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 901 records · Page 50Linked to original sources
PubMed1987

Increased plasma norepinephrine and sympathetic nervous activity in essential hypertensive and uremic humans: effects of clonidine.

We investigated the relationship between hypertension and increased sympathoadrenal activity in previously normotensive, stable maintenance hemodialysis patients (uremics) who developed hypertension subsequent to the onset of chronic renal failure. In age-matched groups, supine morning plasma norepinephrine (NE) concentrations (pg/ml) were elevated in uremics (401 +/- 26, p less than 0.00001, n = 23) and essential hypertensives (340 +/- 23, p less than 0.01, n = 29) compared to normal controls (260 +/- 18, n = 24). To further investigate the functional significance of increased sympathoadrenal activity in uremia, a subset of dialysis patients was studied during chronic clonidine therapy. Compared to placebo baseline, clonidine (mean dose 0.4 mg/day) caused parallel decreases in mean arterial pressure (MAP) (-8 +/- 2 mm Hg, p less than 0.05), heart rate (HR) (-13 +/- 3 b/min, p less than 0.05), plasma NE (-84 +/- 13 pg/ml, p less than 0.01), and plasma epinephrine (-24 +/- 4 pg/ml, p less than 0.01). Clonidine exerted balanced effects on cardiac output and systemic vascular resistance while blood volume and plasma renin activity were slightly increased. We conclude that the increased sympathoadrenal activity in uremia contributes to chronically increased arterial pressure in a pattern similar to essential hypertension. Central sympatholytic drugs are effective antihypertensive agents in uremia.

Adult↗
PubMed1987

Role of the central nervous system in human secondary hypertension.

The central nervous system may initiate or maintain hypertension in humans by a variety of mechanisms. Increased cerebral pressor activity can cause hypertension in some patients with the Guillain-Barré syndrome, where disinhibition of cerebral centres may result from an afferent baroreflex lesion. The brain itself initiates hypertension in patients with cerebral tumours, cerebrovascular accidents, and subarachnoid haemorrhage. The use of drugs (including alcohol), or at times their withdrawal, results in hypertension through neurogenic mechanisms. Impaired cerebral activity also contributes, as in tetraplegic patients in whom paroxysmal hypertension is a consequence of increased spinal sympathetic reflex activity, which is not restrained or appropriately counteracted by the brain because of the cervical spinal cord transection. Neurogenic factors also play a role in the maintenance of hypertension in patients in whom the initiating cause is clearly humoral. In renal artery stenosis for instance, cerebral actions of angiotensin II may later gain ascendance over its peripheral effects, especially as circulating levels fall, as has been demonstrated with the centrally acting sympatholytic agent, clonidine. This is an example of humoroneural coupling that contributes to the hypertension. Increased afferent renal nerve activity may be an additional factor, especially in patients with renal parenchymal disease, where renin appears to play a minor role. The role of the nervous system in other causes of primary hypertension is presently less clear. In phaeochromocytoma noncatecholamine tumour products may have neurogenic effects that could account for the ability of clonidine to lower blood pressure in some patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1989

[Drug therapy of arterial hypertension. Reflections and suggestions].

Treatment of arterial hypertension is an important part of medical care provided in industrialized countries today. When non-drug treatment turns out to be ineffective, or when hypertension levels are higher than target values, or target organ damage is ascertained, drug therapy must be started. This rationale comes from large-scale intervention trials, which have shown that the lowering of elevated blood pressure reduces cardiovascular morbidity and mortality. A logical aim in treatment of hypertension should be both to "normalize" hypertension-induced cardiovascular abnormalities and to maintain the quality of life, without undesirable influence on other cardiovascular risks. Moreover, if we could identify the major hemodynamic impairment behind increased blood pressure and correct it by an appropriate drug therapy, then we would have a satisfactory means to perform individualized treatment. Over the past years the empirical basis for the use of antihypertensive drugs has been replaced by a step-wise approach, but few attempts have been made to provide an approach that fits pathophysiological understanding. For this reason the above-mentioned step-wise approach has been found to be an uncorrected simplification of antihypertensive care. Also, the use of more recent drugs (calcium channel blockers, ACE-inhibitors and serotonin-receptor blockers) as an alternative to beta-blockers and diuretics in first step therapy, has further contributed to the abandonment of the step-wise approach. The different groups of antihypertensive agents are examined with reference to their mechanism of action, pharmacokinetics, indications, and desirable and untoward effects. At present, indirect vasodilators, such as calcium-antagonists, ACE-inhibitors and serotonin-receptor blockers, alone or combined with diuretics, represent an intrinsic part of basic antihypertensive therapy. Beta-adrenoceptor antagonists remain the agents of choice when the principal therapeutic aim is to reduce the adrenergic drive. Both these drugs and direct vasodilators or alpha-adrenoceptor antagonists can be employed in the most severe forms of hypertension. In such cases, combined therapy (vasodilator + antiadrenergic + diuretic agents) is often used. Sublingual nifedipine and intravenous diazoxide or sodium nitroprusside are the drugs of choice for the hypertensive crisis. The use of most of the central or peripheral sympatholytic agents has generally been abandoned. Finally, beta-blockers and calcium-antagonists have been shown to have a secure place in the management of ischemic heart disease complicating arterial hypertension. In this condition captopril also appears to be useful.

Antihypertensive Agents↗
PubMedDate not supplied

[Peripheral-type acute cochleovestibular involvement in the Klippel-Feil syndrome. Comments on 2 clinical cases].

The authors present the clinical observations performed on two medium aged patients with a Klippel-Feil syndrome met with during 1980-1987, in the polyclinic and the hospital. The patients presented themselves to the doctor with acute vestibular suffering of a peripheric type, constantly accompanied by bilateral, symmetric loss of hearing, in various degrees, and, sometimes, associated with neurological signs and some laboratory modifications. The cochleovestibular phenomena made themselves conspicuous together with acute cervical arthritic attacks. If following the treatment with cerebral vasodilator, sympatholytic, analgetic, antiphlogistic, antiemetic and neurotrophic medication the vestibular syndrome was easily compensated and the acute arthritic phenomena improved, the loss of hearing as well as other clinical elements of the syndrome persisted. Concerning these two clinical cases there are presented a series of physiopathologic considerations linked to the importance of the vertebral-basilar periarterial sympathetic system in regulating the dynamics and the biochemistry of the labyrinth liquids. We consider as interesting the presentation of these cases, as being so rare in the ORL practice.

Acute Disease↗
PubMed1989

Disparities in blood pressure control under various antihypertensive regimens.

Ambulatory blood pressure recordings and stress blood pressures during exercise were compared among hypertensive patients effectively treated with oxprenolol, nitrendipine, enalapril or low-dose clonidine. After 6 months of therapy, the means of blood pressure at rest and casual diastolic pressure were nearly identical among the four therapeutic groups. Although all pressures fell to within the normotensive range, casual systolic pressures were lower in patients treated with sympatholytic agents than in those taking enalapril. In contrast, average ambulatory blood pressure was less controlled in patients given clonidine or enalapril than in those given oxprenolol or nitrendipine. During physical stress patients taking clonidine showed the highest stress blood pressures and those taking oxprenolol the lowest pressures. The study demonstrated that although blood pressure was reduced to within the normotensive range in all four therapeutic groups, analysis of values of ambulatory blood pressure and stress blood pressure during physical activity showed a disparate pattern of antihypertensive efficacy.

Antihypertensive Agents↗
PubMed1985

[Typical spontaneous changes in heart rate in pheochromocytoma].

Investigations in 13 hospitalized patients with pheochromocytomata showed peculiar characteristics of heart rate variation at rest, when compared with normals. All patients were given alpha- and beta-sympatholytic drugs. In one case alpha-methyl-Tyrosine caused I-II degree AV blocks and a stable high frequency sinus rate without physiological variations. Resting heart rate in pheochromocytoma varied interindividually from 55-105/min, in the absence of clinical attacks of the underlying disease. The frequency profile was characterized in 12 patients by sudden and inadequate rises of heart rate (200%) of short duration, which were often recorded within 20 seconds of the onset of muscular activity. A similar but less pronounced heart rate modulation was found 1-2 weeks after operation in 3 cases. Our observations indicate that the heart rate profile described may be a sensitive parameter of dysfunction of the autonomous nervous system in pheochromocytoma. Whether the heart rate characteristics are of diagnostic value has to be assessed by further studies.

Adolescent↗
PubMed1989

[Local cortical and medullary blood flows to the single kidney in chemical sympathectomy].

Topological shifts of intracortical and intramedullary blood flow were studied with the hydrogen clearance technique in the single kidney of Wistar rats. A hyperperfusion of the cortex due to contralateral nephrectomy and vasodilating effect of sympatholytic agent, was found during first 24 hours. Cortical blood flow decreased and medullary one increased within 7 days, which was due to compensatory shifts in the kidney necessary for the adaptation of the kidney to the tissue deficit of adrenergic transmitter, and for the maintenance of the water-salt homeostasis in conditions of a systemic peripheral sympathectomy .

Adaptation, Physiological↗
PubMedDate not supplied

[Pathophysiologic characteristics of the reactive toxic stage of acute suppurative peritonitis and ways to enhance the effectiveness of intensive therapy].

The oxygen regimen, circulation, and metabolism were studied in 95 patients in the reactive-toxic stage of diffuse purulent peritonitis. The results of cluster analysis made it possible to determine the clinical and pathophysiological features of the phases of the disease. The phase of compensation was characterized by disorders of mass exchange of plasma water which led to increased index of transcapillary exchange and increased excess of lactate. These parameters of tissue metabolism were grouped into one cluster together with the oxygen regimen value and mean arterial pressure. The other cluster was formed of the values of oxygen consumption and the values of oxygen systemic and vascular tissue transport and the hemodynamic parameters. In the phase of decompensation the homeostasis parameters were grouped into another 2 clusters. The first contained the indices of transcapillary exchange of oxygen and water, the other--those of the intensity of blood oxygen transport function and metabolism. Surgical treatment and inclusion of the sympatholytic agent ornid and the beta-adrenergic agonist alupent in the complex of intensive therapy from the stages of preoperative and anesthesiological management brought homeostasis to a level characteristic of the phase of compensation, as a result of which fatal outcomes were absolutely excluded.

Acute Disease↗
PubMed1989

Reviewing geriatric concerns with commonly used drugs.

The most important special consideration for drug use in the last years of life is that the medications prescribed do what is intended and do not contribute to morbidity or premature mortality. Key factors in appropriate use are reviewed for analgesics, anti-inflammatories, corticosteroids, thyroid drugs, anti-diabetic agents, digoxin, newer antiarrhythmics, beta-blockers, diuretics and potassium supplements, sympatholytic and vasodilatory antihypertensives, warfarin and heparin, anxiolytics, neuroleptics, anticonvulsants, antidepressants, antimicrobials, laxatives, gastrointestinal and bronchodilatory agents, and nutritional supplements and vitamins.

Aged↗
PubMed1989

Methyldopa-related convergence insufficiency.

A case report of convergence insufficiency related to the use of methyldopa is presented. Methyldopa is a systemic antihypertensive agent. It has sympatholytic properties which lower blood pressure by decreasing peripheral vascular resistance. The proposed effects of methyldopa on binocular vision are reduced accommodative convergence and increased demand on fusional convergence. These effects would create a susceptibility to convergence insufficiency. To my knowledge, an association between methyldopa and convergence insufficiency has not been previously reported.

Accommodation, Ocular↗
PubMedDate not supplied

[Aldosterone content of the blood and tissues in rats with an altered level of adrenergic activity].

The content of aldosterone (A) was studied in rat adrenal glands, blood plasma and peripheral tissues--in the myocardium, skeletal muscles, thymus and liver--1 h after the administration of alpha-adrenergic stimulator noradrenaline and beta-adrenergic stimulator isoprenaline and after simultaneous administration of alpha- and beta-blockers and a sympatholytic agent (pyrroxan, propranolol and bretylium tosylate respectively). Adrenergic stimulation did not change the level of A in the adrenal glands, raised its blood concentration and, to a greater extent, its level in the peripheral tissues. A marked increase in the blood concentration of A resulted from isoprenaline and its accumulation in tissues--from noradrenaline. A decrease in the level of adrenergic activity considerably lowered the A content in the adrenal glands, blood plasma and peripheral tissues excluding the myocardium where this value was higher than in the blood.

Adrenal Glands↗
PubMed1988

Efficacy and renal effects of enalapril therapy for hypertensive patients with chronic renal insufficiency.

The antihypertensive efficacy and renal effects of enalapril maleate therapy were evaluated in 13 hypertensive patients with chronic renal failure. Enalapril was administered as follows: alone; added to furosemide, clonidine hydrochloride, or atenolol; or in combination with any of the aforementioned drugs. Three patients did not complete the study; uncontrolled hypertension was the cause in two of these patients. In the remaining ten patients, short-term (mean +/- SD, 63 +/- 9 days) enalapril maleate therapy decreased the patient's seated blood pressure from 161/98 +/- 19/8 to 130/80 +/- 13/7 mm Hg. Furosemide was administered to eight patients; the dose of concomitant sympatholytic therapy was decreased in five of five patients. Serum potassium concentration increased from 4.1 +/- 0.3 to 4.5 +/- 0.3 mmol/L. Levels of urinary total protein excretion decreased from 2.23 +/- 2.05 to 1.08 +/- 1.45 g/d. Renal function (creatinine clearance, 0.58 +/- 0.21 mL/s) did not change from baseline. During long-term therapy, the rate of progression of renal insufficiency seemed to slacken in three of four patients with diabetic nephropathy. Thus enalapril can reduce blood pressure and proteinuria in hypertensive patients with chronic renal insufficiency. The possibility that enalapril can slow the progression of diabetic nephropathy remains to be confirmed by future studies.

Adult↗
PubMed1985

Contractile performance following regression of left ventricular hypertrophy in hypertensive patients.

The left ventricular end systolic stress-end systolic dimension (ESS-ESD) relation was used to assess the effect of regression in left ventricular hypertrophy on myocardial contractility in 14 hypertensive patients (mean age 47 years) treated with guanfacine (a sympatholytic central alpha-adrenergic agonist) for 10 weeks. Echocardiography (M-mode under two-dimensional guidance) was used to determine left ventricular dimensions, posterior wall thickness (PWT) and septal thickness (ST) before and during the last week of therapy. Left ventricular mass (LVM) expressed as cross-sectional area (CSA) and meridianal wall stress at end systole were derived. Echocardiography was carried out at rest and during i.v. infusion of sodium nitroprusside to alter left ventricular afterload. A minimum of four systolic arterial pressure-ESD points were available for analysis and the value for the slope ESS-ESD was calculated for each patient. Guanfacine produced a significant decrease (P < 0.005) in arterial pressure, wall thickness and CSA. The linear ESS-ESD slope was similar in patients with and without left ventricular hypertrophy and did not change in the whole group or in four patients who had a decrease in CSA of > 10%. It is concluded that guanfacine can induce regression of left ventricular hypertrophy in hypertensive patients and that a decrease in LVM does not influence the intrinsic contractile performance of the left ventricular.

Adult↗
PubMedDate not supplied

Use of antihypertensive agents in patients with glucose intolerance.

The selection, use, and potential adverse effects of antihypertensive agents in patients with glucose intolerance are reviewed. Thiazide diuretics frequently impair glucose tolerance, but this deterioration is usually modest and should not preclude use of these agents in most patients with glucose intolerance. The loop diuretics furosemide and ethacrynic acid have also been associated with decreased glucose tolerance. The beta-adrenergic blocking agents may inhibit insulin secretion, but few patients will experience clinically important elevations in blood glucose. Rather than producing glucose intolerance, these agents may delay recovery from hypoglycemic episodes and may mask catecholamine-induced symptoms of hypoglycemia. In certain cases, use of cardioselective beta blockers or avoidance of beta-blocker therapy may be indicated, especially in insulin-dependent diabetics. The calcium-channel blocking agents nifedipine and verapamil have been reported to produce diabetogenic effects in a few studies, but further investigations are needed to define the extent of these effects. Available evidence indicates that sympatholytic agents such as guanethidine and reserpine, alpha 2-adrenergic agonists such as methyldopa and clonidine, the alpha 1-blocking agent prazosin, and the vasodilators captopril and hydralazine produce few, if any, clinically important changes in glucose tolerance. While no antihypertensive agents are absolutely contraindicated in patients with glucose intolerance, patients with glucose intolerance who are receiving thiazide diuretics, beta blockers, and calcium-channel blocking agents should be monitored with extra care for hyperglycemia or deterioration in glucose tolerance.

Adrenergic alpha-Agonists↗
PubMed1987

Local and neurally mediated effects of sufentanil on canine skeletal muscle vascular resistance.

The present study examines both the local and neurally mediated effects of sufentanil, a new synthetic opioid, on the vascular resistance of the isolated, separately perfused canine gracilis muscle. Infusions (50 micrograms/min) of sufentanil into the gracilis arteries of nine denervated gracilis muscles did not produce a direct vascular effect. Because morphine has been previously shown to produce a central sympatholytic effect, the neural effect of sufentanil was examined in 12 innervated muscles under conditions of either low or high background sympathetic activity produced by either hemorrhage or transfusion of the dog. After i.v. sufentanil (20 micrograms/kg), all dogs experienced a rapid parallel fall in gracilis vascular resistance (GVR) and mean arterial pressure. The GVR decreased under conditions of high and low sympathetic activity. With low sympathetic tone, the GVR decreased from a control value of 24.1 +/- 4.4 S.E.M. to 6.6 +/- 0.8 resistance units (RU), a value below the subsequently denervated level (13.2 +/- 2.5 RU) (P less than .05). In hemorrhaged animals with elevated control sympathetic tone, resistance declined from 38.4 +/- 9.1 to 26.1 +/- 4.4 RU (P less than .05) but did not reach the denervated level (12.4 +/- 2.7 RU). Local intra-arterial pharmacologic blockade of the gracilis muscle was performed in animals with low sympathetic tone. Intra-arterial atropine did not effect the neurogenic vasodilatory response to sufentanil, whereas prazosin abolished it. Intra-arterial H1 and H2 receptor blockade prevented the decline of GVR secondary to sufentanil below the denervated level. Thus, vasodilation associated with sufentanil administration is mediated solely through neurogenic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗
PubMed1988

Urapidil in patients with severe hypertension and in long-term treatment.

In order to evaluate the usefulness of urapidil in the treatment of severe hypertension and in the long-term treatment of essential hypertension, two open multicentre studies were performed. In one study, 34 outpatients with diastolic blood pressure exceeding 105 mmHg following treatment with a combination of a diuretic and a sympatholytic or a diuretic and a beta-blocker were additionally given 15-60 mg urapidil twice a day for 8 weeks or more. The responder rate was 73.5%. The pulse rate did not change throughout. Side effects such as dizziness and malaise were observed in five patients (14.7%), but they were slight and did not require withdrawal of treatment. The other study included 95 outpatients with essential hypertension (World Health Organization stages I or II), 15-60 mg urapidil twice a day for 1 year or more in monotherapy (n = 48) or in combined therapy with a thiazide (n = 47). Under both therapies, diastolic blood pressure was reduced significantly at week 4, further reduced at week 12 and remained stable until week 52. Responder rates were 82.9% in monotherapy and 78.4% in combined therapy. Two patients (4.2%) taking monotherapy and six patients (12.8%) taking combined therapy were withdrawn due to inadequate blood pressure control or to side effects. These results indicate that urapidil is useful in severe and in long-term hypertension.

Adrenergic beta-Antagonists↗
PubMed1987

Effects of serotonin1 and serotonin2 receptor agonists and antagonists on blood pressure, heart rate and sympathetic nerve activity.

Previous studies indicate that serotonin (5-HT) neurons provide a tonic excitatory input to central sympathetic neurons. The purpose of the present study was to utilize a number of 5-HT agonists in order to provide insights into the general function of the serotonergic system in the regulation of central sympathetic pathways. The 5-HT1A agonists 8-hydroxy-dipropylaminotetralin and p-aminophenyl-ethyl-m-trifluoromethylphenyl piperazine produced a dose-related inhibition of sympathetic nerve discharge (SND) recorded from either the postganglionic inferior cardiac nerve or the preganglionic splanchnic nerve in chloralose-anesthetized cats. The sympatholytic effects of 8-hydroxy-dipropylaminotetralin and p-aminophenyl-ethyl-m-trifluoromethylphenyl piperazine were accompanied by hypotension and bradycardia. The effects of 5-HT1A agonists were reversed by the 5-HT1A antagonist spiperone. In contrast, spiperone alone produced decreases in blood pressure, heart rate and SND. The 5-HT1B agonists 1[3(trifluoromethyl) phenyl]-piperazine, 1-(3-chlorophenyl) piperazine and 1-(2-methoxyphenyl) piperazine all produced variable effects on SND. In some experiments, SND was increased by these agents, whereas it was decreased in others. The 5-HT2 agonist 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane produced a marked increase in SND. A second 5-HT2 agonist, MK212, produced similar effects. The role of 5-HT receptor subtypes in mediating the 5-HT excitation of sympathetic neurons is discussed. It is suggested that 5-HT1A agonists inhibit SND through a process of disfacilitation by inhibiting the firing rate of 5-HT neurons. Possible mechanisms by which 5-HT2 agonists increase SND are proposed.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1988

[Preventive antifibrillatory treatment of sudden cardiac death in acute myocardial infarct].

The pathophysiological basis of sudden cardiac death due to ventricular arrhythmias in acute myocardial infarction has been extensively investigated in experimental as well as in some clinical studies. Numerous clinical studies have been performed with the aim to establish the feasibility of antifibrillatory prophylaxis of sudden cardiac death by pretreatment with antiarrhythmic drugs. Using class I-antiarrhythmic drugs the reported findings were contradictory. While the antiarrhythmic efficacy of Lidocaine and other, newer class I-antiarrhythmic drugs is well established, the antifibrillatory effects of these drugs in the early phase of acute myocardial infarction remain uncertain. In clinical studies with the endpoint of mortality in patients at risk, longterm administration of orally effective class I-antiarrhythmic drugs did not prove to be superior to placebo. However, beta-sympatholytic agents have been shown to reduce mortality in patients at risk in several large clinical studies. The basic mechanism seems to be primarily a reduction in sudden cardiac death which is caused predominantly by ventricular fibrillation. The antifibrillatory properties of beta-blockers was demonstrated as well by a reduction in the number of episodes of ventricular fibrillation. The recognition of patients at risk who profit most from chronic beta-blocker therapy remains the main problem when treatment of numerous low-risk patients is avoided. In the ISIS I-study with Atenolol intravenous administration of a beta-blocker in the early phase of acute myocardial infarction has been shown to be beneficial if hemodynamic monitoring, for example using flow-directed heart catherization is performed. In general this does not apply to the treatment with calciumantagonists, especially with Verapamil and Nifedipine. These drugs do not improve prognosis of acute myocardial ischemia, obviously because of hemodynamic side effects. The antifibrillatory efficacy of Verapamil-type calciumantagonists, shown in the experimental model, could not be demonstrated in the clinical setting. Nevertheless, further clinical studies performing longterm prophylactic treatment of patients at risk before the onset of myocardial ischemia seem to be worthwhile. Concerning class III-antiarrhythmic agents, clinical experience in the setting of acute myocardial infarction is limited; hence a final conclusion about their antifibrillatory efficacy under clinical conditions at present is impossible.

Anti-Arrhythmia Agents↗