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Postural hypotension in diabetic patients with autonomic neuropathy is driven by compromised baroreceptor reflexes and damaged sympathetic innervation.
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Discusses the pathophysiology and clinical challenge of managing postural hypotension in patients with diabetic autonomic neuropathy.
To diabetic patients with circulatory autonomic neuropathy, postural hypotension can be a perpetual source of frustration. They may not be able to come to terms with gravity. To their physicians this disability is a source of perplexity. They may find it difficult to explain why therapy is ineffective when etiology and pathophysiology are seemingly well known. How well understood, in effect, is postural hypotension of autonomic diabetic neuropathy? Normally, a rise to the upright position causes blood to pool in the lower extremities with resulting fall in venous pressure, cardiac output, and arterial blood pressure. These changes provoke instantaneous reflex peripheral vasoconstriction, increased heart rate, and a rise in plasma norepinephrine and renin levels. As a result of these compensatory adjustments, the vascular hemodynamic steady state is restored, and the blood pressure promptly returns to its previous level. Compromised baroreceptor reflexes and damaged sympathetic innervation of the peripheral vasculature have
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Samuel Vaisrub (1978) conducted an editorial in Diabetic autonomic neuropathy with postural hypotension. Postural hypotension in diabetic patients with autonomic neuropathy is driven by compromised baroreceptor reflexes and damaged sympathetic innervation.
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