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(Hypertension. 1997;29:1007-1013.)
© 1997 American Heart Association, Inc.

Articles

4Intracellular Free Calcium Abnormalities in Fibroblasts From Non–Insulin-Dependent Diabetic Patients With and Without Arterial Hypertension

Elena Duner; Francesco Di Virgilio; Roberto Trevisan; Maria Rita Cipollina; Gaetano Crepaldi; ; Romano Nosadini

From Istituto di Medicina Interna, National Research Council (CNR) Center for the Study of Aging, Università di Padova, and Istituto di Patologia Generale, Università di Ferrara (F. Di V.) (Italy).

Correspondence to R. Nosadini, MD, Istituto di Medicina Interna, Patologia Medica I, Policlinico Universitario, Via Giustiniani 2, 35128 Padua, Italy.

Abstract As arterial hypertension is frequently associated with diabetes, it is possible that altered intracellular free calcium ([Ca²⁺]_i) handling, as reported in non–insulin-dependent diabetic patients, is accounted for by abnormalities caused by hypertension rather than diabetes. Our aim was to investigate [Ca²⁺]_i transients triggered by two extracellular agonists, bradykinin and angiotensin II, with or without chronic insulin exposure, in cultured skin fibroblasts from 10 normotensive and 10 hypertensive non–insulin-dependent patients, matched for age, body mass index, and metabolic control, with fibroblasts from 10 healthy control subjects. Long-term cultured fibroblasts were loaded with fura 2-AM for measurement of [Ca²⁺]_i. Resting [Ca²⁺]_i levels were similar in the three groups of subjects. [Ca²⁺]_i spikes stimulated by angiotensin II (0.1 µmol/L) and bradykinin (1 µmol/L) were significantly greater in hypertensive non–insulin-dependent diabetic patients (216±43 and 374±39 nmol/L, respectively) than in normotensive patients (174±16 and 267±55 nmol/L) and control subjects (188±29 and 320±78 nmol/L). Also, ionomycin evoked a greater [Ca²⁺]_i response in hypertensive than normotensive non–insulin-dependent diabetic patients and in control subjects. Chronic insulin exposure increased by 70% to 90% the [Ca²⁺]_i response to both angiotensin II and bradykinin in control subjects and normotensive non–insulin-dependent diabetic patients but not in hypertensive patients. The presence of abnormalities in [Ca²⁺]_i transients in fibroblasts from only hypertensive non–insulin-dependent diabetic patients supports the possibility that these defects are a feature of concomitant arterial hypertension rather than of diabetes or its disturbed metabolic milieu.

Key Words: calcium, intracellular • diabetes, non–insulin-dependent • angiotensin II • bradykinin

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