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Somatostatin Analog Octreotide (SMS 201-995) Prevents the Decrease in Blood Pressure After Oral Glucose Loading in the Elderly^*

Departments of Geriatric Medicine (R. W.M.M.J., W.H.L.H.) and Medicine, Division of General Internal Medicine (J. W.M.L., A.v.t.L.), University Hospital Nijmegen, and the Department of Statistical Consultation, University of Nijmegen (H.J.J.v.L.) Nijmegen, The Netherlands
The Department of Medical Research, Gut Hormone Laboratory, University of Leuven (T.L.P.) Leuven, Belgium

Address requests for reprints to: R. W. M. M. Jansen, Department of Geriatric Medicine, University Hospital Nijmegen, P.O. Box 9101, 6500 HB Nijmegen, The Netherlands.

In elderly subjects blood pressure (BP) may fall after a meal. The mechanism of this phenomenon is unknown, but it has been suggested that it may be mediated by insulin and/or vasoactive gut hormones. We studied in normo- and hypertensive elderly subjects the effects of the synthetic longacting somatostatin analog octreotide (SMS 201–995) on the BP reduction that follows oral glucose administration in subjects who are recumbent and on their postglucose plasma vasoactive intestinal polypeptide (VIP) and insulin concentrations. After placebo treatment, mean arterial pressure fell by 15 ± 1 mm Hg (P < 0.001) in the 10 hypertensive subjects and by 7 ± 2 mm Hg (P < 0.01) in the 10 normotensive subjects. In contrast, when 50 µg octreotide were given sc, BP did not change significantly in either group. Oral glucose did not induce a rise in plasma VIP after either octreotide or placebo administration. The postglucose rises in plasma glucose concentrations were similar after octreotide and placebo treatments in both groups. After placebo administration the postglucose plasma insulin levels increased from 79 to 519 pmol/L in the hypertensive subjects and from 63 to 464 pmol/L in the normotensive subjects, whereas after octreotide treatment plasma insulin increased little in either group. These data indicate that treatment with octreotide holds promise for patients with symptomatic postprandial hypotension, and that VIP does not seem to play a role in this phenomenon.

^* This work was supported by a grant from the Dutch Stimulation Fund for Research of Aging (SOOM 86-1-205).

Received September 15, 1988.

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