We sought to determine whether the sympathetic nervous system plays a role in the hypertensive response to refeeding from a very low-calorie diet (VLCD).
Cycles of weight loss and regain were induced in the obese spontaneously hypertensive rat (SHROB) model of genetic obese hypertension.
A 12-day VLCD (1/6 of baseline calories) was alternated with 4–6 weeks of ad libitum chow refeeding for three cycles. Control SHROB ate chow ad libitum. Urine was collected for 24 h before and after each period of VLCD, and catecholamines were measured radioenzymatically. Tail cuff blood pressures and body weight were measured in parallel with urine collections. Kidneys were collected for assay of α2-adrenergic receptor density.
VLCD induced rapid weight loss, but all the lost weight was regained during refeeding. Blood pressure fell during caloric restriction, but rose above baseline during refeeding. Urinary excretion of norepinephrine, epinephrine and dopamine changed several fold during weight cycling. Urinary catecholamines paralleled the changes in blood pressure, falling during caloric restriction and rebounding during refeeding. Dopamine showed the greatest decreases during weight loss and rises during weight regain, whereas epinephrine changed the least and norepinephrine was intermediate. Weight cycling elevated blood pressure above the initial baseline throughout the rapid weight gain phase of refeeding. The density of α2-adrenergic receptors was decreased in both the renal medulla and cortex of weight cycled SHROB, consistent with receptor down-regulation owing to overstimulation.
The exacerbations of hypertension during weight regain in SHROB coincide with sustained activation of sympathoadrenal activity, as reflected in urinary catecholamine excretion and adrenergic receptor down regulation.