author_facet Kuchel, O
Buu, N T
Hamet, P
Larochelle, P
Bourque, M
Genest, J
Kuchel, O
Buu, N T
Hamet, P
Larochelle, P
Bourque, M
Genest, J
author Kuchel, O
Buu, N T
Hamet, P
Larochelle, P
Bourque, M
Genest, J
spellingShingle Kuchel, O
Buu, N T
Hamet, P
Larochelle, P
Bourque, M
Genest, J
Hypertension
Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
Internal Medicine
author_sort kuchel, o
spelling Kuchel, O Buu, N T Hamet, P Larochelle, P Bourque, M Genest, J 0194-911X 1524-4563 Ovid Technologies (Wolters Kluwer Health) Internal Medicine http://dx.doi.org/10.1161/01.hyp.3.6_pt_2.ii-129 <jats:p>Hypertensive patients with elevated and hyperresponsive plasma norepinephrine and epinephrine (NE + E) associated with low conjugated NE + E were previously identified by determination of the sum of NE + E. Because of their excessive E but not NE responses to glucagon and also hypertension corresponding to E excess, we explored whether an elevated unconjugated E resulting from a selective E conjugation defect could be obscured by the sum of NE + E. We found that nine patients with elevated E (reflected by the normal 4:1 ratio of plasma NE to E reversed in favor of E), had, when compared to 31 patients with plasma NE exceeding E:1) lower plasma conjugated E (mean 0.03 vs 0.27 ng/ml, p less than 0.01), lower degree of E conjugation (8 vs 51%, p less than 0.01), and a higher maximum systolic (p less than 0.05), pulse pressure (p less than 0.02) and higher pulse rates (p less than 0.04), but no differences in the unconjugated and conjugated proportions of plasma NE; and 2) an absence of conjugated E throughout the circulation and relative preponderance of E over NE at sampling points close to the peripheral venous blood (p less than 0.05). The absolutely and relatively decreased plasma conjugated E in patients with E exceeding NE (without difference in conjugated NE) is a preliminary indication that a selective sulfoconjugating defect of E results in plasma E higher than NE in accordance with the hyper-beta-adrenergic features of their hypertension. Epinephrine, a circulating hormone, is more dependent on conjugated E reflect better this defect than those measuring the sum of NE and E.</jats:p> Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma? Hypertension
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title Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_unstemmed Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_full Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_fullStr Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_full_unstemmed Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_short Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_sort unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
topic Internal Medicine
url http://dx.doi.org/10.1161/01.hyp.3.6_pt_2.ii-129
publishDate 1981
physical
description <jats:p>Hypertensive patients with elevated and hyperresponsive plasma norepinephrine and epinephrine (NE + E) associated with low conjugated NE + E were previously identified by determination of the sum of NE + E. Because of their excessive E but not NE responses to glucagon and also hypertension corresponding to E excess, we explored whether an elevated unconjugated E resulting from a selective E conjugation defect could be obscured by the sum of NE + E. We found that nine patients with elevated E (reflected by the normal 4:1 ratio of plasma NE to E reversed in favor of E), had, when compared to 31 patients with plasma NE exceeding E:1) lower plasma conjugated E (mean 0.03 vs 0.27 ng/ml, p less than 0.01), lower degree of E conjugation (8 vs 51%, p less than 0.01), and a higher maximum systolic (p less than 0.05), pulse pressure (p less than 0.02) and higher pulse rates (p less than 0.04), but no differences in the unconjugated and conjugated proportions of plasma NE; and 2) an absence of conjugated E throughout the circulation and relative preponderance of E over NE at sampling points close to the peripheral venous blood (p less than 0.05). The absolutely and relatively decreased plasma conjugated E in patients with E exceeding NE (without difference in conjugated NE) is a preliminary indication that a selective sulfoconjugating defect of E results in plasma E higher than NE in accordance with the hyper-beta-adrenergic features of their hypertension. Epinephrine, a circulating hormone, is more dependent on conjugated E reflect better this defect than those measuring the sum of NE and E.</jats:p>
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author Kuchel, O, Buu, N T, Hamet, P, Larochelle, P, Bourque, M, Genest, J
author_facet Kuchel, O, Buu, N T, Hamet, P, Larochelle, P, Bourque, M, Genest, J, Kuchel, O, Buu, N T, Hamet, P, Larochelle, P, Bourque, M, Genest, J
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description <jats:p>Hypertensive patients with elevated and hyperresponsive plasma norepinephrine and epinephrine (NE + E) associated with low conjugated NE + E were previously identified by determination of the sum of NE + E. Because of their excessive E but not NE responses to glucagon and also hypertension corresponding to E excess, we explored whether an elevated unconjugated E resulting from a selective E conjugation defect could be obscured by the sum of NE + E. We found that nine patients with elevated E (reflected by the normal 4:1 ratio of plasma NE to E reversed in favor of E), had, when compared to 31 patients with plasma NE exceeding E:1) lower plasma conjugated E (mean 0.03 vs 0.27 ng/ml, p less than 0.01), lower degree of E conjugation (8 vs 51%, p less than 0.01), and a higher maximum systolic (p less than 0.05), pulse pressure (p less than 0.02) and higher pulse rates (p less than 0.04), but no differences in the unconjugated and conjugated proportions of plasma NE; and 2) an absence of conjugated E throughout the circulation and relative preponderance of E over NE at sampling points close to the peripheral venous blood (p less than 0.05). The absolutely and relatively decreased plasma conjugated E in patients with E exceeding NE (without difference in conjugated NE) is a preliminary indication that a selective sulfoconjugating defect of E results in plasma E higher than NE in accordance with the hyper-beta-adrenergic features of their hypertension. Epinephrine, a circulating hormone, is more dependent on conjugated E reflect better this defect than those measuring the sum of NE and E.</jats:p>
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spelling Kuchel, O Buu, N T Hamet, P Larochelle, P Bourque, M Genest, J 0194-911X 1524-4563 Ovid Technologies (Wolters Kluwer Health) Internal Medicine http://dx.doi.org/10.1161/01.hyp.3.6_pt_2.ii-129 <jats:p>Hypertensive patients with elevated and hyperresponsive plasma norepinephrine and epinephrine (NE + E) associated with low conjugated NE + E were previously identified by determination of the sum of NE + E. Because of their excessive E but not NE responses to glucagon and also hypertension corresponding to E excess, we explored whether an elevated unconjugated E resulting from a selective E conjugation defect could be obscured by the sum of NE + E. We found that nine patients with elevated E (reflected by the normal 4:1 ratio of plasma NE to E reversed in favor of E), had, when compared to 31 patients with plasma NE exceeding E:1) lower plasma conjugated E (mean 0.03 vs 0.27 ng/ml, p less than 0.01), lower degree of E conjugation (8 vs 51%, p less than 0.01), and a higher maximum systolic (p less than 0.05), pulse pressure (p less than 0.02) and higher pulse rates (p less than 0.04), but no differences in the unconjugated and conjugated proportions of plasma NE; and 2) an absence of conjugated E throughout the circulation and relative preponderance of E over NE at sampling points close to the peripheral venous blood (p less than 0.05). The absolutely and relatively decreased plasma conjugated E in patients with E exceeding NE (without difference in conjugated NE) is a preliminary indication that a selective sulfoconjugating defect of E results in plasma E higher than NE in accordance with the hyper-beta-adrenergic features of their hypertension. Epinephrine, a circulating hormone, is more dependent on conjugated E reflect better this defect than those measuring the sum of NE and E.</jats:p> Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma? Hypertension
spellingShingle Kuchel, O, Buu, N T, Hamet, P, Larochelle, P, Bourque, M, Genest, J, Hypertension, Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?, Internal Medicine
title Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_full Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_fullStr Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_full_unstemmed Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_short Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_sort unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
title_unstemmed Unconjugated hyperepinephrinemia: a hallmark of hypertension imitating pheochromocytoma?
topic Internal Medicine
url http://dx.doi.org/10.1161/01.hyp.3.6_pt_2.ii-129