Blood pressure normally decreases after a meal and reaches a nadir between 30 and 60 min after eating (1). Giugliano et al. (2) showed that acute hyperglycemia in normal subjects significantly increases systolic and diastolic blood pressure. To define the relationship between postprandial plasma glucose excursions and blood pressure variations in type 1 diabetes, we studied 10 normotensive, type 1 diabetic patients (mean ± SD age 39.7 ± 16.7 years, diabetes duration 10.5 ± 5.4 years, A1C 7.4 ± 0.8%, and BMI 23.9 ± 3.5 kg/m2) without microangiopatic complications. All patients were in therapy with continuous subcutaneous insulin infusion. None took any hypotensive drug. Every patient simultaneously performed 24-h ambulatory blood pressure monitoring (Takeda TM2420 Service; A&D Medical, Tokyo, Japan) and continuous glucose monitoring (CGMS System Gold; Medtronic Minimed). Blood pressure monitoring, fitted to the nondominant arm, was programmed to take blood pressure every 30 min. Glucose concentrations were monitored at 5-min intervals by the continuous glucose monitoring system; the means of 30-min values (mean of six blood glucose measurements) were related to concomitant arterial pressure value. Every patient ate three meals during the test. The premeal plasma glucose level, calculated as the mean level during the hour preceding meal presentation, was 131.7 ± 55.3 mg/dl. The mean increase of blood glucose after meals was 61.2 ± 53.5 mg/dl (median 39 mg/dl [range 9–177]). For every meal, we calculated the maximum postprandial increase of glucose. To evaluate the effects of these glycemic excursions on blood pressure, postprandial glycemic profiles were divided into two groups according to the median of maximum postprandial increase of blood glucose (39 mg/dl).
A light, physiological decrease in arterial pressure (systolic blood pressure from 136.2 ± 21.2 to 132.3 ± 14.2 mmHg, P = NS [not significant]; diastolic blood pressure from 87.3 ± 13.8 to 86.4 ± 12.6 mmHg, P = NS) was observed in the group that showed a lower postprandial increase of blood glucose (<39 mg/dl). On the contrary, a significant postmeal increase of arterial pressure was observed (systolic blood pressure from 130.1 ± 17.7 to 146.6 ± 26.4 mmHg, P < 0.05; diastolic blood pressure from 76.4 ± 14.3 to 85 ± 12 mmHg, P < 0.05) in the group that showed a higher postprandial increase of blood glucose (>39 mg/dl).
Our data, obtained in type 1 diabetic patients treated with continuous subcutaneous insulin infusion in good metabolic control, explain the light postmeal increase of blood glucose. Nevertheless, in the group with a higher increase of postprandial glucose there was a concomitant significant elevation of blood pressure. These data confirm previous reports that showed an increase of systolic and diastolic blood pressure starting after 30 min of acute hyperglycemia, induced in healthy subjects with an artificial pancreas (2,3). Differently from these studies, which were performed in experimental conditions, our data were obtained in a population of type 1 diabetic patients monitored during their usual daily activity. Whether repeated daily episodes of postprandial hyperglycemia, a typical feature of type 1 diabetes, may play a significant role in the development of chronic vascular complications, causing higher hemodynamic stress, remains to be elucidated in prospective studies.
