[Methods of influencing life style and risk factors].
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Age Factors↗
Biomedical subjects
L A Ferrara
Publications and source records attributed to L A Ferrara.
Enhancement of exogenous triglyceride removal following calcium channel blockade.
Adrenergic regulation of lipid metabolism is mediated by various intracellular messengers, including calcium ions. Little is known about the role of calcium in the catabolism of triglyceride-rich lipoproteins. Aim of this study was to investigate whether blockade of calcium influx across the cell membrane influences lipid metabolism in man. The calcium entry blocker nitrendipine was administered to 10 hypertensive, normolipidemic subjects for eight weeks at the dose of 10 mg b.i.d. An enhancement in plasma clearance of triglyceride was observed after nitrendipine administration: fractional removal rate of the triglyceride emulsion Intralipid increased by 22% (from 3.13 +/- 1.1 after placebo to 3.81 +/- 1.4% min after nitrendipine, p less than 0.03). Fasting serum triglyceride was not shifted (83 +/- 57 vs 84 +/- 37 mg/dl). Total serum cholesterol and cholesterol in high density lipoproteins were also unchanged during the study. No evidence of change in insulin response was detected. It is hypothesized that calcium plays a role in the modulation of lipoprotein lipase, the enzyme mainly responsible of the removal of exogenous triglyceride from plasma. Alternatively, the increase in the clearance rate of the triglyceride emulsion might be explained by the vasodilating activity of nitrendipine.
Adult↗
Long-term antihypertensive efficacy of ketanserin plus chlorthalidone.
The long-term antihypertensive efficacy of a combination of ketanserin (20 mg), an S2 antagonist with alpha 1 blocking activity, and chlorthalidone (25 mg), given o.d., was evaluated in fifteen patients with primary hypertension of mild to moderate degree, aged 45-65 years, up to a 12-month observation period. Systolic (SBP) and diastolic (DBP) blood pressure, and heart rate (HR) were measured by an automatic recorder (Sentron Bard Biomedical) twice at rest after 5 min in a supine position and after 2 and 5 min in an upright position, 24 h after the last antihypertensive dose. Thirteen patients completed the study whilst two were lost to the follow-up. A significant reduction was observed in both SBP and DBP at rest. In particular, SBP was reduced from 167 +/- 17 mmHg to 152 +/- 21 mmHg (p less than 0.01) after 1 month of therapy and was kept constant at this level throughout the observation period. DBP was also reduced from the first control [99 +/- 7 vs. 90 +/- 9 mmHg (p less than 0.01)] without any increase during the follow-up. HR was unchanged throughout the study. Four patients had dizziness and orthostatic hypotension after the first dose of the drug combination but were able to continue the study without further adverse reactions. These data support the conclusion that long-term treatment with the combination of a small dose of ketanserin and chlorthalidone is able to reduce systolic and diastolic blood pressure, without remarkable untoward side-effects.
Adult↗
Addition of chlorthalidone to slow-release nifedipine in the treatment of arterial hypertension: a controlled study versus placebo.
The use of calcium antagonists and diuretics in combination for treatment of hypertension is controversial. In a single-blind study 16 patients (8 men, 8 women, age range 39 to 62 years) with primary hypertension of mild to moderate degree were given slow-release nifedipine 20 mg twice daily for 6 weeks, thereafter either chlorthalidone 25 mg (Group A) or placebo (group B) daily was randomly added for a further 6-week period. Blood pressure (BP), heart rate, plasma renin activity (PRA), aldosterone, and 24 hour urinary electrolytes were evaluated. Nifedipine decreased supine BP from 159/92 +/- 16/8 to 151/89 +/- 10/6 mmHg in group A and from 162/94 +/- 20/12 to 145/85 +/- 14/6 mmHg in group B. A further fall to 139/84 +/- 7/6 mmHg (p less than .05) was observed after addition of chlorthalidone. PRA significantly increased with combined treatment compared to baseline (3.3 +/- 0.8 to 9.9 +/- 3.3 ng/ml/hr; p less than 0.05). A slight reduction of 24-hour urinary calcium was observed after the addition of chlorthalidone. These data indicate that the combination of nifedipine and chlorthalidone might be beneficial in the treatment of arterial hypertension.
Adult↗
Acute and chronic effects of dihydropyridines on triglycerides in humans.
Several drugs used in the treatment of hypertension have been shown to affect lipid metabolism. A few studies have examined in detail the effects of calcium antagonists on blood lipids. We investigated the effects of nifedipine and nitrendipine on blood lipids using two experimental protocols. The first study was a double-blind, randomized, placebo-controlled trial to assess the effects of acute oral administration of nifedipine 10 mg on blood lipids in 10 patients (9 males, 1 female; age range 26-50 years) with mild hypertriglyceridemia. Serum triglycerides were not significantly affected (from 310 +/- 120 to 280 +/- 110 mg/dl 2 h after nifedipine) but a slight decrease was observed in patients with higher baseline levels. In the second study, an intravenous fat tolerance test (ivFTT, Intralipid 10%, 1 ml/kg body weight, as a bolus) was performed before and after chronic oral administration of nitrendipine 10 mg b.i.d. in 10 mild to moderate hypertensive patients (7 males, 3 females; age range 40-60 years). After nitrendipine treatment, the fractional removal rate (K2) of the lipid emulsion was significantly increased from 3.1 +/- 0.9 to 3.8 +/- 0.9% min (p less than 0.05). The main findings of these studies suggest that the secretion of lipoprotein lipase might be stimulated by calcium antagonists. Alternatively, the vasodilation produced by these compounds may influence triglyceride removal by expanding the capillary bed where the enzyme exerts its activity. In conclusion, calcium antagonists do not seem to cause unwanted side effects on blood lipids and apparently enhance triglyceride removal.
Adult↗
Is the sympathetic nervous system altered in children with familial history of arterial hypertension?
The sympathetic nervous system has been investigated in 42 children with family history of arterial hypertension and 68 children of the same age without hypertensive relatives. Pressure responses to mental arithmetic and to isometric handgrip stress were measured in both groups, along with 24 h catecholamine excretion. Resting blood pressure and heart rate did not show any difference between groups. The increase in diastolic pressure during the mental arithmetic exercise was, however, significantly greater in children with family history of hypertension. A sharp increase in blood pressure and heart rate was observed during isometric handgrip in both groups without any significant difference. Twenty-four hour catecholamine urinary excretion was significantly higher in the group with family history of hypertension (31 +/- 15 vs. 23 +/- 13 micrograms/24 h; p less than 0.05). These results seem to indicate that an initial impairment of the sympathetic activity is already detectable in young offspring of hypertensive patients.
Blood Pressure↗
[Echocardiographic analysis of anatomical and functional changes in the left heart ventricle during antihypertensive treatment with nicardipine].
Changes in hemodynamic variables regulating systolic function were assessed by M-mode echocardiography, under 2D control, in 11 patients with primary uncomplicated hypertension treated with nicardipine (60 mg/daily). At the end of treatment (8 weeks) blood pressure and end-systolic stress were greatly reduced (p less than 0.001), and systolic fractional shortening was increase (p less than 0.02). The percentage increase in fractional shortening was correlated with a decreased in end-systolic stress (r = 0.67). The index of left ventricular performance (systolic pressure/end-systolic dimension ratio) was reduced: no variation was found in the hypertrophy-independent index of the inotropic state (systolic pressure/end-systolic dimension ratio normalized for posterior wall thickness). No change in the inotropic state was caused by a negligible sympathetic reflex outflow: heart rate also remained unchanged. The only index of left ventricular hypertrophy which was slightly reduced after two months of treatment was left ventricular mass (p less than 0.001). In conclusion, the short-term treatment with nicardipine, in hypertensive patients, showed powerful effects in the improvement of systolic function; the possible regression of left ventricular hypertrophy must be confirmed in long-term therapy.
Adult↗
[Treatment of hypertension associated with metabolic anomalies].
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Female↗
Controlled trial of long term oral potassium supplements in patients with mild hypertension.
A 15 week randomised double blind placebo controlled trial of oral potassium supplements (48 mmol daily) was conducted in 37 patients who had mildly increased blood pressure and a normal dietary intake of sodium. After a two month run in and a one week baseline period the patients were randomly assigned to receive either potassium supplements (n = 18) or placebo (n = 19). By the third week of treatment blood pressure in the actively treated group had decreased significantly compared with that in the placebo group, though the decrease reached its maximum after 15 weeks. Urinary potassium excretion increased significantly in the group who received potassium supplements, but no significant changes were found in plasma sodium and potassium concentrations or in urinary sodium excretion. In a subgroup of 13 patients who underwent a further nine weeks of treatment with oral potassium supplements at half of the previous dose (24 mmol daily) their blood pressure, at the end of this second study period, was still significantly lower compared with their baseline value but not with that of the placebo group. These results show that moderate oral potassium supplements are associated with a long term reduction in blood pressure in patients who have mild hypertension.
Administration, Oral↗
Adrenergic system and carbohydrate metabolism. Effects of beta-receptor blockade on insulin secretion and peripheral insulin sensitivity in normoglycaemic patients.
The effects of 3 weeks of treatment with the beta-receptor blocking agent propranolol and a placebo on glucose tolerance, insulin secretion and peripheral insulin sensitivity have been evaluated in 7 normoglycaemic hypertensive patients by an oral glucose tolerance test and the insulin clamp technique. Significant changes in systolic and diastolic blood pressure and heart rate were observed at the end of propranolol treatment, but there were no associated changes in glucose tolerance, insulin secretion or peripheral insulin sensitivity. No difference was observed in glucagon, growth hormone and free fatty acids between propranolol and placebo treatment. The results support the view that the hypothetical pancreatic glucoreceptor, at least in non-acute studies, is not affected by beta blockade. In addition, there was no effect on tissue sensitivity to insulin.
Adrenergic beta-Antagonists↗
Left ventricular mass and blood pressure during ergometric exercise in primary hypertension.
The pathophysiology of left ventricular hypertrophy (LVH) in hypertensive patients is still an intriguing point. The lack of a close relationship between LVH and systolic or diastolic blood pressure at rest, previously observed by other investigators, was confirmed in our group of 45 patients with uncomplicated primary hypertension. The strength of correlation between echocardiographic left ventricular mass (LVMe) and blood pressure, expressed as incremental area (IA = total area under the curve--basal area), however, increased during bicycle exercise testing (r = 0.33, p less than 0.05 for diastolic blood pressure; r = 0.39, p less than 0.01 for systolic blood pressure; r = 0.41, p less than 0.01 for mean arterial pressure). Other echocardiographic parameters of myocardial mass such as LVM index (LVMI) and septal thickness (ST) were also significantly correlated with blood pressure during exercise. These results suggest either that blood pressure during exercise is a better index of the cardiac workload than resting blood pressure or that the pathogenesis of cardiac hypertrophy involves an enhanced reactivity to adrenergic drive, particularly stimulated during ergometric exercise. Increased blood pressure alone, however, only partly accounts (about 20%) for the increase in myocardial mass in hypertensive patients; other factors, therefore, need to be further investigated for a better understanding of the pathophysiology of left ventricular hypertrophy.
Adult↗
Noninvasive assessment of hemodynamic changes during therapy with nitrendipine in arterial hypertension.
Changes in hemodynamic variables regulating systolic function were examined by M-mode echocardiography in 14 patients with long-duration primary uncomplicated hypertension treated with nitrendipine once daily (20 mg). At the end of treatment (8th week) blood pressure and peripheral resistance were greatly reduced (p less than 0.0001), while the indices of cardiac function (ejection fraction and cardiac index) showed significant increases (p less than 0.01). The variations in ejection fraction were analyzed by multiple linear regression and were mainly influenced by the decrease in end-systolic stress (contribution: 60%). At baseline, despite no radiographic or clinical signs of heart failure, 6 of the studied patients showed impaired systolic function, likely due to the strength of other variables (age, risk factors); in those patients, systolic function was clearly enhanced at the end of treatment, while no change was found in patients with initial normal pump function. Changes in cardiac output were due to a significant increase in heart rate in patients with normal pump function and to improved stroke volume in the others. Left ventricular mass index was slightly reduced (p less than 0.005), primarily because of the reduction in end-diastolic volume (p less than 0.01). When analyzed by the 2 subgroups (with or without impaired systolic function), the left ventricular mass index appeared to be significantly reduced only in those patients with normal basal pump function. This difference was most likely due to the different effects of treatment on end-diastolic volume.
Adult↗
Antihypertensive efficacy of the combination of ketanserin + thiazide in hypertensives older than 50 years.
The antihypertensive effect of the combination of ketanserin, a new antiserotonergic agent, and thiazide has been evaluated in 35 patients with arterial hypertension of mild to moderate degree in the greater than 50-year-old age group. Twenty patients were given ketanserin (20 mg) + hydrochlorothiazide (25 mg) (treatment A) while the others were given ketanserin (40 mg) + hydrochlorothiazide (12.5 mg) (treatment B) once daily, for a period of 6 weeks. Twenty-four-hour blood pressure, measured by an automatic recorder, was significantly reduced by both combinations. In particular, treatment A reduced blood pressure from 169 +/- 15/95 +/- 6 mm Hg before treatment to 146 +/- 11/83 +/- 8, 149 +/- 13/82 +/- 10, 143 +/- 12/81 +/- 9, and 151 +/- 14/84 +/- 7 mm Hg at 2, 6, 8, and 24 h, respectively, after the last dose of drug. With treatment B, blood pressure was reduced from 167 +/- 11/97 +/- 7 mm Hg before treatment to 152 +/- 12/89 +/- 8, 151 +/- 15/85 +/- 8, 150 +/- 16/86 +/- 8, and 158 +/- 13/91 +/- 7 mm Hg at 2, 6, 8, and 24 h, respectively. Heart rate was not affected by both treatments despite the fact that ketanserin has been proved to induce a marked vasodilation. Cardiac workload (systolic blood pressure X heart rate) was slightly reduced by the treatments. Treatment A only induced transient dizziness after the first dose of drug; treatment B, on the other hand, induced drowsiness and more marked dizziness, which in one case was also observed after repeated doses of the drug.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Calcium antagonists and thiazide diuretics in the treatment of hypertension.
The usefulness of the combination of nifedipine and chlorthalidone has been investigated in mild to moderate hypertensive patients (seven men, seven women; age range 39-62 years) by adding the diuretic to nifedipine monotherapy. After a 2 week washout, slow-release nifedipine 20 mg b.i.d. was given for 6 weeks, followed by addition of either chlorthalidone 25 mg (group A) or placebo (group B) q.d. for a further 6-week period. Blood pressure, heart rate, plasma renin activity, and 24-h urinary Na and K excretion were measured at baseline and at the end of each treatment period. Nifedipine decreased blood pressure in the two groups. A further significant fall was observed after chlorthalidone was added. No further change was detected after placebo in group B. Plasma renin activity after 1 h standardized walk significantly increased after combined treatment compared with baseline (3.3 +/- 1.2 to 9.4 +/- 5.3 ng/ml/h; p less than .05). No change was observed in 24 h urinary Na and K in the two groups. Venous distensibility measured by strain gauge plethysmography was slightly reduced during nifedipine monotherapy. Our data therefore suggest that chlorthalidone potentiates the antihypertensive effect of nifedipine despite an increase of renin activity.
Adult↗
Blood pressure during a combination of ketanserin and hydrochlorothiazide.
The antihypertensive effectiveness of a combination of ketanserin 20 mg plus hydrochlorothiazide 25 mg has been evaluated in 20 patients with arterial hypertension of mild to moderate degree in the age group over 50 years (age range 50-78 years). After a wash-out period of at least two weeks, patients were given a single oral dose of ketanserin 20 mg or thiazide 25 mg in a randomized order at two-day intervals and blood pressure, heart rate and cardiac workload (systolic blood pressure x heart rate) were measured during the following 24 h by an automatic recorder. Thereafter patients were given the combination of the two drugs for six weeks and 24 h blood pressure was assessed after the first dose and at the end of the treatment. A significant fall in systolic and diastolic blood pressure was rapidly induced by ketanserin from 2 to 8 h after dosing; thiazide on the other hand did not induce any change in these parameters (169 +/- 15/95 +/- 6 mmHg (22.5 +/- 2.0/12.7 +/- 0.8 kPa) at baseline versus 153 +/- 17/89 +/- 7 mmHg (20.4 +/- 2.3/11.9 +/- 0.9 kPa) at 2 h and 157 +/- 19/87 +/- 8 mmHg (20.9 +/- 2.5/11.6 +/- 1.1 kPa) at 8 h on ketanserin; 166 +/- 15/93 +/- 6 mmHg (22.1 +/- 2.0/12.4 +/- 0.8 kPa) at baseline versus 160 +/- 12/89 +/- 6 mmHg (21.3 +/- 1.6/11.9 +/- 0.8 kPa) at 2 h and 157 +/- 15/89 +/- 5 mmHg (20.9 +/- 2.0/11.9 +/- 0.7 kPa) at 8 h on thiazide).(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Effects of alpha-adrenergic and beta-adrenergic receptor blockade on lipid metabolism.
The role of lipoprotein lipase in the pathophysiology of lipid changes during alpha-receptor or beta-receptor blockade was evaluated in this clinical trial. Thirty hypertensive patients were given 2 mg of prazosin twice daily or 100 mg of metoprolol twice daily for 10 weeks, according to an open, randomized protocol. Both drugs were effective in reducing arterial blood pressure (from 153 +/- 16/102 +/- 6 mm Hg to 146 +/- 12/92 +/- 8 mm Hg with prazosin and from 158 +/- 17/103 +/- 8 to 144 +/- 14/94 +/- 10 mm Hg with metoprolol). Prazosin significantly reduced total plasma cholesterol from 202 +/- 39 to 188 +/- 36 mg/dl and increased high-density lipoprotein cholesterol from 36 +/- 8 to 40.5 +/- 11 mg/dl. Prazosin did not affect plasma triglycerides levels, whereas patients taking metoprolol had a slight rise in these levels, from 122 +/- 42 to 142 +/- 57 mg/dl, along with a decrease in high-density lipoprotein cholesterol from 37 +/- 10 to 31 +/- 8 mg/dl. The concentration of apoprotein B did not change significantly with either treatment. Lipoprotein lipase activity increased in the prazosin group from 28.4 +/- 16 to 37.7 +/- 14 mumol/liter per minute (p less than 0.01), but did not change significantly (29.9 +/- 12 versus 32.8 +/- 8 mumol/liter per minute) in patients treated with the beta blocker. These data, which confirm previous reports of serum lipid changes during antihypertensive therapy, suggest that alpha1 blockers may interfere with lipoprotein lipase, possibly by reducing its catecholamine-mediated inactivation.
Adolescent↗
Response to tilting in hypertensive patients receiving ketanserin.
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Aged↗
Interference by sulphinpyrazone with the antihypertensive effects of oxprenolol.
The interfering effect of sulphinpyrazone, a uricosuric agent which reduces the activity of cyclo-oxygenase, with the antihypertensive activity of oxprenolol, a non-cardioselective beta-blocker with sympathomimetic activity, has been evaluated. Ten patients with primary arterial hypertension of mild to moderate degree entered a randomized double-blind cross-over study versus placebo. They were given oxprenolol + placebo or oxprenolol + sulphinpyrazone for 15 days, and then the treatments were crossed-over for a further 15 days. Oxprenolol significantly reduced blood pressure (161 +/- 3/101 +/- 1 vs 149 +/- 4/96 +/- 2 mmHg) and heart rate (72 +/- 3 vs 66 +/- 3 beats/min). During administration of the combination with sulphinpyrazone the blood pressure increased to its pretreatment level (156 +/- 5/101 +/- 2 mmHg). The effect of oxprenolol on heart rate was not influenced by the combined treatment (67 +/- 6 beats/min). The results may be explained by 1) sulphinpyrazone-induced inhibition of prostaglandin synthesis, which could interfere with the antihypertensive activity of oxprenolol, or 2) sulphinpyrazone-induced acceleration of the metabolism of oxprenolol.
Adult↗