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At least 523 records · Page 29Linked to original sources
PubMed1988

Serum lipoproteins during treatment with antihypertensive drugs.

Hypertension and certain alterations in serum lipoproteins such as a decrease in high density lipoprotein-cholesterol (HDL-C), an increase in low density lipoprotein-cholesterol (LDL-C) and perhaps also elevated triglycerides (Tg), are complementary coronary risk factors. Moreover, it has become evident that several of the drugs used for standard antihypertensive therapy may also interact with lipoprotein metabolism. The following has been observed after 1 to 12 months of treatment. Various diuretics can significantly increase LDL-C and/or very LDL-C and total C/HDL-C ratio, while HDL-C is often largely unchanged; Tg also are often elevated. LDL-C increased in diuretic-treated men and in chlorthalidone-treated postmenopausal women but not in chlorthalidone-treated premenopausal women. The latter may be protected from this side effect. Drug dosages were usually high in these studies. Indapamide, given at a dose of 2.5 mg/day, seems to exert no relevant effect on the lipoproteins. It is not established whether this difference is related to the nature of the drugs or the doses used. There is little doubt that the dose of chlorthalidone used was greater than that required for a full antihypertensive effect of this drug. Several beta-blockers given as monotherapy induce significant increases in Tg and a tendency for decreases in HDL-C. These changes are most prominent on non-selective beta 1+2-blockers without partial intrinsic sympathomimetic activity (ISA), less pronounced on highly selective beta 1-blockers without ISA, and even more discrete or absent on beta-blockers with distinct ISA. Other sympatholytics such as reserpine, methyldopa, debrisoquine, urapidil, clonidine, labetalol, or postsynaptic alpha-blockers (prazosin, trimazosin, doxazosin etc.) did not affect or, postsynaptic alpha-blockers in particular, sometimes even slightly decreased Tg or LDL-C and very LDL-C values. During combination therapy, diuretic-induced increases in LDL-C were at short term prevented or reversed by the concomitant administration of certain beta-blockers, but not by sympatholytics such as reserpine, methyldopa or clonidine. With combined diuretic-prazosin treatment, a tendency for slightly higher HDL-C was reported. Angiotensin converting enzyme inhibitors (captopril, enalapril) and calcium channel blockers (verapamil, nifedipine, nitrendipine, diltiazem) seem to be largely devoid of undesirable effects on serum lipoproteins. Monotherapy with the potent direct vasodilator carprazidil improved blood pressure and significantly increased HDL-C. Whether and to what extent the observed variations in lipoproteins may persist beyond 1 year of treatment is as yet unclear.(ABSTRACT TRUNCATED AT 400 WORDS)

Antihypertensive Agents↗
PubMedDate not supplied

Central imidazoline receptors and centrally acting anti-hypertensive agents.

We have examined the location and contribution of imidazoline receptors (IR) in mediating the hypotensive and sympatholytic actions of first and second generation anti-hypertensive agents in rabbits. We found that the hypotension produced by rilmenidine and moxonidine given intravenously (i.v.) or into the fourth ventricle (4V) was preferentially reversed by the IR antagonists idazoxan and efaroxan (compared to a selective alpha(2)-adrenoceptor antagonist 2-methoxy-idazoxan), suggesting that IR are important in the sympatho-inhibition produced by these agents. Clonidine was not preferentially reversed by the IR antagonists suggesting an action via alpha(2)-adrenoceptors. In anaesthetised rabbits, the rostral ventrolateral medulla (RVLM) was the most potent site for rilmenidine to produce the sympatho-inhibition and modulation of sympathetic baroreflexes. alpha-Methylnoradrenaline was also sympatholytic suggesting alpha(2)-adrenoceptors are also present in this site. Microinjection of the IR and alpha(2)-adrenoceptor antagonists showed that rilmenidine activates IR in the RVLM but that alpha(2)-adrenoceptors are also activated as a consequence. These studies suggest that rilmenidine acts primarily via IR in the RVLM to reduce sympathetic tone but also imply an important association of alpha(2)-adrenoceptors and IR in the region.

Adrenergic alpha-Agonists↗
PubMed1999

Moxonidine: a review of safety and tolerability after seven years of clinical experience.

Centrally acting antihypertensive drugs, or sympatholytics, (reserpine, methyldopa and clonidine) have a long history of efficacy but are now little used in most countries. One of the most important reasons for this is relatively poor tolerability compared to many newer agents. In the case of clonidine there is also the potential danger of rebound hypertension. The most prominent adverse effects have been dry mouth, sedation, dizziness and oedema. These reactions, especially the first two, are thought to be associated with activation of central nervous system and salivary gland alpha2-adrenergic receptors. In the last 15 years it has become possible to produce drugs with selective agonist effect on another class of brainstem receptors, the imidazoline I1-receptors, which appear to have modulate sympathetic activity and blood pressure without affecting alertness or salivary flow: however, they still have some action on alpha2-receptors. Moxonidine and rilmenidine are moderately selective imidazoline agonists which have been in clinical use for several years in many European countries. Trial evidence and postmarketing surveillance indicate that moxonidine may cause dry mouth or sedation in a minority (<10%) of patients, significantly less than with the older drugs. There is no significant incidence of oedema and unexpected or idiosyncratic adverse effects are extremely rare. Moxonidine may improve aspects of glucose and lipid metabolism. In conclusion, moxonidine is a safe as well as an effective antihypertensive, with considerably improved patient tolerability compared to the older sympatholytics.

Antihypertensive Agents↗
PubMed1992

R-pulse wave timing in cardiovascular monitoring: further observations.

Pulse wave arrival times measured from the peak of the R-wave of the electrocardiogram to the onset of a peripheral pulse wave were recorded with a miniature pressure transducer in a group of 72 hypertensive pregnant women, of whom 19 were receiving sympatholytic antihypertensive medication and 53 were not. The mean (+/- SD) pulse wave arrival time of the hypertensive pregnant group was 204 +/- 15 milliseconds, which was significantly shorter than that measured in a group of 49 uncomplicated normotensive pregnant subjects (222 +/- 16 milliseconds) (P less than .001). The mean pulse wave arrival times were shortest in the subset of pregnant hypertensive patients not on sympatholytic medication (201 +/- 13 milliseconds) as compared with patients on such medication (212 +/- 18 milliseconds) (P less than .01). These observations suggest that patients with pregnancy hypertension have much shorter pulse wave arrival times than normotensive pregnant women. Further studies are needed to determine the potential usefulness of this cardiovascular index for evaluation of hypertensive states during pregnancy.

Adult↗
PubMed1991

Atrial natriuretic peptide inhibits sympathetic outflow in NaCl-sensitive spontaneously hypertensive rats.

The current study tested the hypothesis that circulating atrial natriuretic peptide (ANP) inhibits sympathetic outflow, as reflected in lumbar sympathetic nerve activity (LSNA), in NaCl-sensitive spontaneously hypertensive rats (SHR-S) and that this effect is exaggerated by high NaCl feeding. NaCl-resistant SHR (SHR-R) and Wistar-Kyoto (WKY) rats maintained on basal and high-NaCl diets were used as controls. Intravenous administration of ANP to conscious, freely moving rats with intact baroreflexes decreased blood pressure and LSNA in SHR-S, SHR-R and WKY rats maintained on basal or high-NaCl diets for 2-3 weeks. The depressor response to intravenous ANP was greater in 8% NaCl-fed SHR-S than in any other group; the LSNA response was greater in SHR-S on either diet than in any other group. Intracerebroventricular administration of ANP evoked small, transient sympatholytic responses in SHR-S on both diets and minimal responses in SHR-R and WKY rats; these responses could not be attributed to leakage of ANP into the peripheral circulation. Thus, circulating ANP has a sympatholytic effect in SHR-S that is not amplified by high-NaCl feeding and can be only partially accounted for by a central action.

Animals↗
PubMed1991

[ACE inhibition: mechanisms of cardioprotection in heart hypertrophy].

Epidemiologic studies have revealed that in arterial hypertension left ventricular hypertrophy is an important risk factor for cardiac failure. Accordingly antihypertensive therapy should aim at preventing or regressing left ventricular hypertrophy. Reduction of blood pressure does not necessarily induce reversal of left ventricular hypertrophy. Vasodilators like hydralazine and minoxidil, which lead to augmented plasma levels of norepinephrine, were not able to diminish left ventricular hypertrophy. In contrast, a sympatholytic therapy with methyldopa caused a reversal of left ventricular muscle mass. These experimental findings in spontaneously hypertensive rats led to the hypothesis that catecholamines control the onset and progression of myocardial hypertrophy mostly independent of blood pressure. This hypothesis was supported by the experimental findings, that subhypertensive dosages of norepinephrine induce left ventricular hypertrophy and that this hormone promotes alpha-receptor mediated growth of isolated myocytes. Recent studies have revealed that also the renin-angiotension-system has trophic effect on the myocardium. Clinical investigations have documented regression of cardiac hypertrophy due to antihypertensive therapy with sympatholytic drugs, ACE-inhibitors, calcium-channel blockers and beta-receptor blockers. Diuretics failed to decrease left ventricular muscle mass along with blood pressure normalization.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1990

[A pupillographical study on the presence of organochlorine pesticides in autonomic nerve disturbance].

It is well known that the effect of organophosphate pesticides on the autonomic nervous system is a cholinergic reaction. However no study has been done assessing the effect of organochlorine pesticides on the autonomic nervous system. We evaluated the autonomic nerve function using open-loop pupillography in 20 patients who had exposure to the organochlorine pesticides. Significant differences were seen in pupil area (p less than .006), velocity of both constriction and dilatation (p less than .001), and dilatation time (p less than .02), when compared with 18 normal subjects. Autonomic nerve disturbances were detected in eighteen of 20 patients (90%) by evaluating the pupillary light reflex in each patient. Sympathetic nerve inhibition i.e. sympatholytic pattern, was recognized in ten of 18 patients (55%). Four patients with sympatholytic pattern had a disturbance not only in the sympathetic nerve, but also parasympathetic nerve involvement suggesting pandysautonomia. The residue blood level of the organochlorine pesticides was examined in each patient. A high frequency of the DDE was recognized (85%). It was concluded that the toxicity of the organochlorine pesticide on the autonomic nerve appear as an inhibitory effect on pupil light reflex.

Adult↗
PubMed1975

Drug effects on myocardial 45Ca uptake in conscious rats.

The myocardial content of 45Ca++ in conscious rats is increased by single s.c. injections of sympathomimetics. A dose dependent inhibition of this effect is achieved by simultaneous administration of calcium antagonists or beta-receptor blocking agents. The myocardial 45Ca++ content of conscious rats is increased by i.v. administration of dibutyrylcycloadenosinemonophosphate (DBcAMP). The effect of the cyclic nucleotide is suppressed only by a calcium antagonist but not by a beta-receptor blocker. The following conclusions may be drawn: 1. Calcium antagonists and beta-sympatholytics have different sites of action in the heart. 2. The lack of DBcAMP-antagonism of the beta-sympatholytics permits a simple discrimination between both types of substances. After pretreatment with sympathomimetics for 7 days (0.3 mg/kg isoprenaline s.c.), neither high doses of isoprenaline nor doses of DBcAMP and aminophylline increased the myocardial 45Ca content in rats. This effect only lasted briefly (for about two weeks); the site of its action is so far unknown.

Adrenergic beta-Antagonists↗
PubMed1988

Risk factors for severe bradycardia during oral clonidine therapy for hypertension.

We identified eight hypertensive patients who developed severe bradycardia during oral clonidine hydrochloride therapy. Seven patients had sinus bradycardia, four had long sinus pauses, two had junctional bradycardia, and two had high-degree atrioventricular block. Three populations at risk for severe bradycardia during oral clonidine therapy were identified: patients with renal insufficiency, patients with clinical sinus node dysfunction, and patients who had developed bradycardia while taking other sympatholytic agents or who were currently receiving another sympatholytic drug. Clonidine effects were dissociated in two patients who were not hypotensive despite severe bradycardia. Asymptomatic patients required only dose reduction or discontinuation of clonidine therapy. Symptomatic patients responded inconsistently to intravenous atropine sulfate therapy; one responded to isoproterenol therapy, and one required temporary artificial pacing. Awareness of the variable presentation and response of this bradycardia to medical therapy will assist patient management. The incidence of this complication is low (less than 0.3%), but attention to risk factors should make clonidine-induced bradycardia even less frequent.

Administration, Oral↗
PubMed1987

Characterization of the central sympathoinhibitory action of ketanserin.

The present study was designed to determine whether the central sympatholytic effects of ketanserin result from the ability of the drug to block serotonin2 or alpha-1 adrenergic receptors. Ketanserin produced a dose-related inhibition of sympathetic nerve discharge recorded from the inferior cardiac nerve in chloralose-anesthetized cats. Administration of a large dose of prazosin (1 mg/kg i.v.) decreased arterial blood pressure and inhibited sympathetic activity for several hours. Additional doses of prazosin failed to further inhibit sympathetic nerve discharge. Pretreatment with prazosin (1 mg/kg i.v.) also blocked the ability of ketanserin to inhibit sympathetic activity. Conversely, pretreatment with ketanserin blocked the central sympatholytic action of prazosin. In contrast, the alpha-2 adrenergic agonist clonidine inhibited sympathetic activity in animals pretreated with prazosin. The highly selective serotonin2 antagonist, LY 53857, failed to affect arterial blood pressure, heart rate or sympathetic activity recorded from the inferior cardiac nerve. These data, along with earlier results from our laboratory, provide strong evidence to indicate that ketanserin produces a centrally mediated inhibition of sympathetic nerve discharge as a result of the ability of the drug to block alpha-1 adrenergic receptors.

Animals↗
PubMed1984

[Treatment of hypertension emergencies].

Hypertensive emergencies are defined as situations where a seriously elevated blood pressure threatens the patients life or vital organ functions. Since treatment of hypertensive emergencies by a rapid reduction of blood pressure can be complicated by serious unwanted effects, the treatment indications should be defined cautiously. In addition the principles of autoregulation of blood flow and vascular resistance in hypertensive patients should be considered as well as the widely differing effects of the drugs used in hypertensive emergencies like alpha- and beta-adrenergic blocking substances, central sympatholytics and vasodilating agents. A reduction of cardiac output as a consequence of betablockade or central sympatholytics may be beneficial in patients with aneurysms, but may result in severe central hypoperfusion in others which can also be induced by vasodilators by local and systemic steal effects. Therefore we propose a treatment scheme for hypertensive emergencies based on pathophysiological considerations with special regard to cerebral perfusion. In many instances calcium-antagonists can be considered as drugs of first choice since they lower blood pressure in relation to pretreatment blood pressure and have only a weak negative inotropic effect. In addition they exert their vasodilating action predominantly in vessels with a high vasoconstrictor tone and do not reduce cerebral perfusion despite a marked reduction of blood pressure within a short time. In every case the initial emergency treatment should be followed by a careful long term management of hypertension.

Administration, Oral↗
PubMed1996

Prolonged central effects of quinpirole on cardiovascular regulation.

Central cardiovascular effects of the dopamine D2 receptor agonist quinpirole were studied in conscious rats. The i.v. injection of 0.3 mg/kg of quinpirole in spontaneously hypertensive rats (SHR) caused a rapid but short-lasting increase in blood pressure. Heart rate showed little change. Pretreatment with the centrally acting selective dopamine D2 receptor antagonist raclopride, but not the D1 antagonist SCH23390, completely prevented the rise in blood pressure. A second injection of quinpirole, 30 min after the first injection, induced little change in blood pressure, although at 4 or 24 hr after quinpirole treatment, we observed partial and complete recovery of the pressor response, respectively. This pattern of desensitization was similar to that seen after administration of the dopamine D2 receptor agonists N-propylnorapomorphine (0.3 mg/kg) or quinelorane (0.1 mg/kg), and was similar in spontaneously hypertensive rats, Wistar Kyoto and Sprague-Dawley rats. At 30 min after treatment with quinpirole, the hypotension induced by i.v. injection of clonidine (0.01 mg/kg) or of 8-hydroxy-dipropylaminotetralin (0.1 mg/kg) was markedly reduced when compared to that in saline-pretreated spontaneously hypertensive rats, suggesting a prolonged effect of quinpirole at the level of sympathetic regulation. The rapid fall in blood pressure caused by i.v. injection of the ganglion blocker pentolinium (10 mg/kg) was slightly, but significantly enhanced by treatment with quinpirole, which suggests an overall prolonged increase in resting sympathetic vasomotor tone. This would be difficult to reconcile with an inhibition of the action of sympatholytic drugs, unless it is hypothesized that the increase in sympathetic vasomotor tone was differential between different sympathetic beds or different neuronal populations in the brain. This may prohibit any additional pressor responses and, through a central feedback mechanism, may inhibit the action of sympatholytic drugs. No evidence was found for lasting changes in circulating levels of vasopressin, angiotensin or atrial natriuretic factor, nor were there changes in hematocrit. Cardiac sympathetic tone appeared to be enhanced, although vagal tone was normal and no major changes in baroreflex sensitivity were observed.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1996

Reflex sympathetic dystrophy. The controversy continues.

The chronic pain syndrome encompassed by the term RSD is poorly understood. The confusion is caused in large part by frequent misdiagnosis and excessive use of sympatholytic procedures in inappropriate circumstances. Recently, pain specialists have redefined the specific criteria for regional pain syndromes having sympathetic maintaining factors, emphasizing application of placebo testing in diagnosis and attention to anatomic principles in pharmacologic and surgical treatment. The authors believe that three-phase bone scanning is a valuable adjunct to clinical judgment in making the proper diagnosis. Current thinking suggests that sympathetic maintained pain exists but that it may comprise only approximately 10% of regional pain cases. Once the appropriate diagnosis is made, classically described sympatholytic procedures are reasonably used. Alternative techniques, such as spinal cord stimulation, may have an important role in refractory cases of sympathetically maintained pain.

Hand↗
PubMed1985

C-Alkylpiperazines structurally related to piribedil. XI.

The synthesis of a new series of 1-alkoxybenzyl-4-(2-pyrimidyl)piperazines 2-methyl or 2,6-dimethyl substituted, related to piribedil, is described. Besides compounds (IV)-(IX a, b), the isomer (XI) of (V) was also prepared. Central dopaminergic and alpha-blocking activities both in vitro and in vivo were determined for all compounds. Derivatives (IV), (VII), (XI) were also studied for peripheral vasodilator and sympatholytic activities.

Adrenergic alpha-Antagonists↗
PubMed1980

Sympathetic nervous system activity during sodium restriction in essential hypertension.

Sympathetic nervous system activity was studied in 38 patients with essential hypertension during high- and low-sodium diets. Salt restriction was associated with a modest (6 mmHg) decline in mean arterial pressure, while the urinary excretion of catecholamines, metanephrines, and vanillylmandelic acid increased significantly. Plasma renin activity also increased. It is concluded that short-term low-sodium diet therapy for essential hypertension results in only small decrements in mean arterial pressure and may be limited in hypotensive effect by activation of the sympathetic nervous system. Support is offered for the rationale of sympatholytic drug therapy as an initial step in the management of hypertensive patients requiring arterial pressure reductions greater than those afforded by diet alone.

Adult↗
PubMed1977

[Disturbances of micturition after general surgical operations (author's transl)].

Impaired micturition after general surgical operations can be due to three causes, which occur individually or in combination. The first comprises side effects of anesthetics upon the autonomic nervous system. Inhibition of the abdominopelvic reflex, initiating micturition, due to the operative trauma represents the scond cause. Both the vegetative and the mechanical traumas, lead to decompensation of the urinary bladder, whose function is impaired by neuropathic factors and outflow obstruction. Pulmonary, cerebral, and abdominal insufficiency prolong the effects of both traumas. The third cause is direct operative injury of the sacroplexus pelvus.--Approximately 25% of all patients undergoing surgery will shown voiding disturbances in the postoperative period. The treatment consists sympatholytic therapy. In cases of neuropathic and obstructed bladders, the treatment of choice is transurethral correction of the bladder outlet.

Anesthetics↗
PubMed2002

Characterization of sucrose-induced changes in cardiac phenotype.

The neuroendocrine factors responsible for long-term regulation of cardiac contractile performance remain ill defined. We examined influences of diet on the expression of myosin isozymes, sarcoplasmic reticulum (SR) Ca(2+) uptake and serum parameters. Dietary regimens (ad libitum feeding, intermittent fasting and 32% sucrose feeding) were used to alter the neurohumoral status of rats. Intermittent fasting decreased serum insulin levels ( P<0.05) and was associated with decreased SR Ca(2+) uptake and myosin V1 proportion ( P<0.05). Sucrose (32%) feeding increased myosin V1 of fasted and ad libitum fed rats ( P<0.05) but had no effect on insulin or SR Ca(2+) uptake. Expression of the alpha-myosin heavy chain correlated with serum insulin. Treatment of sucrose-fed rats with the sympatholytic compound moxonidine and the hypoglycaemic compounds BM13.907 and ciglitazone partially prevented the increase in myosin V1 ( P<0.05) but had no effect on SR Ca(2+) uptake and insulin. The data show that adrenergic activity and metabolic signals are important for an increase in myosin V1 in sucrose-fed rats, which can be associated with an unaltered SR Ca(2+) uptake rate.

Animals↗
PubMed1993

Comparative mechanisms of action of antiarrhythmic drugs.

The most widely used classification of antiarrhythmic drugs, formulated by Singh and Vaughan Williams, divides antiarrhythmic agents into 4 categories: (1) sodium channel blockers; (2) sympatholytic agents; (3) drugs that delay repolarization; and (4) calcium antagonists. Despite some controversy regarding its value, the available evidence indicates that this classification relates well to the most important clinically relevant mechanisms of antiarrhythmic drug action. Amiodarone is unique in that it possesses properties belonging to all 4 of the Singh and Vaughan Williams classes; moreover, all 4 properties contribute to the beneficial actions of the drug. Class 1 effects are responsible for amiodarone's ability to slow ventricular tachycardias, making them hemodynamically better tolerated, and are likely important in amiodarone's premature ventricular complex-suppressing properties. Class 2 effects may contribute to atrioventricular (AV) node-suppressing actions and may confer protection against sudden death in the postmyocardial infarction population. Class 3 actions contribute to amiodarone's ability to prevent reentrant atrial and ventricular arrhythmias, and may be responsible for a superior ability to maintain sinus rhythm after cardioversion of atrial fibrillation. Class 4 properties contribute to amiodarone's ability to slow the ventricular response in atrial fibrillation and to prevent AV node reentrant arrhythmias. Calcium channel antagonism may also suppress arrhythmias (such as torsades de pointes) caused by early after-depolarizations and contribute to the apparent infrequency of torsades, despite substantial QT prolongation, among patients treated with amiodarone. Consideration of the link between amiodarone's pharmacologic properties and clinical effects illustrates well the various mechanisms of antiarrhythmic drug action.

Action Potentials↗