The role of sympathetic-adrenergic activity in the regulation of acid-base homeostasis and renal sodium excretion under acute physical stress in type-I diabetic children (IDDM).

T. Tulassay, A. Yasar, L. Madácsy, A. Körner, L. Szücs

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Abstract

To evaluate the ability of stress response, plasma and urinary catecholamine concentrations, urinary electrolytes and acid-base status were measured in IDDM children (Group I: newly diagnoses 2-4 weeks, n = 7; Group II: duration 5-7 yr, n = 9; Group III: duration 10-13 yr, n = 12). The data were compared to healthy controls, n = 7, (mean +/- SD). Physical stress was induced by 2 W/kg/10 min bicycle ergometer. IDDM children exhibited metabolic acidosis under stress (pH: Group I = 7.24 +/- 0.08; Group II = 7.25 +/- 0.05; Group III = 7.19 +/- 0.03 vs C = 7.36 +/- 0.02). Stress induced an increase in the concentration of plasma norepinephrine (PNE in each group, the most pronounced elevation was seen in Group I (19.36 +/- 8.8 nmol/I vs C = 8.3 +/- 3.2, p <0.2). Baseline PNE level showed a significant decrease with the duration of IDDM. Excretion of urinary NE (UNE) also increased under stress, however, the highest levels were measured in Group III (580 +/- 209 pmol/min/l. 73m2 vs 290 +/- 124 in Group I, p <.01). Baseline urinary dopamine (UDA) excretions were similar in each group. Stress caused an elevation in UDA only in C (2.05 +/- 1.8 vs 4.59 +/- 2.9 pmol/min.l. 73m2). The ratio of baseline UNE/UDA was similar in Groups I, II and C, but higher in Group III. Stress induced a shift towards NE excretion only in diabetic children which was most pronounced in children having IDDM more than 10 years. Stress did not affect urine output in Groups I. and II., but a decrease was observed in Group III (1.1 +/- 0.3 vs 0.7 +/- 0.3 ml/min.1.73 m2, p <.007). Urinary sodium excretion also decreased in Group III after physical loading (130 +/- 47 vs 66 +/- 33 umol/min/1.73 m2). The data show, that physical stress induces a severe lactic acidosis in IDDM. In spite of the decreased systemic sympathetic activity, the renal catecholamine response showed a shift towards vasoconstriction, sodium and fluid retention under physical stress in IDDM. These changes correlate with the duration of the underlying disease.

Original languageEnglish
Pages (from-to)175-186
Number of pages12
JournalActa bio-medica de L'Ateneo parmense : organo della Società di medicina e scienze naturali di Parma
Volume63
Issue number1-2
Publication statusPublished - 1992

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Type 1 Diabetes Mellitus
Adrenergic Agents
Homeostasis
Sodium
Acids
Dopamine
Catecholamines
Lactic Acidosis
Acidosis
Vasoconstriction
Electrolytes
Renal Elimination
Norepinephrine
Urine
Kidney

ASJC Scopus subject areas

  • Medicine(all)

Cite this

@article{3afcf0ced33e4731a2d402ce79ffa5ad,
title = "The role of sympathetic-adrenergic activity in the regulation of acid-base homeostasis and renal sodium excretion under acute physical stress in type-I diabetic children (IDDM).",
abstract = "To evaluate the ability of stress response, plasma and urinary catecholamine concentrations, urinary electrolytes and acid-base status were measured in IDDM children (Group I: newly diagnoses 2-4 weeks, n = 7; Group II: duration 5-7 yr, n = 9; Group III: duration 10-13 yr, n = 12). The data were compared to healthy controls, n = 7, (mean +/- SD). Physical stress was induced by 2 W/kg/10 min bicycle ergometer. IDDM children exhibited metabolic acidosis under stress (pH: Group I = 7.24 +/- 0.08; Group II = 7.25 +/- 0.05; Group III = 7.19 +/- 0.03 vs C = 7.36 +/- 0.02). Stress induced an increase in the concentration of plasma norepinephrine (PNE in each group, the most pronounced elevation was seen in Group I (19.36 +/- 8.8 nmol/I vs C = 8.3 +/- 3.2, p <0.2). Baseline PNE level showed a significant decrease with the duration of IDDM. Excretion of urinary NE (UNE) also increased under stress, however, the highest levels were measured in Group III (580 +/- 209 pmol/min/l. 73m2 vs 290 +/- 124 in Group I, p <.01). Baseline urinary dopamine (UDA) excretions were similar in each group. Stress caused an elevation in UDA only in C (2.05 +/- 1.8 vs 4.59 +/- 2.9 pmol/min.l. 73m2). The ratio of baseline UNE/UDA was similar in Groups I, II and C, but higher in Group III. Stress induced a shift towards NE excretion only in diabetic children which was most pronounced in children having IDDM more than 10 years. Stress did not affect urine output in Groups I. and II., but a decrease was observed in Group III (1.1 +/- 0.3 vs 0.7 +/- 0.3 ml/min.1.73 m2, p <.007). Urinary sodium excretion also decreased in Group III after physical loading (130 +/- 47 vs 66 +/- 33 umol/min/1.73 m2). The data show, that physical stress induces a severe lactic acidosis in IDDM. In spite of the decreased systemic sympathetic activity, the renal catecholamine response showed a shift towards vasoconstriction, sodium and fluid retention under physical stress in IDDM. These changes correlate with the duration of the underlying disease.",
author = "T. Tulassay and A. Yasar and L. Mad{\'a}csy and A. K{\"o}rner and L. Sz{\"u}cs",
year = "1992",
language = "English",
volume = "63",
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T1 - The role of sympathetic-adrenergic activity in the regulation of acid-base homeostasis and renal sodium excretion under acute physical stress in type-I diabetic children (IDDM).

AU - Tulassay, T.

AU - Yasar, A.

AU - Madácsy, L.

AU - Körner, A.

AU - Szücs, L.

PY - 1992

Y1 - 1992

N2 - To evaluate the ability of stress response, plasma and urinary catecholamine concentrations, urinary electrolytes and acid-base status were measured in IDDM children (Group I: newly diagnoses 2-4 weeks, n = 7; Group II: duration 5-7 yr, n = 9; Group III: duration 10-13 yr, n = 12). The data were compared to healthy controls, n = 7, (mean +/- SD). Physical stress was induced by 2 W/kg/10 min bicycle ergometer. IDDM children exhibited metabolic acidosis under stress (pH: Group I = 7.24 +/- 0.08; Group II = 7.25 +/- 0.05; Group III = 7.19 +/- 0.03 vs C = 7.36 +/- 0.02). Stress induced an increase in the concentration of plasma norepinephrine (PNE in each group, the most pronounced elevation was seen in Group I (19.36 +/- 8.8 nmol/I vs C = 8.3 +/- 3.2, p <0.2). Baseline PNE level showed a significant decrease with the duration of IDDM. Excretion of urinary NE (UNE) also increased under stress, however, the highest levels were measured in Group III (580 +/- 209 pmol/min/l. 73m2 vs 290 +/- 124 in Group I, p <.01). Baseline urinary dopamine (UDA) excretions were similar in each group. Stress caused an elevation in UDA only in C (2.05 +/- 1.8 vs 4.59 +/- 2.9 pmol/min.l. 73m2). The ratio of baseline UNE/UDA was similar in Groups I, II and C, but higher in Group III. Stress induced a shift towards NE excretion only in diabetic children which was most pronounced in children having IDDM more than 10 years. Stress did not affect urine output in Groups I. and II., but a decrease was observed in Group III (1.1 +/- 0.3 vs 0.7 +/- 0.3 ml/min.1.73 m2, p <.007). Urinary sodium excretion also decreased in Group III after physical loading (130 +/- 47 vs 66 +/- 33 umol/min/1.73 m2). The data show, that physical stress induces a severe lactic acidosis in IDDM. In spite of the decreased systemic sympathetic activity, the renal catecholamine response showed a shift towards vasoconstriction, sodium and fluid retention under physical stress in IDDM. These changes correlate with the duration of the underlying disease.

AB - To evaluate the ability of stress response, plasma and urinary catecholamine concentrations, urinary electrolytes and acid-base status were measured in IDDM children (Group I: newly diagnoses 2-4 weeks, n = 7; Group II: duration 5-7 yr, n = 9; Group III: duration 10-13 yr, n = 12). The data were compared to healthy controls, n = 7, (mean +/- SD). Physical stress was induced by 2 W/kg/10 min bicycle ergometer. IDDM children exhibited metabolic acidosis under stress (pH: Group I = 7.24 +/- 0.08; Group II = 7.25 +/- 0.05; Group III = 7.19 +/- 0.03 vs C = 7.36 +/- 0.02). Stress induced an increase in the concentration of plasma norepinephrine (PNE in each group, the most pronounced elevation was seen in Group I (19.36 +/- 8.8 nmol/I vs C = 8.3 +/- 3.2, p <0.2). Baseline PNE level showed a significant decrease with the duration of IDDM. Excretion of urinary NE (UNE) also increased under stress, however, the highest levels were measured in Group III (580 +/- 209 pmol/min/l. 73m2 vs 290 +/- 124 in Group I, p <.01). Baseline urinary dopamine (UDA) excretions were similar in each group. Stress caused an elevation in UDA only in C (2.05 +/- 1.8 vs 4.59 +/- 2.9 pmol/min.l. 73m2). The ratio of baseline UNE/UDA was similar in Groups I, II and C, but higher in Group III. Stress induced a shift towards NE excretion only in diabetic children which was most pronounced in children having IDDM more than 10 years. Stress did not affect urine output in Groups I. and II., but a decrease was observed in Group III (1.1 +/- 0.3 vs 0.7 +/- 0.3 ml/min.1.73 m2, p <.007). Urinary sodium excretion also decreased in Group III after physical loading (130 +/- 47 vs 66 +/- 33 umol/min/1.73 m2). The data show, that physical stress induces a severe lactic acidosis in IDDM. In spite of the decreased systemic sympathetic activity, the renal catecholamine response showed a shift towards vasoconstriction, sodium and fluid retention under physical stress in IDDM. These changes correlate with the duration of the underlying disease.

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