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Background and Aim: The effects of the alpha-1-adrenergic blocker terazosin on blood pressure and fasting and postprandial glucose and lipid metabolism were assessed in type 2 diabetic patients with hypertension., Methods and Results: In this single-blind, randomized, crossover, placebo-controlled pilot study, thirteen patients were given terazosin for three months. Blood pressure and metabolic parameters were measured after a 14-hr overnight fast. In addition, a 800-calorie test meal was administered after placebo and terazosin to evaluate blood glucose and lipid changes following a standardized physiological stimulus. Blood pressure was significantly reduced and HDL-cholesterol significantly increased after terazosin. A significant decrease at fasting with a smaller reduction after the meal test was observed for free fatty acids when terazosin was given in comparison to placebo, suggesting an improvement in insulin resistance. A slight decrease in fasting and postprandial triglycerides was also observed. Cardiovascular risk, calculated according to the Framingham formula, was significantly reduced at the end of the terazosin treatment., Conclusions: Antihypertensive treatment with terazosin is effective, has no adverse effects on fasting and postprandial glucose and lipid metabolisms, and appears to improve the cardiovascular risk profile of hypertensive patients with associated metabolic diseases.

This study evaluates prospectively the relationship between impaired glucose tolerance (IGT) and blood pressure. From a population of 1376 men and women aged 40-59 years, all those with IGT (n = 54) plus 133 age- weight- and sex-matched normoglycaemic control subjects were selected after excluding treated hypertensive patients. Blood pressure, fasting and postload blood glucose and plasma insulin were measured. At 11.5 years after the first visit 76% of the IGT patients and 80% of the control subjects were re-examined. At baseline blood pressure was significantly higher in IGT patients than in control subjects (systolic 135.5 +/- 2.3 vs 127.9 +/- 1.4 mmHg, p < 0.001; and diastolic 88.0 +/- 1.5 vs 84.7 +/- 0.7 mm Hg, p < 0.05) independent of age, gender, weight, antihypertensive medication and insulinaemia. Accordingly, hypertension was more frequent in subjects with IGT (odds ratio 2.1, 95% confidence, interval (CI) 0.9-4.9). Postload insulin was significantly associated with hypertension--both at univariate and multivariate analysis--in normoglycaemic subjects, but not in those with IGT. At follow-up systolic blood pressure increased in both groups; the increase was smaller in patients with IGT (6.0 +/- 2.4 vs 12.3 +/- 1.6 mm Hg p < 0.05). Likewise, the 11.5 years' cumulative incidence of hypertension was not significantly different in subjects with baseline IGT or normoglycaemia; if anything it was lower in the IGT group (odds ratio 0.36, 95% CI 0.1-1.2). In multivariate analysis incidence of hypertension was associated positively with baseline blood pressure (p < 0.0003) and negatively with IGT status p < 0.03), while no significant association was found with insulin. In conclusion, the findings of this study question IGT as a risk factor for hypertension. Furthermore, these data do not indicate a major role for hyperglycaemia and hyperinsulinaemia per se in the aetiology of hypertension and suggest that IGT and hypertension share one or more pathogenetic factor(s) (i.e., insulin resistance, hyperactivity of the sympathetic nervous system, etc.), which induce deterioration of blood pressure control first, and hyperglycaemia later.

A close correlation between body weight and blood pressure has been frequently observed in both clinical and epidemiological studies. The aim of this clinical trial was to evaluate whether, in obese patients, there is any relationship between blood pressure, at rest or during sympathetic stimulation, and blood glucose and serum insulin, both while fasting and during an oral glucose challenge. Twenty obese patients (age 26-65 years, body weight 97 +/- 16 kg, 11 normotensive and 9 hypertensive) entered the study. After a 4-week run-in period on an isocaloric diet with normal intake of sodium, blood pressure and heart rate were measured at rest and during sympathetic stimulation induced by cold and isometric testing. Responses of glucose and insulin to a standardized 75 g oral glucose tolerance test were also evaluated. The responses of glucose and insulin to glucose challenge were not statistically different in normotensive and hypertensive obese patients. Levels of insulin in the serum in the serum in the fasting state and during glucose load were significantly correlated with the response of blood pressure to cold and isometric exercise, but not to blood pressure at rest. The response of heart rate to cold was closely related to insulin only in the subgroup of normotensives. The present findings support the hypothesis that the sympathetic nervous system, which influences secretion of insulin and regulation of blood pressure, is involved in the pathophysiology of the association of obesity and hypertension.

Certain acute and chronic metabolic effects of nicardipine have been studied in 20 patients with non-insulin dependent diabetes (NIDD). An intravenous glucose tolerance test (i.v. GTT, glucose 0.33 g/kg as a bolus) and the corresponding insulin response were assessed at the end of a 4 week placebo period, after the first dose and on administration for 12 weeks of nicardipine 20 mg t.i.d. The glucose and insulin responses to the i.v.GTT, evaluated as incremental AUCs, did not change significantly (glucose 30.5 mg/dl.90 min on placebo, 33.1 mg/dl.90 min acutely and 31.4 mg/dl.90 min on chronic administration of nicardipine; insulin 2.08 microU/ml.90 min on placebo, 1.87 microU/ml.90 min acutely and 1.93 microU/ml.90 min after chronic nicardipine). Glucose removal rate (KG) following the i.v.GTT was 0.73%/min on placebo 0.75%/min on acute administration and 0.8%.min-1 with chronic nicardipine. Active treatment produced a significant reduction of blood pressure (from 187/96 mm Hg on placebo to 166/89 mm Hg acutely and 152/83 mm Hg after 12 weeks of nicardipine treatment). It is concluded that the calcium antagonist nicardipine was an effective antihypertensive drug, and that it did not cause deterioration of metabolic control in hypertensive patients with NIDD.

After a placebo run-in period (one week) 32 hypertensive patients suffering also from other disorders (cardiovascular pathology, diabetes, psychic or neurotic pathology) were treated with ketanserin (20 mg twice daily p.o. for 15 days followed by 40 mg twice daily for another 65 days). The patients' (13 men, 10 women) ages ranged from 54-94 years (average 69 years). Therapeutic results became manifest gradually with significant reductions of systolic and diastolic blood pressure; heart rate, too, had decreased slightly at the end of the treatment period. Global evaluation yielded favorable results in 59% of patients. Topical and systemic tolerance was satisfactory.