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Previous Volume 335:1240-1242 October 17, 1996 Number 16 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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To the Editor: The prevalence of hypertension is increased in patients with insulin resistance and hyperinsulinemia. This observation has led to the hypothesis that insulin causes hypertension, and insulin-induced stimulation of renal sodium reabsorption, vascular smooth-muscle growth, and sympathetic-nerve activity have been proposed as potential pathogenetic mechanisms.¹ The proposal that sympathetic-nerve activity is a pathogenetic mechanism is based on the observations that short-term insulin infusions in lean subjects stimulate sympathetic-nerve activity and that obesity (a state characterized by hyperinsulinemia) is associated with sustained sympathetic activation.^2,3 However, the sympathoexcitatory effects of sustained hyperinsulinemia cannot be established on the basis of such . . . [Full Text of this Article]

References

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