Excerpt
Six patients had essential hypertension (four females and two males), and seven patients had polycystic kidney disease (five females and two males; serum creatinine < 200 μmol/l). All had systolic blood pressure above 145 mmHg and/or diastolic blood pressure above 90 mmHg on three occasions before the study. Antihypertensive medication was stopped 3 weeks before the study. The patients were given a high-sucrose diet (39.7 ± 0.3% of total energy intake) for 6 weeks, in a lemonade, which consisted only of sucrose, flavours and pigment. The composition of the diet was adjusted to maintain an isocaloric intake and electrolyte content. Twenty-four-hour ambulatory blood pressure was meas ured by a SpaceLabs 90207 device (SpaceLabs Medical Products, Dee Why, Australia) before the sucrose diet started, after 2, 4 and 6 weeks of the diet and 2 weeks after stopping the diet. Before and after the high-sucrose diet, insulin resistance was measured after an overnight fast with the euglycaemic hyperinsulinaemic glucose clamp. Biochemical variables were measured in blood sampled before the glucose clamp was started. A 24 h urine collection was made on 3 consecutive days before the diet started and on the last 3 days of the diet. Blood pressure data were analysed by analysis of variance for repeated measures, and biochemical data by paired t test. Data are given as means ± SEM.
Body weight remained constant over the dietary period in all subjects (Table 1), confirming adherence to the dietary regimen that was aimed at constant energy intake, in order to avoid obesity-related increases in blood pressure. No side effects were observed. There were decreases in high-density lipoprotein cholesterol levels (P < 0.05) and increases in plasma triglyceride levels (P < 0.05), which are known effects of a high sucrose intake [8], confirming adherence to the diet. There were no significant changes in fasting plasma insulin levels or glucose infusion rates during the euglycaemic hyperinsulinaemic clamp.
In the patients with essential hypertension, clonidine caused significant decreases in blood pressure before and after 6 weeks of dietary sucrose intake. However, no difference was observed in the magnitude of the decrease, suggesting that there was no increase in adrenergic activity during the test period. The results of captopril tests at these times were also practically congruent. No differences were found in plasma renin activity and aldosterone (Table 1). The latter observations, in combination with an unchanged 24 h sodium excretion, make it unlikely that the high sucrose intake changed the sodium status of the subjects.