Despite years of investigation our fundamental and clinical knowledge of the major public health problem,
obesity-
hypertension, is relatively meager and certainly inadequate. We are at a loss to explain why the pathophysiological mechanisms of
obesity and
hypertension are so inextricably intertwined. Adding to this frustration is the inadequacy of the treatment for
obesity. Hemodynamically, we recognize that the expanded plasma volume caused by
obesity imparts a significant volume overload on the heart, thereby increasing cardiac output, while the
hypertension compounds this ventricular stress by an associated pressure overload. Thus, the ventricle has an eccentric as well as a concentric adaptive
hypertrophy. Associated with
obesity is an increased burden of pressor (e.g.,
catecholamine,
angiotensin II);
peptide (e.g.,
endothelin,
insulin,
leptin, natriuretic); hormonal (e.g., growth,
steroids, thyroid); and neural mechanisms. Further complicating these alterations are electrolytic,
lipid,
uric acid, and other metabolic factors. Both diseases (
obesity and
hypertension) are exacerbated by frequently encountered comorbid pathophysiological disorders including
atherosclerosis,
ventricular dysfunction,
diabetes mellitus,
hyperlipidemias, and
sleep apnea. To add to these issues,
therapy for
obesity-
hypertension is suboptimal. Behavioral modification (of
overweight and
obesity) is commonly characterized by recidivism, and
pharmacotherapy of
obesity is woefully inadequate; the present agents either raise arterial pressure or are fraught with adverse effects. Fortunately, there are no
contraindications imparted by
obesity that complicate the
drug treatment of the associated
hypertension. Each of the lifestyle modifications and seven classes of
antihypertensive therapy that is discussed herein is done in light of the coexistent
hypertension and comorbid diseases.