Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “SYMPATHOLYTICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed1993

Time-dependent efficacy of antihypertensive agents in spontaneously hypertensive rats.

The efficacy of antihypertensive agents was compared when given at different time points in the circadian rhythm. Spontaneously hypertensive rats (SHRs) were kept on a 12/12-h cycle with lights on/off at 07:00/19:00 h. A computerized system was used to measure intraarterial blood pressure and heart rate continuously. Agents or vehicle were intravenously injected at two time points. One at the beginning of the sleeping period, at which low efficacy was expected (T = 10), and one at T = 16, which is 3 h before the circadian peaks in blood pressure (BP) and heart rate (HR), aimed at reducing the rise in BP and HR at awakening. The hypotensive effect of propranolol, metoprolol, labetalol, prazosin, clonidine, and rilmenidine was greater when injected at T = 16 than at T = 10 (p < 0.05 for propranolol, metoprolol, and rilmenidine). In contrast, the renal vasodilators captopril and tertatolol were more potent after injection at T = 10. Felodipine was equally effective at both time points. Thus, the effects of antihypertensive agents are related to the phase of the circadian rhythm. The data on the sympatholytic agents in general and beta-blockers and centrally acting agents in particular support antihypertensive regimens with timed administrations.

Animals↗
PubMed1994

Relevance of plasma noradrenaline concentrations to estimate autonomic effects of antihypertensive drugs.

The sympathetic nervous system is important in regulating cardiovascular function. It is therefore of interest to study the influence of antihypertensive drugs on sympathetic nerve activity. For this purpose, measurements of noradrenaline concentrations in forearm venous plasma have often been used. For several reasons, this provides limited information: i) the sympathetic nervous system is highly differentiated, i.e. activity may be high in some organs and low in others; ii) noradrenaline in forearm venous plasma is largely derived from sympathetic activity to the forearm skeletal muscle; iii) plasma noradrenaline concentrations are determined not only by noradrenaline spillover from sympathetic nerve endings, which is related to sympathetic nerve activity, but also by noradrenaline clearance. Under most circumstances plasma noradrenaline concentrations are not high enough to produce hormonal effects. Many types of antihypertensive drugs may cause acute and long-term increases in forearm venous noradrenaline concentrations. The mechanisms underlying these increases are not fully understood but seem to differ between drug classes: Diuretics increase renal noradrenaline spillover; beta-blockers do not affect spillover but reduce total noradrenaline clearance; calcium antagonists and alpha-blockers probably increase noradrenaline spillover, but it is not known which organs are involved, particularly during long-term treatment. ACE inhibitors seem to have a sympatholytic action, which counteract reflex increases in sympathetic nerve activity during blood pressure reduction, and plasma noradrenaline concentrations are generally not affected. To be able to judge the possible clinical consequences of changes in plasma noradrenaline concentrations during chronic antihypertensive treatment, assessments of noradrenaline spillover from individual organs are needed.

Antihypertensive Agents↗
PubMed1986

Renal vascular responses to saralasin in conscious chemically denervated rabbits and patients with tetraplegia.

To determine the relative contributions of direct angiotensin-II-like myotropism and sympathetic nerve stimulation to the partial agonist effect of saralasin, the renal vascular responses to i.v. saralasin (5, 10, 20 micrograms/kg/min) were assessed in normal conscious rabbits before and after sympatholytic treatment with guanethidine (24 mg/kg/day for 9 days) and in 6 chronic tetraplegic patients (0.5, 1, 5 micrograms/kg/min) before and after alpha-adrenoreceptor blockade with i.v. thymoxamine (1 mg/kg/h). In rabbits saralasin reduced effective renal plasma flow (ERPF) and glomerular filtration rate (GFR), and increased renal vascular resistance (RVR) without affecting mean arterial blood pressure (BP). Responses were similar in both groups, but recovery following saralasin was more prolonged after treatment with guanethidine. When 0.1 microgram/kg/min (one fiftieth of the smallest i.v. dose) was infused just proximal to the renal arteries in 4 conscious rabbits (chronically cannulated), renal perfusion fell and RVR increased. In tetraplegics saralasin produced a transient rise in BP and variable increase in RVR; neither response being altered by thymoxamine. These results suggest that saralasin-induced renal vasoconstriction is independent of central and peripheral sympathetic activation, and is probably due to an intrinsic angiotensin-II-like myotropic action.

Adult↗
PubMed1987

Production and reversal of DOCA-salt hypertension in baboons.

We describe for the first time a non-human primate model of mineralocorticoid-salt hypertension. Baboons instrumented for chronic, direct measurement of arterial pressure, underwent sodium chloride loading (8.6 or 17.1 mEq/kg/day) by different routes for several weeks and deoxycorticosterone acetate (DOCA) 5 mg/2 days i.m., in addition to sodium chloride, for periods lasting up to several months. Salt loading alone at 8.6 mEq/kg/day had no chronic effect on mean arterial pressure (MAP). Salt loading at both doses in combination with DOCA produced increases in MAP within a few days which became progressively larger over weeks to months. DOCA-salt hypertension was associated with hyporeninemia and mild hypokalemia, without consistent changes in heart rate or plasma catecholamines. A biofeedback procedure applied to three animals failed to reduce tonic blood pressure. In two of these animals, administration of clonidine or atenolol also had no antihypertensive effect, whereas a diuretic combination (hydrochlorothiazide and triamterene) rapidly abolished the hypertension. The absence of amelioration of the hypertension by a central sympatholytic agent or a beta-adrenoceptor blocker, coupled with the absence of increased plasma catecholamines, suggests that increased sympathetic activity may not contribute to the hypertension in contrast with findings in lower animals but consistent with clinical reports.

Animals↗
PubMed1987

Neurogenic components of hypertension in human renal artery stenosis.

In renal artery stenosis activation of the renin-angiotensin system elevates blood pressure by direct peripheral effects and probably through stimulation of sympathetic activity, which can be induced by angiotensin-II either centrally or peripherally. In animals specific brain lesions and afferent renal denervation can either attenuate or prevent renovascular hypertension. We investigated the neurogenic mechanisms responsible for hypertension in 21 patients with unilateral renal artery stenosis off drug therapy, by studying the cardiovascular and hormonal effects of Clonidine. The responses to Captopril served as an indicator of the peripheral effects of angiotensin-II. Both oral and intravenous Clonidine lowered blood pressure substantially and for a prolonged period even in patients who had been refractory to multiple antihypertensive drug therapy. Levels of plasma renin activity were unchanged after Clonidine. Plasma noradrenaline levels fell. Pressor responses to infused angiotensin-II were not reduced. These data suggest that Clonidine lowers blood pressure independently of hormonal and peripheral vascular interactions and is consistent with its predominantly central sympatholytic effects. Oral Captopril, unlike Clonidine, had variable hypotensive effects directly related to the basal level of plasma renin activity. The largest reductions were observed in those with the highest level of renin. Our studies indicate that neurogenic mechanisms, probably centrally mediated, have an important and often major role in maintaining hypertension in human renal artery stenosis. These may result from the central effects of angiotensin-II, and/or from increased afferent renal nerve activity, as demonstrated experimentally. The neurogenic components maintaining hypertension in renal artery stenosis are largely dependent on renal ischaemia as revascularisation (by surgery or angioplasty) or nephrectomy, either ameliorates or cures the hypertension in the majority of our patients.

Aortography↗
PubMed1988

Vascular effects of clonidine in patients with tetraplegia and unilateral brachial plexus injury.

Evidence from studies in both animals and in tetraplegics with complete cervical spinal cord transection and preganglionic lesion, indicates that clonidine lowers blood pressure predominantly by a centrally mediated action. We have investigated the haemodynamic basis of this action and performed additional studies in patients with unilateral brachial plexus injury and postganglionic lesions, to further determine the site and mechanism of its action. Blood pressure fell after clonidine in normal subjects but not in tetraplegics. In normal subjects, the fall in blood pressure was associated with a fall in cardiac output, due to a fall in both heart rate and stroke volume. Digital skin vasodilatation occurred after clonidine in normal subjects and only in the innervated limb in patients with unilateral brachial plexus injury. In tetraplegics and in the denervated limb in unilateral brachial plexus injury, there was no vasodilatation; instead a vasoconstrictor response occurred, due to the peripheral adrenoceptor action of clonidine. We conclude that the fall in blood pressure and cardiac output in normal subjects after clonidine were due to its central sympatholytic action. Digital skin vasodilatation after clonidine in normal subjects and the innervated limb in unilateral brachial plexus injury was due to the withdrawal of vasoconstrictor tone and requires intact descending sympathetic pathways.

Adult↗
PubMed1990

Risk reduction following regression of cardiac hypertrophy.

Cardiac hypertrophy in essential hypertension is documented to be an independent risk factor for congestive heart failure, coronary heart disease and cardiac sudden death. Reduction of left ventricular hypertrophy therefore emerged as a new challenge of antihypertensive treatment. Sympatholytic agents, calcium entry blockers, and angiotensin converting enzyme inhibitors have been found to reduce left ventricular hypertrophy, whereas vasodilators (and most likely also diuretics) are unable to reduce left ventricular mass despite good control of arterial hypertension. Several studies indicated that reduction of left ventricular hypertrophy is not detrimental to cardiac pump function: systolic and diastolic function were found to be maintained at rest and during exposure to increased pressure load. In hypertensive patients with left ventricular hypertrophy ventricular arrhythmias have been reported to be increased and to be the pathophysiological link for the increased risk of cardiac sudden death. Reduction of cardiac hypertrophy was found to be accompanied by a reduction of prevalence and severity of ventricular arrhythmias if treated with betablockers, calcium entry blockers or converting enzyme inhibitors. Whether reduction of cardiac hypertrophy indeed decreases the cardiovascular risk attributed to left ventricular hypertrophy is unknown at present, although clinical studies support such a viewpoint.

Antihypertensive Agents↗
PubMedDate not supplied

Effects of beta-adrenergic blockade on short-term variability of blood pressure and heart rate in essential hypertension.

Short-term fluctuations in blood pressure (BP) and heart rate (HR) were analysed in a group of twelve males with essential hypertension. Indirect finger BP was measured by a Finapres device. The effect of a 7-day administration of a cardioselective beta-adrenoceptor blocker, acebutolol (400 mg/day), was studied in a double-blind, randomized, placebo-controlled cross-over study. Compared with placebo, acebutolol caused a significant decrease in BP and HR. In addition, the standard deviation (SD) of BP and HR were reduced after acebutolol in the standing position. Spectral analysis of fluctuations in BP showed a reduction in the variability underlying the SD changes of BP and HR. This reduction predominated in the mid frequency (MF) region corresponding to Mayer waves. This effect was marked for HR since the MF component for standing HR after acebutolol was 46% the placebo level. The average reduction in MF component for standing Systolic BP (SBP) was 36%. No significant correlation was found between the Mayer wave reduction and the systolic, diastolic BP or HR lowering effect of acebutolol. No significant changes in the gain of the transfer function between MF SBP and HR fluctuations in the standing position were observed. The reduced MF component of HR and BP variability after acebutolol could be due to a peripheral cardiac and non-cardiac sympatholytic effect of chronic beta-adrenoceptor blockade.

Acebutolol↗
PubMed1994

Guanabenz induced hypothermia in a poisoned elderly female.

Guanabenz (Wytensin Wyeth-Ayerst Laboratories, Philadelphia, PA) is a centrally acting alpha 2 adrenergic agonist. Guanabenz shares structural and pharmacologic properties with the more commonly known sympatholytic agent clonidine. Little is known about guanabenz in overdose. Eleven cases of guanabenz poisoning have been reported in the literature and to the manufacturer to date and followed a clinical course comparable to clonidine poisoning. We report this case of guanabenz poisoning in an elderly woman who sustained protracted hypothermia following overdose. Hypothermia has been commonly associated with clonidine toxicity but has not been previously reported with guanabenz. Postulated mechanisms of clonidine induced hypothermia are discussed.

Aged↗
PubMed1989

Thermographic evaluation of the autonomic effects of nerve blocks in the foot.

The authors evaluated regional skin temperatures of the foot following the administration of a variety of local anesthetic nerve blocks with either Xylocaine (lidocaine hydrochloride) or Sensorcaine (bupivacaine hydrochloride). The study was carried out on ten randomized parallel groups of five subjects, each group being tested with one drug and one regional nerve block. The results indicated that both Xylocaine and Sensorcaine, when administered as a posterior tibial block, result in a significantly increased blood flow to the foot. Nerve blockade of the remaining nerves of the foot did not significantly increase the sympatholytic effect obtained by posterior tibial nerve block alone.

Adult↗
PubMed1976

[Presence of the blood depot in orthostatic position and after physical exertion].

In healthy individuals and in patients with essential hypertension in the orthostatic position and on physical effort an insignificant reduction in the volume of the circulating blood and of the packed cell volume were in evidence; this being due to the outflow of the liquid part of the blood into the tissues. Even in instances of a well-marked orthostatic hypotonia, during medication with sympatholytic agents in particular, the circulating blood volume in the orthostatic position does not show any significant change. The results obtained by the authors and an analysis of the published data suggest that all of the blood is in circulation with none of it being repository or leaving the depot either in the orthostatic position or on physical effort.

Antihypertensive Agents↗
PubMed1976

Cardiovascular and antihypertensive actions of 1-methyl-3-keto-4-phenylquinuclidinium bromide.

The sympatholytic and norepinephrine depleting drug 1-methyl-3-keto-4-phenylquinuclidinium bromide (MA540) possessed significant chronic antihypertensive activity in mecamylamine- and renal-hypertensive dogs. The compound was approximately four times more potent than guanethidine in the former model and three times as potent in the latter. MA540 reduced orthostatic blood pressure responses in unanesthetized rabbits, but was approximately ten times less potent than guanethidine. The quinuclidine derivative did not affect cardiac output, heart rate or stroke volume in anesthetized open chest dogs and moderately increased mean blood pressure and total peripheral resistance. It produced diuresis and saluresis in anesthetized dogs, but did not influence water or electrolyte urinary excretion in conscious rats. In the latter test, guanethidine produced antidiuresis and antisaluresis. It was concluded that MA540 is a potent, orally effective antihypertensive agent acting through adrenergic neuron blockade, that it lacks undesirable effects on cardiac and renal functions, and that compared with guanethidine, it is more potent in lowering blood pressure but less so in interfering with orthostatic cardiovascular reflexes.

Animals↗
PubMed1999

[Preoperatively asymptomatic left adrenal incidentaloma].

Since the introduction of new, very sensitive imaging procedures (ultrasonography, CT, MRI) the incidence of incidentally discovered, asymptomatic adrenal masses has clearly increased. These tumours are a new challenge to develop therapy and preoperative evaluation strategies, as the following case report shows. In a 29-year-old asymptomatic female patient a large adrenal tumour on the left side was discovered on abdominal ultrasonography during pregnancy. The further endocrinological examinations were normal. The patient was operated on post partum. During intraoperative manipulation of the tumour we observed an excessive increase in blood-pressure and heart rate. Shortly after removal of the tumour and immediate sympatholytic treatment the situation was under control. The intraoperative clinical situation and histological work-up of the tumour led to the diagnosis of phaeochromocytoma. The problem of adrenal incidentalomas is discussed on the basis of the current literature and an algorithm for preoperative evaluation is presented.

Adrenal Gland Neoplasms↗
PubMed1999

Taurine attenuates hypertension and improves insulin sensitivity in the fructose-fed rat, an animal model of insulin resistance.

Fructose feeding induces moderate increases in blood pressure levels in normal rats, which is associated with hyperinsulinemia, insulin resistance, and impaired glucose tolerance. Increased vascular resistance, sodium retention, and sympathetic overactivity have been proposed to contribute to the blood pressure elevation in this model. Taurine, a sulphur-containing amino acid, has been reported to have antihypertensive and sympatholytic actions. In the present study, the effects of taurine on blood pressure, plasma levels of glucose and insulin, glucose tolerance, and renal function were studied in fructose-fed rats. Fructose-fed rats had higher blood pressure and elevated plasma levels of insulin and glucose. The plasma glucose levels were higher in fructose-fed rats than in controls at 15, 30, and 60 min after the oral glucose load. Treatment with 2% taurine in drinking water prevented the blood pressure elevation and attenuated the hyperinsulinemia in fructose-fed rats. The exaggerated glucose levels in response to the oral glucose load was also prevented by taurine administration. Thus, taurine supplementation could be beneficial in circumventing metabolic alterations in insulin resistance.

Animals↗
PubMed1976

[Amiodarone hydrochloride and anesthesia in heart surgery. Use of an injectable form in the correction of peroperative rhythm disorders].

The amiodarone is studied in the context of cardiac surgery to evaluate its anti-arrythmic properties in its injectable form and possible interference with the anaesthetic drugs. Two groups of patients were established: - the first group of 10 patients received the amiodarone per-os in the immediate pre-operative period, - the second group of 19 patients received injectable amiodarone either by direct intraveinous injection at a dose of 5 mg/kg or in I.V. drip for rhytmic irregulatities during surgery. The anti-arrythmic property of the product is confirmed. No incompatibility with the anaesthetics employed (neuroleptanalgesia) was observed. Howerer, a potentialization of the sympatholytic alpha-effects by the anaesthesia is observed. The fall in arterial pressure, when it is measureable, is of the order of a third of the initial value, with a return to the previous level within about ten minutes.

Adolescent↗
PubMed2000

[Treatment of glaucoma with brimonidine (Alphagan 0.2%)].

PURPOSE: The main purpose of our study was to assess the systemic safety of brimonidine tartrate 0.2%, an alpha 2 highly selective agonist in patients with glaucoma or ocular hypertension MATERIAL-METHODS: Brimonidine was administered alone or in combination in 128 patients suffering from glaucoma or ocular hypertension in order to improve the IOP effect and/or to replace a drug which prescription was limited due to its secondary effects. In addition to the standard follow up and IOP reduction evaluation, our study was focused on the appreciation of the systemic tolerance to brimonidine. RESULTS: The average age of our patients was 65.2 +/- 13.8 years and the mean follow up was 4.5 +/- 3.4 months. Brimondine was administered in monotherapy in 15 patients (7.8%) and in combination with another drug in the others (92.2%), the combination with a beta-blocking agent being the most frequent combination. 113 among the 128 patients suffered from POAG. 51.6% of patients described systemic side effects at various degrees (drowsiness, fatigue, general uneasiness, mouth dryness.). All these systemic side effects were significantly more frequent in patients older than 60 years (p<0.05). They did not seem to be influenced by an intercurrent illness or a systemic concurrent treatment with drugs potentially acting with the noradrenergic transmission (monoamine oxydase inhibitors, tricyclic antidepressants, mianserine, alpha-sympatholytics.). Brimonidine was interrupted in 82 patients (64.1%) secondary to a systemic intolerance in 21 patients, an allergic blepharo-conjunctivitis in 12 patients, and a non optimal IOP reduction in 42 patients. Considering the all patients and treatments, IOP dropped from 20.5 +/- 3.6mmHg to 19.8 +/- 4.6mmHg at the last examination (p<0.05). In bitherapies, the observed IOP reduction was not significantly different from the one achieved with the previous association. CONCLUSION: Our medium-term results have shown that brimonidine was an efficient ocular hypotensive agent and had a satisfactory ocular tolerance in nearly all the patients. However, its systemic tolerance appeared to be less favourable than previously reported. A systematic eyelid closure and punctal occlusion following each instillation is advisable in older patients.

Adolescent↗
PubMedDate not supplied

Diuretic therapy in congestive heart failure.

The principal goals of treatment of the patient in heart failure are the relief of their symptoms and improvement in their prognosis. Of all antiheart failure drugs currently available, the diuretics are therapeutically superior in their efficacy in relieving clinical symptoms and signs. Whether administered intravenously or orally, all diuretics result in a substantial reduction in the raised pulmonary vascular pressures in combination with a small reduction in cardiac output. Diuretics stimulate release of renin with subsequent activation of the renin-angiotensin-aldosterone system, particularly if used in large doses, although their quantitative impact on the neuroendocrine profile at different stages of heart failure remains to be defined. In patients with mild heart failure, diuretics reduce plasma catecholamine concentrations, but their sympatholytic effects in more severe cases are unknown, as are their effects on the metabolically active tissues in these patients. Diuretic resistance can be circumvented by segmental nephron blockade with a combination of low-dose diuretics that simultaneously block sodium reabsorption in the proximal tubule, the loop of Henle, the distal tubule, and the collecting duct. Diuretics improve symptoms of breathlessness and signs of peripheral edema in patients with congestive heart failure in direct relationship to the induced diuresis. These benefits are frequently associated with a substantial improvement in patients' appreciation of quality of life and economic capacity. There are few adverse reactions to chronic diuretic therapy, but the serum electrolytes should be monitored for hypokalemia and hypomagnesemia. The impact of diuretics on prognosis of patients with congestive heart failure is unknown; however, diuretics have been a major ingredient of the therapies used in all the survival trials with vasodilators, angiotensin-converting enzyme inhibitors, and beta-blocking drugs. In addition to their clinical benefits, diuretics are the most cost-effective treatment of any single drug group currently available for the treatment of patients with congestive heart failure.

Adult↗
PubMed1975

Interaction between centrally acting hypotensive drugs and tricyclic antidepressants.

From clinical experience it is known that the hypotensive action of clonidine and alpha-methyl-DOPA is antagonized by desipramine. This antagonism was investigated in detail in chloralose-anaesthetized cats. Both the centrally acting hypotensive agents and the tricyclic antidepressants where infused into the left vertebral artery. (1) The central hypotensive action clonidine was antagonized by desipramine, imipramine, amitriptyline, protriptyline and mianserine. For the inhibition of the hypotensive action of clonidine by protriptyline a parallel shift of the dose-response curve was obtained, indicating the possibility of a competitive antagonism. The central hypotensive action of alpha-methyl-DOPA was antagonized by desipramine and imipramine and that of amphetamine by imipramine. (2) The modest central hypotensive action of tricyclic antidepressants themselves and that of cocaine is explained by means of the inhibition of noradrenaline re-uptake in the CNS, brought about by these compounds. (3) It seems likely that the antagonism occurs at the level of central alpha-adrenoreceptors in the brain stem. (4) The antagonism probably reflects a general interaction between centrally acting hypotensive drugs and tricylclic antidepressants. The alpha-sympatholytic properties of the tricyclic antidepressants probably give rise to a blockade of the central alpha-adrenoreceptors, stimulated by clonidine, noradrenaline (via amphetamine) and alpha-methylnoradrenaline (from alpha-methyl-DOPA). The cocaine-like activity of antidepressants does not play a part.

Amphetamine↗