INTRODUCTION
Obesity has been studied for years and is still being studied today (2). The leading cause of mortality worldwide is cardiovascular diseases, hypertension and diabetes, and this is associated with obesity. There are many contributing factors to obesity than one would think. Some of the health issues that could be life threatening are hypertension, diabetes, coronary disease, heart failure, etc. (2). Obesity is the most common health disorder in the United States, and affects the majority of adults in the country (5).
Obesity has many causes that do not have a single explanation, but there are factors that are associated with obesity like; Ethnicity, social economic status, region of residence, season, and urban living (5). Obesity ultimately results from an imbalance between energy intake and energy expenditure, meaning not being able to burn calories as fast as they are being consumed (3).
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MATERIALS AND METHODS
Upon researching the APUS Library about Obesity and its causes and effects on hypertension, the topic, “Obesity: Causes and Effects on High Blood Pressure” came into thought. During this research process, 5 articles and 1 graph were selected to provide the information needed to complete this essay. This study reflects information about hypertensive patients that were followed up on at an outpatient clinic and had a documented history of chronic high blood pressure without any causes or underlying issues (1). The study is conducted by The Cardiology Branch of the National Heart, Lung, and Blood Institute (NHLBI).
This study was on 27 hypertensive patients and 28 healthy patients and was designed to investigate the vivo vasoconstrictor activity of ET-1 (endothelin receptor) in hypertension (1). Patients were not taking any medications and any that were being taken was stopped 2 weeks before the study. Volunteers that were normal are selected as a control group and matched with patients of approximate race, gender, and age (1). The studies were performed in the mornings, in a room with the temperature of 76°F and participants was asked to not drink alcohol or caffeine for 24 hours before the studies (1). Each study had an infusion of drugs into the brachial artery and measurement of the response of the forearm vasculature by use of strain-gauge venous occlusion plethysmography. The blood pressure was recorded directly from this arterial catheter.
Graph 1 Bars show FBF responses to BQ-123 according to BMI in normotensive subjects (right panel) and hypertensive patients (left panel). Values (each is average of 6 measurements taken every 10 minutes during drug infusion) represent mean+SEM. Probability values refer to changes in FBF from baseline during selective ET blockade by 1-way ANOVA for related measures (1).
Many studies have found a relationship between obesity and hypertension (4). These studies investigate the linkages of being overweight and health issues caused by the obesity. Hypertension is a massive relation and is life threatening to say the least. Obese individuals have many commonalities, like; depression, lack of activity, pain, sicknesses, loss of sexual desire, etc. (5). These linkages are studied to find common grounds and helpful information to hopefully assist in reducing obesity and hypertension along with it. The study listed above covers just one side of the many studies out there.
RESULTS
Arterial pressure and heart rate did not drastically change after infusion of any of the drugs used in the study. The findings indicated that the drug effects were limited to the infused forearm. ET-1 caused a significant vasoconstrictor response in both obese normotensive and hypertensive subjects (1). There are many lines of reasoning that suggest a potential role of the activated ET-1 in the pathophysiology of complication of obesity-related hypertension (1).
CONCLUSION
The main finding of the study is that blockade of ET-1 receptors results in important vasodilation in overweight and obese subjects, but not in lean hypertensive subjects. It doesn’t determine any significant hemodynamic change in normotensive controlled subjects, irrespective of their body mass (1).
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