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Humoral mechanisms in the pathogenesis of postprandial hypotension in patients with essential hypertension.
Wien Klin Wochenschr. 2001 Jun 15; 113(11-12):424-32.WK

Abstract

OBJECTIVE

To examine the role of catecholamines and insulin in the development of postprandial hypotension (PPH) in hypertensive patients.

PATIENTS

Forty patients with essential hypertension (25 men, 15 women, mean age 68 +/- 2 years).

METHOD

Blood pressure and heart rate were recorded in all subjects immediately after a 1903 kJ test meal and at 15-minute intervals for up to 1 hour after the meal. At these time points, circulating levels of norepinephrine, epinephrine, dopamine and C-peptide were measured.

RESULTS

Twenty-three patients (58%) had PPH. By 15 minutes norepinephrine had significantly increased in PPH-negative subjects while it rose more slowly in PPH-positive patients and peaked by 45 minutes after the meal. Norepinephrine levels in 15 minutes were lower in PPH-positive than in PPH-negative ones (159.8 +/- 9.7 vs. 212.3 +/- 21.1 pg/ml, p = 0.01). Epinephrine levels rose only in PPH-negative subjects and did not differ significantly at the different time points. However, the area under curve analysis showed significantly lower epinephrine values in PPH-positive subjects (2903 + 247 pg.min.ml-1 vs. 3710 + 284 pg.min.ml-1, p = 0.03). Dopamine increased in both groups, although it was lower in subjects with PPH during the entire study (15 minutes: 68.6 +/- 3.7 vs. 93.7 +/- 11.7 pg/ml, p = 0.02; 30 minutes: 68.8 +/- 3.7 vs. 86.1 +/- 7.7 pg/ml, p = 0.03; 45 minutes: 60.5 +/- 4.2 vs. 79.7 +/- 5.2 pg/ml, p = 0.006). The postprandial C-peptide response did not differ between patients with PPH and those without PPH.

CONCLUSIONS

In patients with essential hypertension, a marked decline in postprandial systolic blood pressure is associated with lower postprandial levels of norepinephrine, epinephrine and dopamine as compared to subjects without postprandial hypotension. This indicates that impaired sympatho-adrenal activation after ingestion of a meal may contribute to the development of PPH. Insulin appears not to be involved in the pathogenesis of postprandial hypotension.

Authors+Show Affiliations

Mitro P
Department of Internal Medicine II, University Hospital Kosice, Slovak Republic. pmitro@kosice.upjs.sk
Feterik K
No affiliation info available
Lenártová M
No affiliation info available
Cvercková A
No affiliation info available
Curmová A
No affiliation info available
Rybárová E
No affiliation info available
Petrásová D
No affiliation info available
Rybár R
No affiliation info available
Trejbal D
No affiliation info available

MeSH

Adrenal MedullaAgedBlood PressureCatecholaminesFemaleHeart RateHumansHypertension, MalignantHypotensionMalePeptidesPostprandial PeriodSympathetic Nervous System

Pub Type(s)

Journal Article

Language

eng

PubMed ID

11467088

Citation

Mitro, P, et al. "Humoral Mechanisms in the Pathogenesis of Postprandial Hypotension in Patients With Essential Hypertension." Wiener Klinische Wochenschrift, vol. 113, no. 11-12, 2001, pp. 424-32.
Mitro P, Feterik K, Lenártová M, et al. Humoral mechanisms in the pathogenesis of postprandial hypotension in patients with essential hypertension. Wien Klin Wochenschr. 2001;113(11-12):424-32.
Mitro, P., Feterik, K., Lenártová, M., Cvercková, A., Curmová, A., Rybárová, E., Petrásová, D., Rybár, R., & Trejbal, D. (2001). Humoral mechanisms in the pathogenesis of postprandial hypotension in patients with essential hypertension. Wiener Klinische Wochenschrift, 113(11-12), 424-32.
Mitro P, et al. Humoral Mechanisms in the Pathogenesis of Postprandial Hypotension in Patients With Essential Hypertension. Wien Klin Wochenschr. 2001 Jun 15;113(11-12):424-32. PubMed PMID: 11467088.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Humoral mechanisms in the pathogenesis of postprandial hypotension in patients with essential hypertension. AU - Mitro,P, AU - Feterik,K, AU - Lenártová,M, AU - Cvercková,A, AU - Curmová,A, AU - Rybárová,E, AU - Petrásová,D, AU - Rybár,R, AU - Trejbal,D, PY - 2001/7/27/pubmed PY - 2001/8/31/medline PY - 2001/7/27/entrez SP - 424 EP - 32 JF - Wiener klinische Wochenschrift JO - Wien Klin Wochenschr VL - 113 IS - 11-12 N2 - OBJECTIVE: To examine the role of catecholamines and insulin in the development of postprandial hypotension (PPH) in hypertensive patients. PATIENTS: Forty patients with essential hypertension (25 men, 15 women, mean age 68 +/- 2 years). METHOD: Blood pressure and heart rate were recorded in all subjects immediately after a 1903 kJ test meal and at 15-minute intervals for up to 1 hour after the meal. At these time points, circulating levels of norepinephrine, epinephrine, dopamine and C-peptide were measured. RESULTS: Twenty-three patients (58%) had PPH. By 15 minutes norepinephrine had significantly increased in PPH-negative subjects while it rose more slowly in PPH-positive patients and peaked by 45 minutes after the meal. Norepinephrine levels in 15 minutes were lower in PPH-positive than in PPH-negative ones (159.8 +/- 9.7 vs. 212.3 +/- 21.1 pg/ml, p = 0.01). Epinephrine levels rose only in PPH-negative subjects and did not differ significantly at the different time points. However, the area under curve analysis showed significantly lower epinephrine values in PPH-positive subjects (2903 + 247 pg.min.ml-1 vs. 3710 + 284 pg.min.ml-1, p = 0.03). Dopamine increased in both groups, although it was lower in subjects with PPH during the entire study (15 minutes: 68.6 +/- 3.7 vs. 93.7 +/- 11.7 pg/ml, p = 0.02; 30 minutes: 68.8 +/- 3.7 vs. 86.1 +/- 7.7 pg/ml, p = 0.03; 45 minutes: 60.5 +/- 4.2 vs. 79.7 +/- 5.2 pg/ml, p = 0.006). The postprandial C-peptide response did not differ between patients with PPH and those without PPH. CONCLUSIONS: In patients with essential hypertension, a marked decline in postprandial systolic blood pressure is associated with lower postprandial levels of norepinephrine, epinephrine and dopamine as compared to subjects without postprandial hypotension. This indicates that impaired sympatho-adrenal activation after ingestion of a meal may contribute to the development of PPH. Insulin appears not to be involved in the pathogenesis of postprandial hypotension. SN - 0043-5325 UR - https://www.unboundmedicine.com/medline/citation/11467088/Humoral_mechanisms_in_the_pathogenesis_of_postprandial_hypotension_in_patients_with_essential_hypertension_ L2 - https://www.diseaseinfosearch.org/result/8360 DB - PRIME DP - Unbound Medicine ER -