1. Hyperinsulinaemia and insulin resistance are thought to be intimately involved in the development of hypertension, but controversy remains as to whether hyperinsulinaemia is a consequence or a cause of hypertension per se, and whether it plays a role in the short-term regulation of blood pressure.

2. We studied six hypertensive patients [blood pressure 161(9)/101(2) mmHg] and seven normotensive control subjects [blood pressure 122(6)/76(4) mmHg], (P < 0.005) using two oral glucose tolerance tests of 3 h duration. In one of these tests the endogenous insulin response was inhibited with subcutaneous octreotide.

3. After placebo, hypertensive patients had slightly but significantly higher blood glucose levels than controls (P < 0.0001), but comparable insulin concentrations (P > 0.5). Plasma noradrenaline levels were consistently lower in the hypertensive group (P < 0.001). Blood pressure did not change in either group during the 3 h after glucose ingestion.

4. Octreotide completely abolished the immediate insulin response to glucose in all subjects (both P < 0.0001) and caused a delayed and significantly increased glycaemic response in born groups (P < 0.0001). There were no significant differences in plasma glucose responses between groups; however, after octreotide, the hypertensive subjects had a greater insulin suppression than the controls (P < 0.02). Octreotide suppressed noradrenaline levels in the normotensive group (P < 0.001); they were also suppressed in the hypertensive group, but just failed to reach significance (P = 0.056). Throughout the study the hypertensive group's noradrenaline levels remained generally lower than those in the control group (P < 0.0001).

5. In this study there were no differences between hypertensive and normotensive subjects in fasting or post-glucose insulin levels, nor any significant change in blood pressure in either group when post-glucose hyperinsulinaemia was suppressed. This argues against insulin playing a direct role in the short-term regulation of blood pressure.

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