Insulin increases forearm vascular resistance in obese, insulin-resistant hypertensives.

Abstract:

OBJECTIVE:To determine whether acutely lowering insulin levels with somatostatin in obese, insulin-resistant hypertensive individuals reduces arterial pressure and forearm vascular resistance; and whether these changes are reversed by restoring insulin levels during continuing somatostatin infusion. SUBJECTS:Subjects were 11 obese (body mass index 36 +/- 4 kg/m2) insulin-resistant, hypertensive men (systolic/diastolic blood pressures 153 +/- 6/94 +/- 2 mmHg, aged 51 +/- 7 years, fasting insulin level 17 +/- 8 mU/l). METHODS:Arterial pressure, forearm blood flow and vascular resistance were measured during 2 h of somatostatin infusion and during 2h of somatostatin plus insulin infusion (hyperinsulinemic or euglycemic clamp). RESULTS:Somatostatin infusion decreased plasma insulin levels from 17 +/- 2 to <3 mU/l. Insulin infusion raised plasma insulin levels to 86 +/- 7 mU/l. The forearm vascular resistance decreased significantly during somatostatin infusion and increased significantly during infusion of somatostatin plus insulin. Somatostatin also caused small but significant reductions in arterial pressure whereas insulin infusion during somatostatin infusion increased arterial pressure. Control experiments in six obese hypertensives indicated that the changes in forearm vascular resistance (but not in arterial pressure) were caused neither by time nor by vehicle. Control studies in six young normotensives indicated that somatostatin does not block the vasodilator response to insulin previously demonstrated in this group. CONCLUSIONS:The present results suggest that insulin causes forearm vasoconstriction in obese, insulin-resistant hypertensive humans.

journal_name

J Hypertens

journal_title

Journal of hypertension

authors

Gudbjörnsdottir S,Elam M,Sellgren J,Anderson EA

subject

Has Abstract

pub_date

1996-01-01 00:00:00

pages

91-7

issue

1

eissn

0263-6352

issn

1473-5598

journal_volume

14

pub_type

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