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Biomedical subjects

C H Darwin

Publications and source records attributed to C H Darwin.

3 recordsLinked to original sources

Decreased polymorphonuclear leukocyte deformability in NIDDM.

OBJECTIVE: To determine the rheological properties of polymorphonuclear leukocytes (PMN) from non-insulin-dependent diabetes mellitus (NIDDM) patients. RESEARCH DESIGN AND METHODS: The deformability of PMN from 33 NIDDM subjects, 13 with impaired glucose tolerance (IGT), and 22 with normal glucose tolerance (NGT) was studied. A Cell Transit Analyzer that measures the transit time of PMN through 8-microns pores was used. Studies were performed under three different conditions: 1) basal state; 2) after incubation with cytochalasin B (20 microM) to dissociate f-actin from the cytoskeleton; and 3) following activation with N-formyl-methionyl-leucyl-phenylalanine (fMLP, 1 nM). RESULTS: PMN from diabetic patients were more rigid (i.e., had longer transit time) than those from subjects with NGT or IGT under basal conditions and after cytochalasin B, but not after stimulation with fMLP. The deformability of PMN from subjects with IGT was similar to those of the NGT group. In the pooled data, basal transit time correlated with age; systolic and diastolic blood pressure; HbA1c; and serum creatinine, cholesterol, and triglyceride concentrations (r = 0.29, 0.34, 0.37, 0.48, 0.25, 0.36, 0.29, respectively, P < 0.05 for each). Hypertensive diabetic patients had less deformable PMN than normotensive ones. No relation was found between PMN deformability and the duration of diabetes, type of treatment, or the presence of retinopathy. CONCLUSIONS: These data indicate increased rigidity of PMN in NIDDM that may contribute to development of microcirculatory disturbances and microangiopathy.

Adult↗

Insulin and hypertension: are they related?

It has been postulated that insulin resistance and the concomitant compensatory hyperinsulinemia contribute to the pathogenesis of hypertension; possible by stimulating the sympathetic nervous system, promoting renal sodium reabsorption, modulating cation transport, and/or stimulating vascular smooth muscle hypertrophy. The purpose of this article is to present a comprehensive up-to-date review of the literature and critically examine the insulin resistance-hyperinsulinemia-hypertension hypothesis.

Animals↗

Insulin and hypertension: are they related?

It has been postulated that insulin resistance and the concomitant compensatory hyperinsulinemia contribute to the pathogenesis of hypertension, possibly by stimulating the sympathetic nervous system, promoting renal sodium reabsorption, modulating cation transport, and/or stimulating vascular smooth muscle hypertrophy. The purpose of this article is to present a comprehensive up-to-date review of the literature and critically examine the insulin resistance-hyperinsulinemia-hypertension hypothesis.

Animals↗