TY - JOUR
T1 - Disorders of sympathetic neural function in human diabetes mellitus
T2 - Hypoadrenergic and hyperadrenergic postural hypotension
AU - Cryer, Philip E.
N1 - Funding Information:
From the Metabolism Division, Department of Medicine, Washington University School of Medicine. St. Louis. MO. Supported in part by USPHS grants AA420579 and RR00036 and by Grants from the Diabetic Children’s Welfare Association/American Diabetes Association, Greater St. Louis AJiliate. Address reprint requests to Dr. Philip E. Cryer. the Department of Medicine. Washington University School of Medicine. 660 South Euclid. St. Louis, MO. 631 IO. o 1980 by Grune & Stratton, Inc. 0026&0495~80/2913-0012$01.00/0
PY - 1980
Y1 - 1980
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0019254972&partnerID=8YFLogxK
U2 - 10.1016/0026-0495(80)90028-1
DO - 10.1016/0026-0495(80)90028-1
M3 - Article
C2 - 7432176
AN - SCOPUS:0019254972
SN - 0026-0495
VL - 29
SP - 1186
EP - 1189
JO - Metabolism: clinical and experimental
JF - Metabolism: clinical and experimental
IS - 11
ER -