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PubMed1987

Prescription patterns and costs of antihypertensive drugs in two outpatient clinics: Zürich (Switzerland) and Münster (FRG), 1975-1985.

In the present study the prescription patterns and cost of antihypertensive drugs in two outpatient clinics located in two different countries (Zürich, Switzerland, and Münster, FRG), were analyzed from 1975 till 1985 by using representative random samples of hypertensive outpatients. Throughout the observed period the leading positions were held by diuretics and beta-blockers, whereas central sympatholytics and ganglion blockers nearly disappeared. A rapid increase in the use of calcium antagonists occurred within the last 2 analyzed years. Drugs in fixed combination containing reserpin showed a constant decrease during the observed period, whereas beta-blocker-containing combination drugs increased in both clinics. The comparison between the two clinics revealed only minor differences in the prescription pattern of the various known classes of antihypertensive drugs. However, marked differences were observed within given classes between the preferred products. Both in Zürich and Münster the mean annual drug cost per patient doubled from 1975 to 1985. Especially during the last few years these changes took place with a remarkable rapidity, obviously the result of a more intense promotion of new antihypertensive drugs.

Adrenergic beta-Antagonists↗
PubMed1997

Effect of sympathoinhibition on exercise performance in patients with heart failure.

BACKGROUND: In patients with heart failure, excessive sympathetic activation during exercise could interfere with exercise performance by impairing arteriolar dilation in working muscle and by adversely altering skeletal muscle metabolic behavior. To test this hypothesis, we examined the effect of sympathoinhibition with clonidine, a central sympatholytic agent, on skeletal muscle blood flow and metabolism in patients with heart failure. METHODS AND RESULTS: Swan-Ganz and femoral venous catheters were inserted in 20 patients with chronic heart failure and exercise intolerance (peak exercise VO2 = 9.3 +/- 1.4 [SEM] mL.min-1.kg-1). Central hemodynamic measurements, leg blood flow determined by thermodilution, and systemic and leg metabolic parameters were measured during maximal treadmill exercise before and 2 hours after clonidine 2 micrograms/kg IV (n = 15) or 0.9% normal saline (n = 5). During-control exercise before the administration of clonidine, leg blood flow increased from 0.3 +/- 0.1 to 1.8 +/- 0.2 L/min and plasma norepinephrine increased from 485 +/- 61 to 2155 +/- 186 pg/mL (both P < .01). Treatment with clonidine markedly suppressed norepinephrine levels during exercise (matched peak exercise workload: control, 2137 +/- 187 versus clonidine, 1430 +/- 161 pg/mL), increased leg blood flow (control, 1.8 +/- 0.2 versus clonidine, 2.3 +/- 0.4 L/min), reduced systemic oxygen consumption (control, 1002 +/- 70 versus clonidine, 966 +/- 68 mL/min), reduced pulmonary artery lactate concentration (control, 3.2 +/- 0.3 versus clonidine, 2.6 +/- 0.2 mEq/L), and decreased minute ventilation (control, 39.7 +/- 2.1 versus clonidine, 34.9 +/- 2.4 L/min) (all P < .05). CONCLUSIONS: These findings suggest that sympathetic activation during exercise reduces leg blood flow, increases muscle glycolysis, and decreases muscle efficiency in patients with heart failure.

Cardiomyopathy, Dilated↗
PubMed1991

Raynaud's phenomenon. An update.

The pathogenesis of primary Raynaud's phenomenon remains an enigma. Most evidence favors a local abnormality in the digital arteries as opposed to an increased activity of the sympathetic nervous system. The local fault may involve the alpha 2-adrenergic receptors, which are most important in reflex sympathetic vasoconstriction. Cooling blood vessels increase the sensitivity of alpha 2-adrenergic receptors, increased levels of alpha 2-adrenergic receptors are present in primary Raynaud's disease, and patients show an increased sensitivity to alpha 2-adrenergic receptor agonists on finger blood flow. Serotonin has also been implicated, but the evidence is not compelling. In secondary Raynaud's phenomenon, vasospastic attacks can often be explained by a low arterial distending pressure, a thickened vessel wall, or absence of beta-adrenergic receptor activity. Diagnosis of primary Raynaud's disease relies on a typical history and normal physical examination, laboratory studies, and nailfold capillaroscopy. Finger systolic blood pressures during local cooling with ischemia may be helpful to document vasospastic attacks but does not distinguish primary from secondary Raynaud's phenomenon. The treatment of Raynaud's phenomenon is usually conservative. Pavlovian conditioning or biofeedback may be beneficial. When drug therapy is necessary, the calcium channel entry blocker nifedipine or sympatholytic agents have been shown to decrease the frequency and duration of vasospastic attacks in about two thirds of patients, although subjective improvement does not usually correlate with objective testing. Direct-acting vasodilators have not been shown to be of definite benefit. New therapies include prostaglandins, captopril, and the serotonergic antagonist ketanserin. Surgical sympathectomy has not been beneficial.

Calcium Channel Blockers↗
PubMedDate not supplied

Role of reactive hyperreninemia in blood pressure changes induced by sodium depletion in patients with refractory hypertension.

Sixteen patients with refractory hypertension were submitted to vigorous sodium depletion while cardiovascular homeostasis was monitored with measurements of hormonal and hemodynamic parameters and repeat saralasin tests. This regimen resulted in a negative sodium balance by an average of 300 mEq. The loss of sodium closely correlated to the decrease of body weight (r = 0.70, p less than 0.005). Blood pressure (BP) decreased from 176/166 +/- 8/3 to 155/109 +/-6/3 mm Hg. There was a significant correlation between percent increments in plasma renin activity (PRA) and the rise in plasma norepinephrine (r = 0.68, p less than 0.05) and a close negative correlation between percent increase in PRA and the ratio of fall in mean blood pressure (MAP) per unit of weight loss (r = -0.73, p less than 0.005). Thus, patients with the least percent increase in PRA demonstrated the greatest fall in BP per unit of weight loss, indicating that relative rather than absolute elevation of renin may be the factor limiting antihypertensive efficacy of sodium depletion. Sodium depletion induced increase in peripheral resistance and decrease in cardiac output, both mostly attributable to relative hyperreninemia. Indeed, the adverse hemodynamic changes were reversed by angiotensin inhibition, during which BP normalized. It is concluded that vigorous sodium depletion complemented by angiotensin blockade or suppression with sympatholytic agents improves management of otherwise refractory hypertension.

Adult↗
PubMedDate not supplied

Causes of inadequate response to antihypertensive drugs. Volume factors.

Diuretic therapy, by producing a negative salt and water balance, eliminates the false tolerance to sympatholytic drugs that often occurs during long-term monotherapy. This tolerance results from salt and water retention produced by the drugs. Review of published results suggests a primacy for arterial pressure reduction in this fluid because suppressed renal sympathetic activity should facilitate salt and water excretion through lessened alpha-adrenergic influence on tubular reabsorption, and beta-adrenergic inhibition would diminish renin release thus promoting natriuresis. The return of hypertension that characterizes the false tolerances seems paradoxical because these drugs cause venodilation, which should provide ample storage of expanded blood volume without affecting cardiac output. However, animal studies have suggested that dilated veins have decreased compliance; if that is so, in humans it would mean that fluid retention would be accompanied by a redistribution of blood into the central circulation, with a rise in cardiac output.

Animals↗
PubMedDate not supplied

Antihypertensive therapy in diabetic patients.

Hypertension in diabetic patients is more common than in controls, contributes substantially to their increased cardiovascular morbidity and mortality, and should be treated as accurately as diabetes mellitus itself. After appropriate exclusion of secondary forms, the first therapeutic step consists of reduction of overweight, salt intake, and smoking; the omission of interfering drugs; and adequate instruction. Step 2 has usually been the prescription of a diuretic drug, in spite of its known side effects on carbohydrate and lipid metabolism. A new possible alternative may be a calcium antagonist. Results in 10 hypertensive diabetic persons suggest that at a dose that normalizes blood pressure, neither carbohydrate nor lipid metabolism is altered, uric acid decreases, the exaggerated cardiovascular reactivity toward norepinephrine becomes normal, and the pressor dose for angiotensin II tends to rise. Body weight, blood volume, exchangeable sodium, as well as plasma and urinary sodium, potassium, and creatinine levels were unchanged. The third therapeutic step is the addition of a cardioselective beta blocker in a moderate dose. This avoids the disadvantages of beta 2-adrenergic blockade such as decreased insulin output, prolonged hypoglycemia, diminished glucagon secretion, and increased vasospasticity during hypoglycemic states, as well as aggravation of peripheral vascular disease. Alternatives are other sympatholytics with their known tendency to cause or increase orthostatic and sexual problems or, again, a calcium antagonist. In step 4, a hydralazine-type drug or prazosine is added. The fifth step, which adds minoxidil or captopril to the previous drugs, should only be taken after a specialist reevaluates the overall situation.

Adrenergic beta-Antagonists↗
PubMed1998

The effects of clonidine on the fear-inhibited light reflex.

We have shown previously that pupil diameter increases and the amplitude of the pupillary light reflex is reduced when subjects are under threat of an aversive event (electric shock), and that light reflex amplitude correlates negatively with subjective anxiety. Furthermore, we have shown that the threat-induced reduction in light reflex amplitude is sensitive to the effect of the anxiolytic drug diazepam. We have suggested that the 'fear-inhibited light reflex' paradigm could be used as a laboratory model of human anxiety. In the present study, we examined whether a single oral dose (200 microg) of the sedative-sympatholytic drug clonidine would antagonize the effects of threat on the pupillary light reflex. Twelve healthy male volunteers participated in two sessions separated by seven days in which they ingested clonidine 200 mg or placebo in a double-blind, balanced, cross-over design. Light stimuli (0.43 mW/cm2, 200 msec) were generated by a green (peak wavelength 565 nm) light-emitting diode, and pupil diameter was monitored by computerized binocular infrared television pupillometry in the dark. The light reflex response was recorded during either the anticipation of a shock ('threat' blocks) or periods in which no shocks were anticipated ('safe' blocks). The shock was a single square wave current pulse (1.5 mA, 50 msec) applied to the median nerve at the end of the experiment. Following each 'threat' or 'safe' block, subjects rated their anxiety using visual analogue scales. Two-factor ANOVA (treatment x condition) showed that clonidine treatment antagonized both the threat-induced increase in pupil diameter and the threat-induced reduction in light reflex amplitude. These effects, however, were not threat-specific since clonidine also reduced pupil diameter and enhanced light reflex amplitude in the 'safe' condition. Clonidine also reduced subjective alertness but not subjective anxiety in the 'threat' condition. These findings suggest that the mutual antagonism between clonidine and threat is likely to reflect the opposite effects of the two variables on the central noradrenergic control of pupillary functions, rather than a specific anxiolytic effect.

Adult↗
PubMed1997

Cardiotonic activity of the rhizome of Polygonatum sibiricum in rats.

The cardiotonic effect of the rhizome of Polygonatum sibiricum was investigated in the left atria of rats. The methanol extract of the rhizome of Polygonatum sibiricum (OM) (1-7 mg/ml) concentration-dependently increased the developed tension of the left atrium. It also strongly inhibited cAMP phosphodiesterase. The increase cAMP level correlated the increase in left atrial contraction. On the other hand, OM did not inhibit Na+, K+-ATPase. The cardiotonic effect of OM was strongly inhibited by reserpine, a sympatholytic agent. Furthermore, OM-treated left atria inhibited the tension produced by propranolol, a beta adrenocepter antagonist. These findings suggested that the cardiotonic effect is due to stimulating beta adrenoceptors through activation of sympathetic nerves.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1984

Hypertension in pregnancy. Pathophysiology and management.

Hypertension in pregnancy has implications for both maternal and fetal welfare. Extrapolation from concepts of mechanisms operating in hypertension in general to pregnancy-related hypertension is not justified. In the latter, the major features are a hyper-adrenergic state, plasma volume reduction and an increased systemic resistance. A reduction in uteroplacental perfusion may result from or may activate the mechanisms that elevate blood pressure. Humoral factors (e.g. hormonal attenuation of vascular reactivity) and prostacyclin deficiency may be central to the disordered physiology. Treatment of hypertension in pregnancy should aim at avoiding the vascular damage due to blood pressure elevation but not cause a reduction in uteroplacental perfusion. Unlike earlier antihypertensive regimens using centrally acting sympatholytics, adrenergic neuron blockers or diuretics, regimens using beta-blockers or combinations of beta-blockers with alpha-blockers or vasodilating agents such as hydralazine permit effective blood pressure control, even in severe hypertension, and pregnancy can often proceed until term or until fetal maturity is secured. Adverse effects on the fetus (growth retardation, cardiorespiratory depression, hypoglycaemia, hyperbilirubinaemia) formerly attributed to beta-blockers are more likely related to poorly controlled hypertension. Specific benefits of maternal beta-adrenoceptor blockade are suggested by evidence for prevention of proteinuric deterioration and a decrease in the incidence and severity of respiratory distress in premature infants. Hypertension in pregnancy still presents a formidable therapeutic challenge and requires comprehensive management with close monitoring of fetal welfare. The presence or development of proteinuria in a hypertensive pregnant woman implies a major increase in risk to the fetus and warrants immediate admission to hospital for specialist management.

Adrenergic alpha-Antagonists↗
PubMed1988

Central sympathoplegic and norepinephrine-depleting effects of antioxidants.

Carbon disulfide (CS2), tetraethyl lead (TEL), tetraethyl tin (TeET), dithiothreitol (DTT), and gossypol acetic acid (GAA) significantly decreased brain norepinephrine (NE) in rats. The central dopamine (DA) increased after ip administration of CS2, TEL, and DTT, but decreased after TeET and GAA. The brain serotonin decreased only after TeET. Two doses of DTT decreased the NE longer than one dose (24 vs 2 hr) but did not increase DA. L-DOPA, given SC with DTT, delayed the decrease in NE by 24 hr. The similar behavioral and autonomic effects of each of these compounds suggest a central sympatholytic effect and an antipsychotic type of sedation and rigidity. A possible mechanism is reversible inhibition of dopamine beta-hydroxylase through the reduction of the copper ion of the enzyme. Each of these reducing agents, together with the boranes previously studied, has similar behavioral and autonomic effects and a common effect on NE concentration, suggesting that the agents act through a physicochemical property rather than by combination with a cellular component. These data have applications to the toxicity of the single agents. They also provide an index of activity, previously lacking, of systemic antioxidant effect.

Animals↗
PubMed2004

Systematic review: antihypertensive drug therapy in black patients.

BACKGROUND: Hypertension occurs more frequently and is generally more severe in black persons than in white persons, leading to excess morbidity and mortality. PURPOSE: To systematically review the efficacy of different antihypertensive drugs in reducing blood pressure, morbidity, and mortality in hypertensive black adults. DATA SOURCES: The following databases were searched from their inception through November 2003: MEDLINE, EMBASE, LILACS (Literatura Latino-Americana y del Caribe en Ciencias de la Salud), African Index Medicus, and the Cochrane Library. PubMed was also searched from September 2003 through March 2004. Searches were conducted without language restriction. STUDY SELECTION: Randomized, controlled trials of drugs versus placebo (blood pressure outcomes) or drugs versus placebo or other drugs (morbidity and mortality outcomes). DATA EXTRACTION: 2 reviewers independently extracted data. DATA SYNTHESIS: The efficacy of beta-blockers in reducing systolic blood pressure and the efficacy of angiotensin-converting enzyme inhibitors in achieving diastolic blood pressure goals did not significantly differ from that of placebo (weighted mean difference for beta-blockers, -3.53 mm Hg [95% CI, -7.51 to 0.45 mm Hg]; relative risk for angiotensin-converting enzyme inhibitors, 1.35 [CI, 0.81 to 2.26]). In the pooled analyses, other reviewed drugs (calcium-channel blockers, diuretics, central sympatholytics, alpha-blockers, and angiotensin II receptor blockers) were more effective than placebo in reducing blood pressure, but only calcium-channel blockers remained effective in all prespecified subgroups, including patients with a baseline diastolic blood pressure of 110 mm Hg or greater. Main morbidity and mortality outcomes did not differ significantly between treatment groups when drugs were combined to reach blood pressure goals. However, trial results indicated a greater occurrence of diabetes with diuretics and a higher risk for cardiovascular events with drug regimens that included angiotensin-converting enzyme inhibitors. LIMITATIONS: This meta-analysis evaluated the blood pressure lowering-efficacy of monotherapy only. CONCLUSIONS: Drugs differ in their efficacy for reducing blood pressure in black patients, but there is no solid evidence that efficacy for reducing morbidity and mortality outcomes differs once patients achieve the blood pressure goal.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Mechanism of the diuretic effect of eufillin].

In acute experiments on rats the xanthine diuretic euphylline did not block the short-circuited current in the proximal tubule, nor did it lower the transtubular potential and the transepithelial resistance of the nephron wall. The diuretic speeded up significantly the passage of the tubular fluid along the proximal region of the nephron and Henle's loop. The dihydroergotoxin and inderal blocking of adrenoreceptors did not produce any influence on the renal effects of the xanthine agent. Reserpine totally blocked the diuretic and saluretic effects of euphylline, whereas other sympatholytics, such as alpha-methyl-dofa, anthabus and hemedin, did not modify the action of the diuretic.

Aminophylline↗
PubMed2002

Sympatho-inhibitory properties of various AT1 receptor antagonists.

It is well known that angiotensin II (Ang II) can facilitate the effects of sympathetic neurotransmission. In the present study, using various experimental models, we investigated the inhibitory effects of several Ang II subtype 1 receptor (AT1) antagonists on this Ang II-induced facilitation. We compared the sympatho-inhibitory potencies of the AT1 blockers with their respective potencies regarding inhibition of the direct vasoconstrictor effects of Ang II. In the isolated mesenteric artery, we investigated the effects of Ang II in the presence and absence of losartan, irbesartan and telmisartan on stimulation-induced vasoconstrictor responses. In the pithed rat, we studied the effect of AT1 blockade on the sequelae of electrical stimulation of the thoracolumbar sympathetic outflow (presynaptic AT1 blockade) as well as on dose-response curves elicited by exogenous Ang II (postsynaptic AT1 blockade). Additionally, we compared the sympatho-inhibitory of irbesartan in spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. In the isolated mesenteric artery, Ang II (10 nM) significantly enhanced stimulation-induced vasoconstrictor responses. The enhancement could be antagonized in a concentration-dependent manner by losartan (1 nmol/l to 1 mumol/l), irbesartan (0.1 nmol/l to 0.1 mumol/l) and telmisartan (0.01 nmol/l to 0.01 mumol/l). The sympatho-inhibitory potency was telmisartan > irbesartan > losartan. In the pithed normotensive rat, the stimulation-induced increase in diastolic blood pressure (DBP) as well as the Ang II-elicited DBP response were dose-dependently reduced by all the AT1 receptor blockers investigated. The order of potency with respect to sympatho-inhibition was eprosartan > valsartan = candesartan = embusartan = telmisartan > losartan > irbesartan (comparison of doses which at 2 Hz reduced delta DBP by 20 mmHg, differences significant at P < 0.05). The order of potency regarding inhibition of the Ang II-induced DBP increase was candesartan > embusartan = valsartan = eprosartan = telmisartan > irbesartan > losartan (comparison of the antagonist concentration, in the presence of which twice the agonist concentration, in the presence of which twice the agonist concentration is needed to cause the same effect [pA2 values], differences significant at P < 0.05). In the pithed SHR and the normotensive WKY rat the sympatho-inhibitory potency of irbesartan did not differ significantly between both strains. It can be concluded that all AT1 receptor antagonists appear to possess sympatho-inhibitory properties, which may be of potential interest in the treatment of hypertension and heart failure. Our findings suggest differences in pre- and postsynaptic inhibition between the various compounds, since for eprosartan and losartan the sympatholytic doses and postsynaptic inhibitory doses differed far less than for the other AT1 receptor antagonists.

Angiotensin Receptor Antagonists↗
PubMed2004

Treatment of postmenopausal hypertension with moxonidine, a selective imidazoline receptor agonist.

This study compared the effects of two sympatholytic agents--one central (moxonidine) and one peripheral (atenolol)--on blood pressure and other metabolic syndrome factors in postmenopausal hypertensive women who were not taking hormone replacement therapy. Atenolol and moxonidine led to a statistically significant reduction in diastolic blood pressure of 9.5 mmHg and 5.5 mmHg, respectively. A clear rebound effect was observed in the atenolol patients whereas the moxonidine group exhibited a slightly further decrease in blood pressure. Moxonidine also caused a profound decrease in both mean plasma-glucose area under the curve (AUC) during oral glucose tolerance test (-0.96 mmol/L x H, NS) and mean plasma-insulin AUC (-6.15 mU/L x H). Therefore, moxonidine displayed a slightly less potent antihypertensive effect than atenolol in hypertensive postmenopausal women, but it demonstrated a better metabolic effect. To conclude, moxonidine could benefit hypertensive postmenopausal women who display other signs of metabolic syndrome.

Antihypertensive Agents↗
PubMed2004

[Clonidine and anesthesia].

The alpha2-adrenoceptor agonists have several beneficial actions during the perioperative period. They exert a central sympatholytic action, improving haemodynamic stability in response to endotracheal intubation and surgical stress, reducing the anesthetic and opioid requirements and causing sedation, anxiolysis and analgesia. Furthermore, alpha2-adrenoceptor agonists may offer benefits in the prophylaxis and treatment of perioperative myocardial ischaemia. Recent alpha2-adrenoceptor agonists with short duration of action (dexmedetomidine and mivazerol) are adapted for the administration to patients at high risk for coronary artery disease during surgery. The alpha2-adrenoceptor agonists have an analgesic action at several sites of the peripheral and central nervous system as well as the prolongation of epidurally or intrathecally administered local anesthetics and opioids.

Adrenergic alpha-Agonists↗
PubMed1989

Antihypertensive treatment of the elderly in general practice.

In order to assess the antihypertensive care received by the elderly, where clear therapeutic guidelines are lacking, a population of 3,858 aged over 64 years was studied. Data were derived from a large Italian 'Study on Blood Pressure in the Elderly', carried out in general practice. Over 90% of the 2,059 known hypertensive patients were receiving drug treatment, with no age or sex-related differences. A single drug was prescribed to 50.2% of treated patients; only 5.5% were receiving three or more drugs. Diuretics and older sympatholytic agents were by far the most frequently prescribed categories, with four drugs (hydrochlorothiazide, amiloride, methyldopa and chlorthalidone) accounting for over 50% of all prescriptions. Low-dosage treatment schedules were frequently used, often associated with less-often-than-daily drug administration. Our study shows that physicians' attitudes to the treatment of arterial hypertension in the elderly are fairly uniform, with treatment of all subjects but with low drug dosages.

Aged↗
PubMed1988

Participation of the sympathetic system in acetic acid-induced writhing in mice.

We investigated the participation of a sympathetic component in the abdominal contortions induced by intraperitoneal injection of 0.6% acetic acid in the mouse. The beta blocker propranolol (4 mg/kg, sc) caused a small significant (19%) blockade of the contortions but strongly potentiated (greater than 80%) the effect of indomethacin (30% at 5 mg/kg, sc). Significant inhibition of writhing was also observed with sympatholytics such as guanethidine (27% at 30 mg/kg, sc) and by a specific dopamine-I antagonist, SCH 23390 (62% at 400 micrograms/kg, sc). Tyramine, which releases sympathomimetic amines, and cocaine, which partially blocks the uptake of amines, potentiated acetic acid writhing. Intraperitoneal administration of noradrenaline (187 micrograms/kg)potentiated acetic acid-induced writhing. These results are consistent with the suggestion of Nakamura and Ferreira (1) that inflammatory nociception has a dual component: one mediated by cyclooxygenase metabolites and another by sympathetic amines, possibly acting through a DA-1 type receptor.

Acetates↗
PubMed1986

[Differential approach to restoring motor function of the intestines in peritonitis].

The authors have made a comparative estimation of the effectiveness of different methods of treatment of 330 patients with peritonitis with special reference to subdivision of motor disorders into 4 stages (compensated, subcompensated, decompensated stages and enteroplegia). It was established that sympatholytic drugs and continuous peridural anesthesia were effective in the compensated stage. Continuous intubation of the gastro-intestinal tract with the help of a rigid probe ensuring decompression in the postoperative period was the operation of choice in decompensated disturbances of the motor-evacuatory function.

Anesthesia, Epidural↗