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Biomedical subjects

H P Dustan

Publications and source records attributed to H P Dustan.

At least 19 recordsLinked to original sources
PubMed1996

Controlling hypertension. A research success story.

In the past 2 decades, deaths from stroke have decreased by 59% and deaths from heart attack by 53%. An important component of this dramatic change has been the increased use of antihypertensive drugs. This remarkable success resulted from broad-based and diverse research programs supported by the federal government, pharmaceutical companies, voluntary health agencies, and private foundations. It included basic research, drug development programs, epidemiologic studies, health surveys of US citizens, clinical research, and large-scale drug trials. Four of the categories of antihypertensive drugs in wide use--diuretics, beta-blockers, calcium antagonists, and angiotensin-converting enzyme inhibitors--emerged from widely different areas of investigation. In the beginning, the major breakthroughs that led to the development of these drugs were impossible to forecast, and their ultimate applications were impossible to predict. Although decreases in hypertension-related mortality are impressive, enthusiasm must be tempered because the mechanisms of hypertension are still incompletely understood and prevention is not yet possible. Continued research is needed to extend these advances.

Antihypertensive Agents↗
PubMed1996

Gender differences in hypertension.

The evidence we have for the US, Australia and Korea indicates that men have slightly higher pressures than women and slightly greater prevalence of hypertension. In the US this sex difference is reversed at about age 70 and persists throughout the rest of the lifespan. How much these gender differences affect gender differences in cardiovascular disease manifestations is not clear, but remains an intriguing possibility.

Adolescent↗
PubMed1995

Does keloid pathogenesis hold the key to understanding black/white differences in hypertension severity?

Repeated national surveys have shown that in the United States hypertension is more common and more severe in the black than in the white population. This discussion presents the hypothesis that the racial difference in hypertension severity is because of differences in growth factors (cytokines) affecting vascular smooth muscle cell growth. This hypothesis is derived from studies of keloids, which occur almost exclusively in blacks. Keloid fibroblasts in culture have growth characteristics that differ substantially from those of normal skin. Furthermore, there is evidence that peripheral blood mononuclear cells from patients with keloids produce different amounts of cytokines than do similar preparations from the blood of individuals without keloids. A growing body of evidence indicates that growth factors play a pivotal role in the pathogenesis of atherosclerosis, in experimental forms of hypertension, and in various renal diseases; it may be that they function in clinical hypertension as well.

Adolescent↗
PubMed1992

Cardiovascular consequences of obesity.

Obesity is common in populations that are overnourished and can become a significant public health problem. Obesity predisposes to non-insulin dependent diabetes mellitus, hypertension, dyslipidemia, cholelithiasis, some malignancies and osteoarthritis. These consequences that most directly affect the cardiovascular system are dyslipidemia and hypertension. Nations in which obesity is rare should learn from the experience of the countries where it is prevalent, that prevention of obesity is a public health measure rather than weight reduction.

Coronary Disease↗
PubMed1991

Treatment of obesity-associated hypertension.

Many obese people are hypertensive either because of obesity-associated hypertension or because the two conditions coexist. Weight loss is recommended for all obese hypertensives as some patients benefit by concomitant reductions of arterial pressure and/or decreased requirements for antihypertensive drugs. Since obesity-associated hypertension cannot be diagnosed as a separate entity, available evidence was reviewed to determine the antihypertensive effectiveness of weight loss and effects of weight loss on antihypertensive drug requirements. Generally speaking, patients with mild hypertension appear to respond better to weight reduction than those with moderate and severe hypertension. However, a substantial percentage of patients with mild hypertension may be unresponsive. Weight loss also seems to have potential for lessening requirements for antihypertensive drug therapy. Beneficial effects for both blood pressure and drug requirements are due to weight loss and not caloric restriction, per se. Mechanisms of the beneficial effects are related to consequences of weight loss and appear to involve decreased cardiac output and blood volume. The issue of salt sensitivity of obesity-associated hypertension is unresolved.

Antihypertensive Agents↗
PubMed1991

A perspective on the salt-blood pressure relation.

Current recommendations for a population-wide decrease in dietary salt consumption come from a conclusion that a substantial portion of the population with essential hypertension is salt-sensitive. It is difficult to determine the appropriateness of these recommendations because of critical gaps in knowledge of the salt-blood pressure relation. There is no agreement on a definition of salt-sensitive blood pressure changes. There is no consensus about mechanisms of changes; several have been suggested but none seems universal. In fact, differing results suggest marked heterogeneity in the mechanisms of salt-sensitive hypertension, and some evidence points to the possibility that arterial pressure of hypertensive subjects is controlled differently than that of normotensive subjects during manipulation of salt intake. Because salt-sensitive blood pressure changes are not always related to the magnitude of the positive sodium balance, it seems possible that for some people the current recommendations for modest dietary sodium restriction may be inadequate to influence blood pressure control for the prevention of hypertension.

Blood Pressure↗
PubMed1991

Obesity and hypertension.

There is a close association of obesity with hypertension through mechanisms not now understood. Hypertension occurs frequently in industrialized societies where weight gain with advancing years is a common feature and is rare in primitive societies where weight and age are negatively correlated. Hemodynamically, obesity is characterized by an expanded blood volume and increased cardiac output. Hypertension results if/when systemic vascular resistance fails to decrease as cardiac output increases. When calorie restriction leads to weight loss, both blood volume and cardiac output decrease; when the blood pressure falls, this is because peripheral resistance is unchanged. Weight-loss programs are helpful for the obese hypertensive because when hypertension is mild, blood pressure often (but not always) normalizes. Also, weight loss has been shown to decrease antihypertensive drug requirements. Interest in obesity-associated hypertension focuses on hyperinsulinemia/insulin resistance as causative factors. Although the evidence is tempting, it is far from conclusive and it seems likely that the mechanism of this type of hypertension is as multifactorial as those of other types.

Blood Glucose↗
PubMed1991

Hypertension and obesity.

Obesity is a major risk factor for hypertension that itself is a direct cause of premature cardiovascular morbidity and mortality. When hypertension is mild, weight reduction normalizes it often enough to warrant weight loss instructions for all obese hypertensives. Reasons for the obesity and hypertension relationship are as yet unclear. Although current interest focuses on hyperinsulinemia and insulin resistance, hemodynamic data suggest that the fault lies in an inability to reduce vascular resistance as blood volume and cardiac output rise.

Antihypertensive Agents↗
PubMed1991

Obesity-related hypertension: evaluation of the separate effects of energy restriction and weight reduction on hemodynamic and neuroendocrine status.

PURPOSE: Although weight reduction generally lowers blood pressure, it is unclear whether the response is due to concurrent dietary changes or to reduced body mass itself. In this study, the independent effects of energy restriction and weight reduction were examined prospectively in 24 obese, hypertensive, normoglycemic women whose dietary intake was tightly controlled. SUBJECTS AND METHODS: Sodium, potassium, and calcium intake, the polyunsaturated/saturated fat ratio, and the proportional composition of carbohydrate, fat, and protein were constant throughout the 5-month protocol. Hemodynamic and neuroendocrine status was evaluated in four 10-day hospital phases: two prior to weight loss (energy balance and then 800-kcal intake), and two after an average loss of 13 kg to normal body weight (800 kcal and then return to energy balance). RESULTS: Fasting serum insulin, triiodothyronine:reverse triiodothyronine ratio, resting metabolic rate, and heart rate declined, and sodium and potassium balances were negative during energy restriction. Catecholamines, renin, aldosterone, plasma volume, cardiac output, and blood pressure showed no consistent response to changes in energy intake. By contrast, weight reduction independently lowered blood pressure, plasma volume, cardiac output, and plasma renin activity. Body fat pattern remained unchanged. CONCLUSION: These results demonstrate that weight loss has a blood pressure-lowering effect that is distinct from energy restriction and that is related to changes in blood volume and cardiac output.

Aged↗