Humoral mechanisms in the pathogenesis of postprandial hypotension in patients with essential hypertension.
OBJECTIVE
To examine the role of catecholamines and insulin in the development of postprandial hypotension (PPH) in hypertensive patients.


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


METHODS
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.
Mitro
P
P
Department of Internal Medicine II, University Hospital Kosice, Slovak Republic. pmitro@kosice.upjs.sk
Feterik
K
K
Lenártová
M
M
Cvercková
A
A
Curmová
A
A
Rybárová
E
E
Petrásová
D
D
Rybár
R
R
Trejbal
D
D
D000313:Adrenal Medulla / Q000503:physiopathology; D000368:Aged; D001794:Blood Pressure; D002395:Catecholamines / Q000097:blood; D005260:Female; D006339:Heart Rate; D006801:Humans; D006974:Hypertension, Malignant / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D007022:Hypotension / Q000097:blood / Q000209:etiology* / Q000503:physiopathology; D008297:Male; D010455:Peptides / Q000097:blood; D019518:Postprandial Period; D013564:Sympathetic Nervous System / Q000503:physiopathology
D002395:Catecholamines; D010455:Peptides; C050632:polypeptide C