Disorders of sympathetic neural function in human diabetes mellitus: hypoadrenergic and hyperadrenergic postural hypotension.
Although sympathoadrenal activation occurs in poorly controlled diabetes, particularly diabetic ketoacidosis, abnormalities in sympathoadrenal activity have not been convincingly documented to be a general feature of patients with controlled, nonketotic diabetes. Some stable nonketotic diabetic patients, however, exhibit hypoadrenergic patterns whereas others exhibit hyperadrenergic patterns. Recent evidence indicates that diabetic patients with hypoadrenergic postural hypotension--diabetic adrenergic neuropathy--have a sympathetic postganglionic axonal lesion. However, postural hypotension can occur in patients who exhibit a hyperadrenergic pattern--hyperadrenergic postural hypotension. Intravascular volume contraction, specifically a reduction in red cell mass, at least partially underlies the latter phenomenon in some patients. Thus, postural hypotension in patients with diabetes should not be quickly attributed to diabetic adrenergic neuropathy since potentially remediable factors may contribute to its pathogenesis.
D000311:Adrenal Glands / Q000294:innervation / Q000503:physiopathology*; D000315:Adrenalectomy; D000450:Aldosterone / Q000097:blood; D048909:Diabetes Complications; D003920:Diabetes Mellitus / Q000503:physiopathology; D004491:Edrophonium / Q000494:pharmacology; D004837:Epinephrine / Q000097:blood; D006801:Humans; D007024:Hypotension, Orthostatic / Q000209:etiology*; D009638:Norepinephrine / Q000097:blood; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D000450:Aldosterone; D004491:Edrophonium; D009638:Norepinephrine; D004837:Epinephrine