP) is a known factor that affects the structure of the left ventricle. The association between left ventricular hypertrophy (LVH) and BP in normotensive individuals is poorly understood. All individuals who underwent routine echocardiography and BP measurements as aircrew candidates for the Israeli Air Force in the years 2006 to 2012 were identified. Participants with normal values were included. Associations between echocardiographic characteristics and BP were studied. A total of 2386 participants were included. Mean systolic BP was 125.31±11.18 mm Hg and mean diastolic BP was 68.69±9.02 mm Hg. Interventricular septal (IVS) thickness was positively correlated with systolic BP (P<.001, correlation coefficient 0.121) and significantly inversely correlated with heart rate and hematocrit level (P<.001 for both). Men with evidence of IVS or posterior wall thickening on echocardiography, even within the normal range, may require a closer follow-up of BP.

Effect of buttermilk consumption on blood pressure in moderately hypercholesterolemic men and women

ObjectivesMilk fat globule membrane (MFGM) found in buttermilk is rich in unique bioactive proteins. Several studies suggest that MFGM proteins possess biological activities such as cholesterol-lowering, antiviral, antibacterial, and anticancer properties, but data in humans are lacking. Furthermore, to our knowledge, no study has yet investigated the antihypertensive potential of MFGM proteins from buttermilk. The aim of this study was to investigate the effects of buttermilk consumption on blood pressure and on markers of the renin–angiotensin–aldosterone (RAS) system in humans. MethodsMen and women (N = 34) with plasma low-density lipoprotein cholesterol < 5 mmol/L and normal blood pressure (< 140 mm Hg) were recruited in this randomized, double-blind, placebo-controlled, crossover study. Their diets were supplemented with 45 g/d of buttermilk and with 45 g/d of a macro-/micronutrient-matched placebo in random order (4 wk for each diet). ResultsButtermilk consumption significantly reduced systolic blood pressure (−2.6 mm Hg; P = 0.009), mean arterial blood pressure (−1.7 mm Hg; P = 0.015), and plasma levels of the angiotensin I-converting enzyme (−10.9%; P = 0.003) compared with the placebo, but had no effect on plasma concentrations of angiotensin II and aldosterone. ConclusionShort-term buttermilk consumption reduces blood pressure in normotensive individuals.

Testosterone and Secondary Hypertension

See related article, pp 1263–1271 The absence of estrogen, in males or after menopause in women, is independently associated with increased cardiovascular risk.1 A number of factors have been implicated as the underlying cause, including effects at the cell-organ level (eg, inflammatory activation, increased oxidative stress, and increased vasoconstriction),1 as well as changes in cardiovascular physiology (eg, sympathetic activation, increased blood pressure, and insulin resistance). All of these parameters are sensitive to modulation by sex steroid hormones,1 particularly 17β-estradiol, testosterone, and its more active metabolite, 5α-dihydrotestosterone, which is produced from testosterone by 5α-reductase.1,2 Testosterone is the main male sex steroid hormone but is also produced by women.2 Testosterone is converted to 17β-estradiol by aromatase in numerous tissues, including the vasculature and adipose tissue, representing an important local source of estrogen.3 In obesity, aromatase-derived 17β-estradiol formation may represent an important cause of feminization in males and the increased risk of estrogen-sensitive cancers in obese females.3 ### Androgenic Steroids and Cardiovascular Risk In many countries, including the United Kingdom, the United States, Canada, and Australia, anabolic androgenic steroids, such as testosterone, are controlled substances, and their nonmedical use is considered drug abuse.4,5 Testosterone has been used since the 1930s for nonmedical, athletic purposes, especially in male and female body builders and swimmers.6 Because testosterone abuse may increase arterial blood pressure,7 leading to left ventricular hypertrophy,8 it should be included among the differential diagnoses of secondary arterial hypertension. Moreover, testosterone abuse has been associated with myocardial infarction because of coronary vasospasm9 or thrombosis.10–12 Among the mechanisms of how exogenous, as opposed to endogenous, testosterone contributes to increased in cardiovascular risk, coagulatory activation, as well as accelerated progression of coronary artery disease, have been described.10 Sex steroids dilate human coronary …

Abstract P101: Genetic Variation of Phenylethanolamine-N-methyltransferase Influences Cardiovascular Function in Healthy Humans

Objectives: Genetic susceptibility to hypertension can be caused by alterations in cardiovascular and/or renal function. Previous work using genome-wide association studies have demonstrated that the gene that encodes phenylethanolamine-N-methyltransferase (PNMT) is a candidate for hypertension. Follow-up studies confirmed that the gene that encodes PNMT may alter susceptibility to hypertension in African Americans, although no mechanistic data was assessed. Genetic variation of PNMT alters the catecholamine response to exercise, and variation of PNMT at position -182 has been associated with susceptibility to multiple sclerosis. Methods: We sought to determine the influence of genetic variation of PNMT (A-182G) on renal Na + handling and cardiovascular function in humans. We collected serum epinephrine (Epi) and norepinephrine (NE), 24-hour urine, serum Na + , K + , and creatinine, and measured cardiac output (Q, acetylene rebreathing), heart rate (HR, 12-lead EKG), blood pressure (systolic, SBP, diastolic, DBP, and calculated mean arterial, MAP) and calculated fractional excretion of Na + (F E Na), stroke volume (SV), and systemic vascular resistance (SVR) in 20 normotensive subjects (n: AA=6 and GG=14). Results: We found that the GG genotype had higher Epi and Epi/NE when compared to AA (Epi=98±21 vs. 53±10pg/l; NE= 344±56 vs. 462±79pg/l; Epi/NE= 0.31±0.07 vs. 0.13±0.03, for GG and AA, respectively, mean±SE, p&lt;0.05 for Epi and Epi/NE). We found no differences between the genotype groups in 24hr. renal Na + handling (serum Na + , urine Na + , or F E Na). We found no differences in HR, SBP, or SV between the groups. The GG group had a trend towards a lower DBP, and MAP, but these did not reach statistical significance (DBP= 70±3 vs. 75±2mmHg; MAP= 83±3 vs. 87±2mmHg, for GG and AA, respectively, mean±SE). The GG group had a higher Q and a lower SVR when compared to the AA group (Q= 6.0±0.5 vs. 4.8±0.4 l/min; SVR= 1020±64 vs. 1316±95 dynes*sec/cm 5 , for GG and AA, respectively mean±SE, p&lt;0.05). Conclusion: These results suggest that genetic variation of PNMT can influence resting blood pressure in normotensive individuals and that this may be the result of cardiovascular function, rather than renal Na + handling.

Dietary Approaches to Stop Hypertension (DASH) diet: applicability and acceptability to a UK population

The Dietary Approaches to Stop Hypertension (DASH) diet is widely promoted in the USA for the prevention and treatment of high blood pressure. It is high in fruit and vegetables, low-fat dairy and wholegrain foods and low in saturated fat and refined sugar. To our knowledge, the use of this dietary pattern has not been assessed in a free-living UK population. The DASH diet was adapted to fit UK food preferences and portion sizes. Fourteen healthy subjects followed the adapted DASH diet for 30 days in which they self-selected all food and beverages. Dietary intake was assessed by 5-day food diaries completed before and towards the end of the study. Blood pressure was measured at the beginning and end of the study to assess compliance to the DASH style diet. The DASH diet was easily adapted to fit with UK food preferences. Furthermore, it was well tolerated and accepted by subjects. When on the DASH style diet, subjects reported consuming significantly (P < 0.01) more carbohydrate and protein and less total fat (5%, 6% and 9% total energy, respectively). Sodium intakes decreased by 860 mg day(-1) (P < 0.001). Systolic and diastolic blood pressure decreased significantly (P < 0.05) by 4.6 and 3.9 mmHg, respectively when on the DASH style diet. The DASH style diet was well accepted and was associated with a decrease in blood pressure in normotensive individuals and should be considered when giving dietary advice to people with elevated blood pressure in the UK.

Beetroot juice consumption reduced blood pressure in normotensive individuals in an acute dose-response study

Elevated blood pressure (BP) is a leading preventable cause of morbidity and mortality and an established independent risk factor for CVD and stroke. Fruit and vegetable-rich diets have been shown to reduce systolic blood pressure (SBP) in hypertensive subjects. Green leafy vegetables conferred the strongest protection. These contain high concentrations of nitrate that can act as a substrate for the endogenous formation of the potent vasodilator nitric oxide after consumption. Beetroot juice (BJ) is also rich in nitrate and has been shown to lower SBP by 10 mmHg in normotensive individuals when given as a 500 ml dose. The present study investigated the dose-response effects of BJ on 24 h ambulatory blood pressure (ABP). Twenty-five normotensive volunteers (18 males and 7 females), aged 18–64 years, consumed 3 doses of BJ (100, 250 and 500 ml) and a water/no BJ control in a single-blind, randomized and controlled crossover study. Low-nitrate mineral water was used to match the volume in all drinks to 500 ml. ABP was determined every 15 min for 1 h pre- and 4 h post-drink consumption, every 30 min for a further 9 h and hourly overnight. Urine was collected at 0, 2, 4, 6 and 24 h after BJ consumption. The subjects followed a low-nitrate diet for 48 h and consumed standardised low-nitrate meals the night before and during the study day.

Does nicotinic acid (niacin) lower blood pressure?

Nicotinic acid (niacin) is a well-established treatment for dyslipidaemia – an important cardiovascular disease (CVD) risk factor. However, niacin may also reduce blood pressure (BP), which is another important CVD risk factor. This review examines the limited publicly available data on niacin’s BP effects. Acute administration of immediate-release niacin may lower BP because of niacin’s acute vasodilatory effects. Although not always supported by clinical trial data, the package insert of a prescription, extended-release niacin describes niacin-induced acute hypotension. From a chronic standpoint, larger studies, such as the Coronary Drug Project, suggest that niacin may lower BP when administered over a longer period of time. Post hoc analyses of some of the more recent niacin clinical trials also support a more chronic, dose-dependent, BP-lowering effect of niacin. Because laropiprant [a prostaglandin D2 (PGD2) type 1 (DP1) receptor antagonist] does not attenuate niacin’s BP-lowering effects, it is unlikely that any chronic lowering of BP by niacin is due to dilation of dermal vessels through activation of the DP1 receptor by PGD2. Further research is warranted to evaluate the extent and mechanisms of niacin’s effects on BP.

Prevention and Management of Hypertension Without Drugs

Lifestyle modifications and non-drug therapies are a vast group of measures essential to the prevention and management of hypertension. International experts unanimously recommend some of them. However, not all measures are equally valuable or have the same evidence base. The first step in the management of patients at any age who have hyper- tension should be a reduction in salt intake, either alone or in combination with drug therapy, to which is often additive. A high potassium diet achieved with an increase in the consumption of fruit and vegetables is also recommended. Weight reduction, regular dynamic exercise and reduction of alcohol consumption should be included in management plans for the prevention and non-pharmacological treatment of hypertension. The qualitative composition of diet is also an impor- tant factor to consider for the prevention and management of hypertension. Beyond the benefits associated with specific nutrients, adherence to a dietary pattern based on the DASH (Dietary Approaches to Stop Hypertension) diet, as part of a comprehensive lifestyle intervention, is a suitable, cost-effective approach to prevent high blood pressure in normotensive individuals; moreover, if combined with reduced sodium intake, it may represent an alternative to drug therapy for indi- viduals with mild hypertension willing to comply with long-term dietary changes.

Body weight and weight change in relation to blood pressure in normotensive men

We examined blood pressure (BP) in association with weight change since age 20, body mass index (BMI) at different ages and fat distribution in normotensive individuals using baseline survey data collected in the Shanghai Men's Health Study, an ongoing population-based prospective cohort study of Chinese men aged 40-74 years. All anthropometric and BP measurements were performed by medical professionals. Included in this analysis were 25 619 men who had no prior history of hypertension, diabetes or cardiovascular disease, never took any antihypertensive medication and had both normal systolic BP (SBP) and diastolic BP (DBP) (<140/90 mm Hg). Both SBP and DBP increased linearly across the whole range of weight gain since age 20. The adjusted mean differences between the highest and the lowest quintiles of weight gain were 6.0 mm Hg (95% confidence interval (CI): 5.6, 6.5) for SBP and 3.9 (95% CI: 3.6, 4.2) for DBP. When accounting for BMI at age 20, the multivariate-adjusted odds ratio of prehypertension (SBP, 120-139 and/or DBP, 80-89 mm Hg) was 4.1 (95% CI: 3.7, 4.5; P for trend <0.0001) comparing the extreme quintiles of weight gain. Similar positive associations were also observed for BMI at age 40, current BMI, circumferences of the waist and hips and waist-to-hip ratio. In conclusion, these data suggest that weight gain since age 20 and elevated adiposity may contribute significantly to the rise in BP in normotensive individuals, emphasizing the importance of weight control throughout adulthood in preventing high BP.

Influence of polymorphism of glutathione S-transferase M1 on systolic blood pressure of normotensive individuals

Studies have indicated that systolic (SBP) and diastolic (DBP) blood pressure are multi-factorial traits and significantly heritable. The aims of the present study are to assess whether the glutathione S-transferase M1 (GSTM1) and T1 (GSTT1) genotypes are associated with SBP and DBP of normotensive subjects and to ascertain whether the level of SBP and DBP given exposure to cigarette smoking is modified by the specific genetic polymorphisms of GSTM1 and GSTT1. This cross-sectional study was conducted on 140 subjects (49 females and 91 males) (mean age ± SD: 38.7 ± 14.7). The genotypes were determined using a polymerase chain reaction based method. Individuals were stratified according to the mean values of DBP and SBP, lower than or maximally same as the mean value defines as group I and higher than the mean value defines as group II. The logistic regression analyses were used. The best models fitted by logistic regression analysis for variables were associated with SBP and DBP. For analysis the combination of genotypes, sex, and smoking behavior was used as qualitative variables, and age, body mass index (BMI), and heart rate were used as covariates. Combination of “present-GSTT1, null-GSTM1” genotype (OR = 0.001, 95% CI = 0.00–0.439, P = 0.025), heart rate (OR = 1.065, 95% CI = 1.018–1.114, P = 0.006), and interaction between BMI and combination of “present-GSTT1, null-GSTM1” (OR = 1.319, 95% CI = 1.058–1.644, P = 0.014) was associated with SBP. There was no association between either combination genotypes of GSTs or interaction of genotypes and smoking behavior on DBP. The present results suggest that the GSTM1 gene is one of the candidate genes that alter the baseline of SBP in normotensive individuals.

Nonpharmacologic therapies that reduce blood pressure: a fresh perspective.

Traditional approaches to control the epidemic of blood pressure-related atherosclerotic cardiovascular disease (ASCVD) have largely focused on drug therapy in persons with hypertension. Still, nonpharmacologic therapy, also termed lifestyle modification, has an important and expanding role that complements drug therapy. Specifically, nonpharmacologic therapies can serve as initial therapy in Stage 1 hypertensive patients, facilitate medication step down or withdrawal in patients with well-controlled hypertension, prevent hypertension in high-risk populations, and reduce blood pressure in normotensive individuals and thereby lower their risk of ASCVD. Traditional lifestyle modifications that reduce blood pressure include sodium reduction, weight loss, moderation of alcohol intake, and increased physical activity. Such strategies have been prominently advocated in the Fifth Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Recommendations to increase potassium, magnesium, and calcium intake were based primarily on general health considerations, not for control of high blood pressure. In its sixth and most recent report (JNC VI) published in 1997, the Joint National Committee has extended its recommendations. In addition to the traditional lifestyle recommendations, the JNC VI advocates increased potassium intake for control of high blood pressure. Furthermore, this policy-making body now recommends a healthy dietary pattern, that is, one that is rich in fruits, vegetables, and low-fat dairy products, and reduced in saturated fat, total fat, and cholesterol. This diet, which was rigorously evaluated in the Dietary Approaches to Stop Hypertension (DASH) clinical trial, substantially lowered blood pressure in normotensive and hypertensive individuals. These recent developments reinforce the hypothesis that multiple dietary factors influence blood pressure. Nonpharmacologic approaches have enormous potential as a means to reduce blood pressure and control hypertension, thereby preventing the occurrence of ASCVD. The current challenge to health care providers, government officials, and the general public is to develop and implement effective clinical and public health strategies that lead to desirable lifestyle modifications.

BLOOD PRESSURE RESPONSE TO EXERCISE IN LOW AND HIGH FIT, MIDDLE-AGED WOMEN

1428 An exaggerated increase in exercise blood pressure (BP) is associated with risk for cardiovascular events even in those with normal resting BP. Fitness levels are associated with lower resting BP. Thus, we sought to determine if fitness levels were also associated with lower exercise BP in normotensive individuals. We assessed fitness and BP during a graded exercise test (Bruce Protocol), in 735 middle-aged (43±11) women. All were free of heart disease and antihypertensive medication. They were classified as Low-Fit (n=362) or High-Fit (n=373) based on exercise time to exhaustion (ETE), adjusted for age. Groups were similar in age and resting BP with significant differences in exercise BP (p<0.05); table). Multivariate regression revealed the strongest predictors of BP at 6 minutes of exercise, were ETE, resting BP and age (R2=0.46). For peak exercise BP the predictors were resting systolic BP and age (R2=0.30). The risk of having exaggerated BP during exercise (systolic BP ≥ 190 mm Hg), was 53% lower in the High-Fit vs the Low-Fit group (Odds Ratio=0.47; CI: 0.35-0.64).TableWe concluded that in middle-aged women: 1) physical fitness is associated with lower BP at sub-maximum and maximum exercise workloads; and 2) exaggerated BP response to exercise may be attenuated by increased physical fitness.

Interaction of nonsteroidal anti-inflammatory drugs with antihypertensive and diuretic agents: Control of vascular reactivity by endogenous prostanoids

Indomethacin and some other nonsteroidal anti-inflammatory drugs partially antagonize the blood pressure lowering effect of drugs used to treat hypertension. They can also produce a mild elevation of blood pressure in normotensive individuals. The elevated arterial pressure caused by these agents is associated with Increases in the vascular resistance of mainly the renal and splanchnic beds. This may be due to direct inhibition of the synthesis of vasodilator prostanoids, or it may be due to indirect potentiation of the action of the sympathetic nervous system or of angiotensin II. Nonsteroidal antiinflammatory drugs also cause renal retention of sodium and this probably contributes to their hypertensive effects. In humans, the sodium retention may involve increased reabsorption in the proximal tubule. Although a direct tubular action is possible, these drugs may change proximal sodium reabsorption by their vascular effects. However, the exact mechanism is not understood. These interactions are clinically significant and may complicate the treatment of common diseases.