Gastric inhibitory polypeptide (GIP) is one of the strongest insulinot
ropic gut factors. Its secretion is induced by oral (but not intraveno
us) glucose and it has been implicated in the pathogenesis of hyperins
ulinemic states (NIDDM, obesity). To determine its relevance to hypert
ension, 54 subjects were studied: 26 normotensives (12 with and 14 wit
hout family history of essential hypertension), and 28 essential hyper
tensive subjects. Plasma glucose, serum insulin (IRI), and GIP were ev
aluated after a mixed meal containing a total of 82 g of carbohydrates
, and 2 g sodium chloride. Venous blood was collected at baseline and
every 15 min. during a 3-h period. Baseline levels of glucose, IRI, an
d GIP were comparable in the three groups. At 30 min, however, IRI and
GIP were higher in normotensives with a family history of hypertensio
n and in established hypertensive versus control subjects. Both in nor
motensive and in hypertensive groups, glucose, IRI, and GIP responses
to the meal were significantly correlated. Our data suggest the contri
bution of altered GIP secretion in the pathogenesis of hyperinsulinemi
a in essential hypertension.