Moderate Essential Hypertensive Patients Research Articles

Beta-adrenergic blocking treatment and 24-hour baroreflex sensitivity in essential hypertensive patients.

We dynamically evaluated the effects of beta-blockade on the sensitivity of arterial baroreflex control of heart rate in 10 mild or moderate essential hypertensive patients in whom blood pressure was recorded intra-arterially for 24 hours in ambulatory conditions. Twenty-four-hour baroreflex sensitivity was assessed by both (1) a time-domain approach based on the calculation of the slope of the regression line between linearly related progressive increases in systolic blood pressure and pulse interval (+PI/+SBP sequences) and decreases in systolic blood pressure and pulse interval (-PI/-SBP sequences) and (2) a frequency-domain approach, ie, the ratio between the spectral powers of pulse interval and systolic blood pressure around 0.1 Hz (alpha coefficient). Data were obtained before and after 1 month of administration of either acebutolol (n = 5) or labetalol (n = 5). Before treatment, the 24-hour average slopes of the +PI/+SBP and -PI/-SBP sequences were 4.36 +/- 0.32 and 4.05 +/- 0.27 ms/mm Hg, respectively, while the alpha coefficient was 7.78 +/- 0.7 ms/mm Hg. After beta-blockade, these values were increased by 25.3 +/- 6.8%, 25.0 +/- 8.0%, and 32.1 +/- 9.3%, respectively (P < .01 for all values). Thus, beta-blockers potentiate baroreflex sensitivity in daily life. Time-domain and frequency-domain methods yielded superimposable results in dynamically evaluating 24-hour baroreflex sensitivity and its changes after beta-blockade.

Radial artery compliance in essential hypertension

To evaluate the effects of antihypertensive therapy with lacidipine on the increase in radial artery compliance observed in mild essential hypertensive patients. The study was performed in eight mild to moderate essential hypertensive patients in whom clinic blood pressure, radial artery diameter and radial artery compliance were evaluated before and after 3 months' administration of lacidipine, at a single daily dose of 4 mg. Radial artery diameter and compliance were evaluated by means of a high precision echo-tracking device able to assess arterial compliance over the blood pressure oscillations that characterize the cardiac cycle. Lacidipine treatment caused a significant reduction in clinic systolic and diastolic blood pressure, while the heart rate was not modified by the drug. Radial artery diameter and compliance were both reduced by lacidipine over the entire systolodiastolic blood pressure range. Chronic administration of lacidipine seems to reverse the increase in compliance observed in essential hypertension at the radial artery level. We suggest that lacidipine treatment can reverse an increase in the smooth muscle component in the arterial wall induced by hypertension.

Isobaric compliance of the radial artery is increased in patients with essential hypertension.

Hypertension is known to decrease arterial elasticity and systemic compliance. However, the arterial tree is not a homogeneous system, and whether a distal medium-sized artery such as the radial artery behaves like proximal arteries has not been determined. The aims of the present study were, first, to characterize non-invasively the mechanical properties of the radial artery through the determination of the pressure-diameter curve, the distensibility-pressure curve and the compliance-pressure curve, and, secondly, to compare untreated hypertensive patients with normotensive subjects. A new high-precision echo-tracking device was developed which allows the diameter of peripheral arteries to be measured continuously. By relating the changes in internal diameter (cross-sectional changes) to those in blood pressure, the cross-sectional arterial compliance could be determined. Seventy-eight untreated mild or moderate essential hypertensive patients aged 24-78 years were compared with 44 normotensive subjects aged 22-81 years. In order to increase the database and provide independent assessments of the variables examined, the cross-sectional study was performed independently using a standardized procedure in three different research centres. The major finding was that diameter, distensibility and compliance of the radial artery of hypertensive patients were not significantly different from those of normotensive controls when the two populations were studied at their mean arterial pressure. Furthermore, when the two populations were compared for the same level of blood pressure, using distensibility--and compliance--pressure curves, it was clear that isobaric distensibility and compliance of hypertensives were not significantly lower than those of normotensives, being either unchanged or higher. These findings are in contrast with the well-known decrease in compliance of proximal large arteries due to hypertension. Whether such a difference between proximal large arteries and distal medium-sized arteries may be related to the structural vascular changes observed with long-standing hypertension is still difficult to analyse in humans, and requires further investigation.

The cumulative dose response effect of eicosapentaenoic and docosahexaenoic acid on blood pressure, plasma lipid profile and diet pattern in mild to moderate essential hypertensive black patients

In this study eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) were given in a cumulative manner, every 6 weeks, starting with 10 mg, then 100 mg, 1000 mg and 10 000 mg EPA daily to mild to moderate essential hypertensive black patients. The corresponding DHA doses were 3, 33, 333 and 3333 mg. A control group was given olive oil as placebo for the entire 24 weeks. The placebo group had lower diastolic and systolic blood pressures after 24 weeks than the EPA and DHA group. No effect was seen on plasma triglycerides, cholesterol, HDL-cholesterol and gamma-glutamyltranspeptidase at any stage of the trial. In the EPA group plasma free-EPA increased significantly from 1000 mg onwards and plasma free-arachidonic acid (AA) decreased after 1000 mg EPA. No other plasma free essential fatty acid changed during the trial, although the HDL: cholesterol increased slightly but non-significantly with an increase in EPA and DHA. No significant changes in diet pattern or body mass was observed. It is therefore concluded that EPA and DHA supplementation had no beneficial effects in mild to moderate essential hypertensive black patients except for a lowering of plasma AA.

Severe hypertension induces disturbances of renal autoregulation.

To study if the severity of hypertension could be associated with disturbances of the autoregulation of renal blood flow and glomerular filtration, we compared the renal hemodynamic and functional responses to acute blood pressure reductions of a group of patients with moderate essential hypertension (n = 10) with those of a group of patients with severe hypertension (n = 10). Blood pressure was reduced to normal levels by a stepwise infusion of sodium nitroprusside, and effective renal blood flow (by 131I-hippuran), glomerular filtration rate (by endogenous creatinine clearance), and filtration fraction were determined. After acute blood pressure normalization, effective renal blood flow and glomerular filtration rate were significantly reduced in patients with severe hypertension (-41.6 +/- 8.3% and -44.7 +/- 6.8%, respectively; p less than 0.01 for both) but not in those with moderate hypertension (+4.9 +/- 9.1% and +6.2 +/- 13.3%, respectively; NS). Filtration fraction remained unchanged in both groups. These results show that severe but not moderate essential hypertensive patients have a displacement to the right of the lower limit of the renal autoregulation curve due to impaired vasodilation to maintain adequate renal blood flow during acute reductions of blood pressure. This impairment may be due to anatomic or functional defects of preglomerular vessels, or to both. Furthermore, the inability to maintain adequate glomerular filtration in these circumstances shows that patients with severe hypertension also have an impaired ability to adjust postglomerular vasomotor tone in the face of reductions in glomerular blood flow.

Regulation of vasopressin release in moderately severe essential hypertension

Vasopressin plasma concentrations have been measured in two groups of subjects, 13 moderate essential hypertensive patients without target organ damage and eight control normotensive subjects, before and after the assumption of the upright position, and intravenous infusions of hypotonic saline (0.45% NaCl, 0.25 ml kg-1 min-1 for 1 h) and hypertonic saline (100 mmol NaCl in 50 ml). Plasma vasopressin in recumbent baseline conditions was not significantly different in the two groups. Upright posture and hypertonic challenge augmented, while hypotonic saline reduced plasma vasopressin levels, which were not significantly different between the two groups. Plasma renin activity increased in the upright position, was reduced by administration of hypotonic saline and unaffected by hypertonic saline, with no differences between the hypertensives and normotensives. After hypertonic saline, urinary flow rate and urinary sodium excretion in the hypertensive group increased to values significantly (p less than 0.05) higher than in normotensive subjects. In conclusion our study excludes significant alteration of vasopressin regulation in moderate uncomplicated hypertension. In hypertensives although the response of vasopressin to an osmotic load is preserved, the data suggest that the renal handling of the osmotic load may be altered.

Effects of dilevalol on renal function

Renal function was measured in a total of 35 volunteers and patients who were given dilevalol, the R,R optical isomer of labetalol. Young normotensive volunteers (n = 6) and elderly normotensive volunteers (n = 12) received single 400- and 200-mg doses of dilevalol, respectively. Renal function was determined in these subjects on the same day before and after dosing. In addition, patients with mild to moderate essential hypertension (n = 11) and hypertensive patients with renal insufficiency (n = 6) were treated with placebo to establish baseline blood pressure and then were given dilevalol, 400 to 1,600 mg/day, for 2 to 6 weeks until blood pressure was controlled. Renal function was determined at the end of the baseline period and again at the end of dilevalol treatment. A subgroup of elderly hypertensives from the 2 protocols used to study hypertensive patients was treated as a separate study group. The only effect on parameters of renal function seen in any of the study groups was a statistically significant 15% decrease in glomerular filtration rate after single-dose treatment in the elderly normotensive group. Effective renal plasma flow, filtration fraction, renal blood flow and renal vascular resistance were unchanged before and after treatment in all groups. Mean arterial pressure was reduced significantly in all groups except in the elderly normotensive volunteers. Dilevalol appears to be a well-tolerated, effective therapeutic agent that is neutral regarding its effect on renal function and potentially useful in a variety of patient populations.

Demography predicts blood pressure response to once-daily enalapril monotherapy of mild to moderate essential hypertensive patients.

Enalapril was given once daily in low dose (5 to 10 mg) and high dose (20 to 40 mg) in 25 (15 white and 10 black) mild-to-moderate essential hypertensive patients. The white patients had a significant (p less than 0.005) supine diastolic blood pressure (SDBP) lowering with all doses of enalapril (from 97.2 +/- 1.8 to 85 +/- 2.4 mm Hg lowest). The black patient's SDBP did not decrease significantly (100.8 +/- 2.4 to 96.2 +/- 3.7 mm Hg lowest) with enalapril but addition of hydrochlorothiazide achieved satisfactory SDBP control. It is concluded that hydrochlorothiazide should be added if greater than 10 mg/day of enalapril is needed in white patients and the initial therapy in black patients should be a combination of enalapril and hydrochlorothiazide.

Persistence of the Natriuretic Effect of Calcium Entry Blockers

In order to elucidate whether or not the natriuretic properties of calcium entry blockers persist during the long-term administration of the drug, we have investigated the renal capacity to excrete an intravenous sodium load (2,000 ml of isotonic saline in 4 h) in a group of eight mild to moderate essential hypertensive patients, before and after 1, 8, and 24 weeks of treatment with nitrendipine. The following parameters were measured before and hourly during saline infusion: blood pressure, and plasma and urine sodium and potassium. For 5 days prior to the performance of the test, the patients received a diet containing 120 mEq of sodium daily. Nitrendipine induced a significant fall of both systolic and diastolic blood pressure (p less than 0.05-0.01) that was maintained throughout the study. A significant increase of the cumulative renal sodium output (microEq/min/h) was observed after 1, 8, and 24 weeks (p less than 0.05-0.001) of therapy with the calcium entry blocker. Meanwhile, plasma sodium and potassium and the kaliuresis did not change significantly. These results indicate that the natriuretic effect of calcium entry blockers is still present after long-term treatment.

Large Arteries in Hypertension

Acute effects of a new calcium entry blocker, nitrendipine, on large arteries of the forearm were studied by using arterial pulse strain gauge mecanography and pulsed Doppler velocimetry of the brachial artery in 13 mild to moderate essential hypertensive patients. Ninety minutes after nitrendipine ingestion, patients exhibited significant decreases in blood pressure without changes in heart rate; increases in brachial artery diameter and decreases in brachial to radial pulse wave velocity; increases in arterial compliance and decreases in characteristic impedance; and increases in brachial artery blood velocity and flow and decreases in forearm vascular resistance. Lastly, amplitude of pulse pressure was decreased by nitrendipine and negatively correlated to the level of arterial compliance. These results suggest that nitrendipine exerts a direct benefit effect on the hypertensive large arteries whose two main consequences are a decrease in pulsatility of arterial pressure and an increase in arterial flow.