Obesity and hypertension

A rise in blood pressure is associated with increased body weight. Epidemi-ological studies indicate that obesity is a strong independent risk factor for hypertension (Modan et al., 1985; Stamler et al., 1993). In the Framingham Study, for example, the prevalence of hypertension among obese individuals was twice that of those individuals with normal weight irrespective of sex and age (Hubert et al, 1983). The INTERSALT Study involving 10000 men and women showed that a 10-kg increase in weight was associated with 3-mmHg rise in systolic and 2.3-mmHg rise in diastolic blood pressure (Dyer and Elliott, 1989). This level of blood pressure elevation is associated with a 12 per cent increase risk for CHD and 24 per cent increase for stroke. In the Nurses' Health Study, the relative risk of hypertension in those women who gained 5.0 to 9.9 kg and greater than 25.0 kg was 1.7 and 5.2, respectively (Huang et al., 1998). The risk of hypertension was even higher with abdominal obesity (WHR > 0.9 in men and > 0.85 in women) (Blair et al., 1984).

The exact mechanism of the association of central obesity and hypertension is not fully defined. Insulin resistance may provide a metabolic link perhaps through hyperinsulinaemia. Hyperinsulinaemia enhances sodium reabsorption directly through its effects on distal renal tubules (De Fronzo et al., 1975) and indirectly through the stimulation of central sympathetic nervous system (Moan et al., 1995; Rearen et al., 1996). It also augments angiotensin-II-mediated aldosterone secretion (Landsberg, 1992). The resultant hypervolaemia causes an increase in cardiac output, yet the total peripheral resistance remains near normal with failure of vasodilatation of the systemic vasculature. Vasodilation is thought to be mediated by nitric oxide (NO) and this vasodilatory effect is blunted in obese and hypertensive subjects (Baron et al., 1995; Steinberg et al., 1996).

Another mechanism which may cause increased vascular tone is through alterations in cation transport. Insulin has been shown to stimulate NA/K ATPase activity with accumulation of intracellular sodium along with increase in intra-cellular calcium leading to vascular resistance and hypertension (Sowers and Draznin, 1998).

This link between hyperinsulinaemia and hypertension is not seen in Pima Indians despite commonly having hyperinsulinaemia, insulin resistance and obesity (Saad et al., 1991). These discrepancies might be explained by difference in genetic susceptibility to the development of hypertension or to the effects of insulin on blood pressure. Another explanation is that there might be 'selective insulin resistance' with impaired ability of insulin to cause glucose uptake, but preservation of some actions such as renal sodium retention, activation of the renin-angiotensin system, alteration in cation flux and stimulation of the sympathetic nervous system.

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