Mechanisms mediating postprandial blood pressure reduction in young and elderly subjects.

The objective of this study was to clarify potential differences in hormonal, neurogenic and hemodynamic mechanisms mediating postprandial blood pressure (BP) reduction. In 12 age- and body mass index-matched young normotensive (NT) subjects, 21 elderly NT, 17 young hypertensive (EH) patients, and 32 elderly EH, we measured BP, blood glucose, plasma insulin (IRI), and norepinephrine (NE) levels before and every 30 min for 3 h after a 75 g oral glucose solution ingestion. Cardiac output (CO) and total systemic resistance (TSR) were also measured before and 1 h after oral glucose ingestion. Postprandial BP reduction, defined as 10% or more decline in mean BP was recognized in 3/12 (25%) young NT, 9/21 (43%) elderly NT, 5/17 (29%) young EH, and 20/32 (63%) elderly EH. The most consistent finding was that the IRI response to glucose was high in all subjects with postprandial BP reduction regardless of age or level of BP, although changes in blood glucose levels showed no major differences. The NE level was low in young and elderly NT with postprandial BP reduction, but in EH the level was not different. Increases in CO in elderly subjects with postprandial BP reduction was significantly less than that in subjects without postprandial BP reduction. In addition, the decrease in TSR in young subjects with postprandial BP reduction was significantly greater than that in subjects without postprandial BP reduction, while the decrease in elderly subjects was not different between the subjects with and without postprandial BP reduction. In conclusion, postprandial BP reduction in elderly EH appears to be associated with hyperinsulinemia independent of age and BP status. The vasodilator effects of insulin may contribute to postprandial BP reduction. A second conclusion is that impairment of sympathetic nervous system responses to insulin may also contribute to altered postprandial hemodynamic responses especially in EH, suggesting multiple mechanisms in origin of postprandial BP reduction.

[1]  G. Reaven,et al.  Insulin and blood pressure in obesity. , 1985, Hypertension.

[2]  E A Anderson,et al.  Hyperinsulinemia produces both sympathetic neural activation and vasodilation in normal humans. , 1991, The Journal of clinical investigation.

[3]  J. T. Lee,et al.  Postprandial alterations in hemodynamics and blood pressure in normal subjects. , 1986, The American journal of cardiology.

[4]  W. Hoefnagels,et al.  The effect of oral glucose, protein, fat and water loading on blood pressure and the gastrointestinal peptides VIP and somatostatin in hypertensive elderly subjects , 1990, European journal of clinical investigation.

[5]  W. Hoefnagels,et al.  Hormonal Mechanisms of Postprandial Hypotension , 1991, Journal of the American Geriatrics Society.

[6]  A. Gupta,et al.  Effects of insulin on renal sodium excretion. , 1992, Hypertension.

[7]  A. Mark,et al.  Insulin Increases Sympathetic Activity but Not Blood Pressure in Borderline Hypertensive Humans , 1992, Hypertension.

[8]  W. Anderson,et al.  Assessment of human sympathetic nervous system activity from measurements of norepinephrine turnover. , 1988, Hypertension.

[9]  L. Lipsitz,et al.  Postprandial Blood Pressure Reduction in Healthy Elderly , 1986, Journal of the American Geriatrics Society.

[10]  I. Macdonald,et al.  Effects of meal composition on the postprandial blood pressure, catecholamine and insulin changes in elderly subjects. , 1989, Clinical science.

[11]  Y. Ohkura,et al.  Spectrofluorimetric determination of catecholamines with 1,2-diphenylethylenediamine , 1984 .

[12]  E. Ferrannini,et al.  Insulin resistance in essential hypertension. , 1987, The New England journal of medicine.

[13]  W. Hoefnagels,et al.  Blood pressure reduction after oral glucose loading and its relation to age, blood pressure and insulin. , 1987, The American journal of cardiology.

[14]  S. R. Berger,et al.  Postprandial blood pressure decrease in well elderly persons. , 1989, Archives of internal medicine.

[15]  H. Kennedy,et al.  The effects of sampling site on the two-dimensional echo-Doppler determination of cardiac output. , 1985, American heart journal.

[16]  J. Horgan,et al.  Baroreflex function in elderly hypertensives. , 1983, Hypertension.

[17]  J. Wei,et al.  Postprandial reduction in blood pressure in the elderly. , 1983, The New England journal of medicine.

[18]  L. Lipsitz,et al.  Postprandial hypotension in elderly patients with unexplained syncope. , 1995, Archives of internal medicine.

[19]  R. Hoeldtke,et al.  Effects of aging on catecholamine metabolism. , 1985, The Journal of clinical endocrinology and metabolism.

[20]  M. Mulholland,et al.  Duplex ultrasound measurement of postprandial intestinal blood flow: effect of meal composition. , 1988, Gastroenterology.

[21]  P. Korner,et al.  Norepinephrine Kinetics in Essential Hypertension , 1981, Hypertension.

[22]  R. Townsend,et al.  Insulin enhances pressor responses to norepinephrine in rat mesenteric vasculature. , 1992, Hypertension.

[23]  K. Minaker,et al.  Effect of age on insulin stimulation of sympathetic nervous system activity in man. , 1982, Metabolism: clinical and experimental.

[24]  B. Wallin,et al.  Increased norepinephrine spillover into the jugular veins in essential hypertension. , 1992, Hypertension.

[25]  L. Lipsitz,et al.  Cardiovascular and norepinephrine responses after meal consumption in elderly (older than 75 years) persons with postprandial hypotension and syncope. , 1986, The American journal of cardiology.

[26]  L. Landsberg Hyperinsulinemia: possible role in obesity-induced hypertension. , 1992, Hypertension.