Primary or secondary activation of immune mechanisms has been implicated in the pathogenesis of many forms of hypertension. Changes in serum immunoglobulin levels, alterations in both humoral and cellular immune functions, and inherited abnormalities of the complement system have been identified in patients with essential hypertension. In addition, many models of spontaneous hypertension (such as the Okamoto and Lyon strains of hypertensive rats and the hypertensive New Zealand Black mouse) have identifiable abnormalities in immune function that are associated with their hypertensive disease. Other models (such as partial renal infarct hypertension, post-mineralocorticoid-salt hypertension, and hypertension induced by repeated injections of angiotensin II) also may have primary or secondary immunologic factors contributing to their etiology. Although there is a strong association between alterations in immune function and hypertension, the specific immunologic mechanisms that contribute to the pathogenesis of hypertension are not known. Therefore, further investigation will be necessary to elucidate these mechanisms.

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Abstract-Obesity often leads to symptoms of cardiopulmonary congestion associated with normal systolic but abnormal diastolic function. This study analyzed alterations in passive diastolic compliance in obesity using the rabbit model. New Zealand White rabbits were fed a normal (nϭ8) or 10% added fat diet (nϭ8 Key Words: heart Ⅲ stroke volume Ⅲ obesity Ⅲ computer modeling Ⅲ diastolic pressure-volume relationship O besity is independently associated with an increase in morbidity and mortality, resulting primarily from increased incidence of cardiovascular diseases such as stroke, coronary artery disease, and congestive heart failure. 1 The precise mechanisms leading to greater risk for developing congestive heart failure in obesity are unknown but may stem from the increased work load on the heart imposed by the combination of increased cardiac output, increased intravascular volume, hypertension, and cardiac hypertrophy. 2 Interestingly, some obese patients with symptoms of systemic and pulmonary congestion present with normal systolic function; however, diastolic function is often abnormal. 3 In fact, it has been estimated that 35% to 40% of patients with congestive heart failure present with diastolic dysfunction only. 4 Diastolic dysfunction may be simply described as a condition in which diastolic filling is impeded. However, diastolic filling of the left ventricle is a complex process determined by the interaction of several factors, including active ventricular relaxation and passive properties influencing left ventricular compliance. Active relaxation is related to calcium reuptake by the sarcoplasmic reticulum, whereas passive ventricular filling properties are determined by ventricular wall thickness, the dimensions of the ventricular cavities, and the structural properties of the cardiac tissue itself. A few studies have attempted to examine the diastolic pressurevolume relationship, 5,6 and the data suggested that morbidly obese patients exhibit abnormalities in diastolic filling, with or without the presence of hypertension or cardiac hypertrophy. 7,8 Although there is evidence that diastolic filling is altered in obesity, 7 it is difficult to determine from clinical studies what role altered diastolic compliance plays in diastolic dysfunction. Little is known about the mechanisms underlying abnormal diastolic function in obesity or the relative contributions of decrements in active versus passive relaxation to filling abnormalities. In addition, little is known about how quickly diastolic dysfunction becomes manifest during the development of obesity. Therefore, our purpose was to examine the passive end-diastolic pressure-volume relationship in isolated hearts of obese and control rabbits to determine the presence and extent of obesity-related decrements in passive diastolic compliance. In addition, we used computer models of circulatory function to predict systemic effects resulting from reduced compliance both at rest and during exercise.

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