No abstract

In this investigation we correlated platelet Na-H antiport parameters with blood pressure and serum lipids in a sample population of non-insulin-dependent diabetic obese, nondiabetic obese, and nondiabetic nonobese black women. Parameters of the Na-H antiport were examined in aspirin-treated platelets. These parameters were not altered in resting or in thrombin-stimulated platelets of diabetic patients. The activity index of platelet Na-H antiport after thrombin stimulation was positively correlated with the blood pressure (systolic blood pressure, r=0.5320 and p=0.0001; diastolic blood pressure, r=0-5123 and p=0.0017). Lower high density lipoprotein cholesterol levels were associated with an alkaline shift in the cytosolic pH set point for activation of the Na-H antiport. Highly significant correlations were also observed between the total cholesterol/high density lipoprotein cholesterol ratio and the cytosolic pH set point for activation of the Na-H antiport These correlations were independent of diabetes or the body mass index. Together, these observations indicate that parameters of platelet Na-H antiport are altered with an increase in blood pressure and a decrease in serum high density lipoprotein cholesterol. (Hypertension 1992^0:549-554) KEY WORDS • diabetes mellltus, non-insulin-dependent • lipoproteins, HDL • hypertension, essential N on-insulin-dependent diabetes mellitus(NIDDM) is frequently accompanied by elevated blood pressure, whereas essential hypertension is usually associated with insulin resistance.1 " 4 NIDDM and essential hypertension also share a tendency for accelerated atherosclerotic and thromboembolic complications, 5 " 8 which may arise from serum lipid abnormalities and platelet hyperactrvity 9 "12 that are commonly observed in these diseases.Recent studies have indicated that the activity of the Na-H antiport is increased in platelets of patients with essential hypertension, 13 -17 a process that may relate to platelet hyperactivity. Since NIDDM and essential hypertension appear to express common cellular perturbations, it is possible that these include altered platelet Na-H antiport activity. The present study was therefore designed to answer the following questions: are parameters of platelet Na-H antiport altered in NIDDM and obesity (two conditions commonly associated with essential hypertension) and are there any relations be-