A behavioral treatment program as a therapy in the control of primary hypertension.

In order to assess the effects of a Behavioral Treatment Program in the control of primary hypertension, twenty one unmedicated hypertensives were randomly allocated to three groups: first, a treatment group (BHG) receiving a Behavioral Treatment which included: deep muscle relaxation, peripheral temperature Biofeedback and anxiety management training; second, the placebo attention control group (PHG) and third, a control group of hypertensives too (CHG). Additionally, were compared with seven normotensives subjects (CNG). The post-treatment measures showed a significant reduction (p < 0.001) in systolic and diastolic values only in the (BHG). In a six months follow-up the (BHG) group still showed a significant reduction in the systolic and diastolic BP (p < 0.02; p < 0.01). Moreover individual variations in response to treatment were observed in this group, (BHG).

Echocardiographic assessment of doxazosin on left ventricular mass in patients with essential hypertension.

A single daily dose of doxazosin taken during a 12-week period produced a significant reduction in blood pressure and left ventricular mass index in patients with mild or moderate hypertension. The systolic shortening coefficient was also increased and a trend in the improvement of ejection fraction, rate of circumferential fiber shortening, systolic contraction time, and preejective/ejective ratio was observed. No change in heart rate was recorded and no patients had side effects. The serum lipid profile was modified favorably, particularly with regard to the low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio. By producing a reduction in blood pressure and left ventricular mass while favorably modifying the serum lipid profile, doxazosin produced a beneficial change in the overall coronary heart disease risk profile.

Impaired glucose metabolism in hypertensive patients.

We have studied glucose tolerance under carefully controlled conditions in 79 patients with arterial hypertension. The results show that, in patients with arterial hypertension but without clinical diabetes mellitus, the glucose tolerance was abnormal in 77.3% and normal in 22.3%. The corresponding figure in the control group of normotensive subjects was 0%. In each test the responses to glucose administration were analyzed by plotting the logarithm of the blood glucose concentration against time. For the points between 60 and 120 min, corresponding to the periods following glucose administration, a linear relationship was obtained and showed a decline at an exponential rate, as noted by other observers. An estimate of the volume of distribution of glucose was obtained as follows. Values observed in hypertensives with a pathological percent fall in blood glucose per minute (Kg) were 29.8 +/- 12.0 (mean +/- SD) liters and those in normal subjects with normal Kg values had a mean of 14.35 +/- 2.98, the difference being highly significant (p less than 0.0001). The results of the theoretical glucose concentration are also presented. Those obtained from subjects with normal Kg values (359.0 +/- 58.4 mg/dl) are significantly higher than in subjects with pathological Kg values (257.6 +/- 51.3 mg/dl; p less than 0.0001). All patients with either pathological or normal Kg values had normal glucose concentration levels, fasting blood sugar and no glucose in the urine specimen. The difference between pathological Kg values (107.0 +/- 25.8 mg/dl) and normal Kg values (90.6 +/- 13.0 mg/dl) was not found to be statistically different (p greater than 0.05). The distribution and means of glucose half time in controls with normal Kg values and hypertensives with pathological Kg values were: 63.5 +/- 11.5 and 137.8 +/- 48.1 min, respectively. The difference between normal and pathological Kg values being statistically significant at a confidence level above 99.5%. We also studied the free glucose pool at zero time. A significantly higher level was found in hypertensives with pathological Kg values, again indicating an impairment in glucose metabolism in this group: 90.6 +/- 26.5 vs. 65.0 +/- 5.4 g (p less than 0.0001). Another study showed an estimate of the mean cellular glucose uptake (MCUg) per minute and per kilogram body weight. The MCUg following glucose loading decreased considerably in hypertensives with pathological Kg values. The percentage reduction ranged between 50 and 55% hypertensives with pathological Kg values 4.1 +/- 0.8, and normotensives with normal Kg values, 8.0 +/- 0.6 (p less than 0.0001).(ABSTRACT TRUNCATED AT 400 WORDS)

Acute hypotensive action of clonidine after intravenous infusion in hypertensive emergencies.

Clonidine was administered by intravenous infusion to 12 patients classified as having exaggerated arterial hypertension, their systolic (SAP), diastolic (DAP) and mean (MAP) arterial pressures were significantly reduced from the third min. The maximal percentage reduction (Mean +/- SEM) reached 30.1 +/- 3.1% (SAP) and 24.7 +/- 2.9% (DAP) after 30 to 110 min of infusion. Initially there were transitory initial increases in SAP (3 patients) and DAP (1 patient). The increases in blood pressure were related to low body surface area (BSA). The dose of clonidine per m2BSA able to reduce by 10% either SAP or DAP (active dose-10), and the dose able to reduce SAP or DAP by 10 mmHg in one minute (systolic or diastolic clonidine unit) were calculated, providing indices for detecting clonidine responsiveness in patients with exaggerated hypertension. This method is advantageous when using clonidine intravenously because it diminishes the risk of overdosage.