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PubMed1984

Relationship between plasma aldosterone and angiotensin II before and after noradrenergic inhibition in normal subjects and patients with mild essential hypertension.

The responsiveness of plasma aldosterone to the infusion of angiotensin II at dose rates of 2, 4, and 10 ng/kg X min was assessed in 11 normal subjects and 13 patients with mild essential hypertension before and after 4 weeks of treatment with the sympatholytic agent debrisoquine. Debrisoquine treatment caused a significant (P less than 0.01) decrease in circulating norepinephrine (-45%), but did not modify plasma levels of angiotensin II, renin, aldosterone, or epinephrine or the metabolism of sodium or potassium. In normal subjects, debrisoquine caused a significant shift to the left (P less than 0.05) of the correlation relating plasma aldosterone to plasma angiotensin II levels. In patients with essential hypertension, the aldosterone-angiotensin II interrelationship was not modified. These findings suggest that the sympathetic nervous system exerts an inhibitory influence on aldosterone responsiveness to angiotensin II in normal man, and that this physiological interaction is impaired in patients with essential hypertension.

Adult↗
PubMed1997

Selegiline diminishes cardiovascular autonomic responses in Parkinson's disease.

Selegiline (L-deprenyl), a selective inhibitor of monoamine oxidase type B, is an established adjuvant to levodopa therapy in Parkinson's disease (PD). To evaluate whether selegiline also effects the severity and progression of autonomic nervous system dysfunction in PD, we studied autonomic functions by measuring cardiovascular responses to normal breathing, deep breathing, the Valsalva maneuver, the tilting test, and the isometric contraction test prospectively in 52 PD patients receiving either selegiline (n = 27) or placebo (n = 25) in randomized order in a double-blind parallel trial. The study also continued double-blind after the introduction of levodopa. Recordings of cardiovascular responses were carried out annually, with the median follow-up period being 6 years. Cardiovascular autonomic reflexes were diminished in the patient groups compared with those of healthy control subjects (n = 45). There was no progression (except age-related) in dysautonomia in patients on placebo, but there was a decrease in cardiovascular responses in the selegiline group. The heart rate variability in normal breathing, in the Valsalva maneuver, and in the tilting test was clearly diminished during the selegiline treatment. In addition, in the tilting test, the fall in diastolic blood pressure immediately after tilting and in systolic blood pressure 2 minutes after standing up was more pronounced in the selegiline group than in the placebo group. Levodopa treatment had no effect on the measured autonomic responses. In the isometric contraction test, the two treatment groups showed no difference. We conclude that selegiline treatment diminishes autonomic responses, especially those of the sympathetic division. This sympatholytic effect may signal an increased risk of orthostatic hypotension.

Analysis of Variance↗
PubMed1987

T2 and T3 sympathetic ganglia in the adult human: a cadaver and clinical-radiographic study and its clinical application.

The technique of percutaneous radiofrequency (RF) upper thoracic sympathectomy mandates an exact knowledge of the anatomical location of the sympathetic ganglia. Because conflicting descriptions are given in anatomy texts, we examined the T2 and T3 sympathetic ganglia in 48 sympathetic chains in adult cadavers to measure the exact location of the ganglia. Measurements were made relative to their distances (a) dorsal to the ventral surface of the vertebral body and (b) rostral or caudal to the midpoint of the vertebral body. Median locations of T2 and T3 ganglia were 17 to 20 mm dorsal to the ventral surface of the vertebral body and 2 mm rostral to the T1-T2 and T2-T3 vertebral bodies. The sympathetic chains lay lateral to and between the heads of the ribs at these levels. A clinical-radiographic correlation study of the sympatholytic effectiveness of various needle electrode placement sites during sympathectomy confirmed these findings. These data have been used to modify the technique of percutaneous RF sympathectomy.

Female↗
PubMed2005

Dexmedetomidine for neurological surgery.

Dexmedetomidine is a new intravenous drug gaining popularity in neuroanesthesia and neurocritical care practice. This alpha2-adrenergic receptor agonist offers a unique "cooperative sedation," anxiolysis, and analgesia with no respiratory depression. Cerebral effects are generally consistent with a desirable neurophysiological profile, including neuroprotective characteristics. In addition, sympatholytic and antinociceptive properties allow for hemodynamic stability at critical moments of neurosurgical stimulation. This review will address the neuropharmacology and neurophysiology of alpha2-adrenergic agonists and will specifically consider the rapidly evolving applicability of dexmedetomidine as an adjuvant to neurosurgical case management.

Adrenergic alpha-2 Receptor Antagonists↗
PubMed2003

Acute metabolic effects of thiopental anesthesia on fed and fasted rats chronically treated with bromocriptine.

We investigated the acute effects of thiopental anesthesia (4 mg/100 g, i.v.) on plasma glucose, insulin, triacylglycerol, and prolactin levels in rats treated with bromocriptine (BR) (0.4 mg/100 g body wt, i.p., for two weeks). Thiopental anesthesia induced a rapid increase in plasma insulin that was more pronounced in the animals treated with BR (116%, P <0.05). Thiopental anesthesia also produced a 55% decreased in plasma prolactin levels (P <0.01) in control fed rats, and a 22% reduction in plasma triacylglycerol (P <0.05) in both controls and BR-treated rats. We conclude that BR may constitute and additional sympatholytic factor in animals submitted to thiopental anesthesia.

Anesthesia↗
PubMed1995

Mechanism of hypertension induced by chronic inhibition of nitric oxide in rats.

In order to clarify the mechanism of hypertension induced by a nitric oxide (NO) synthase inhibitor, L-NG-nitro-L-arginine (LNNA), metabolites of NO, catecholamines, and hemodynamic parameters were measured during 7 days of oral administration of LNNA in rats. Control rats received either L-arginine (L-Arg) or the vehicle. systolic blood pressure, measured by the tall-cuff method was elevated throughout the period of LNNA administration, but that in the two control groups was not influenced by treatment. Heart rate decreased on the second day only in LNNA-treated rats. Although L-Arg treatment had no influence, LNNA markedly decreased the plasma level and the urinary excretion of nitrate ions (NO-3). Urinary excretion of noradrenaline was significantly decreased on the second day of LNNA administration and returned to the control level thereafter. When hemodynamic changes were measured by using radioactive microspheres, LNNA was found to increase blood pressure by markedly increasing total peripheral resistance. Cardiac output was decreased by LNNA. L-Arg, again, did not influence the hemodynamic variables as compared with the vehicle control group. The regional vascular resistance index was increased by LNNA in many tissues and organs, except the brain and the heart. Regional blood flow, on the other hand, was significantly decreased only in the liver and skin by LNNA. The marked reduction in NO3- in urine by LNNA-treatments may indicate that the measured NO3- is exclusively of endogenous origin, and that inhibition of NO production causes elevation of blood pressure by constricting peripheral arteries. Sympatholytic responses by the baroreceptor reflex were thereby evident only on the second and the third days, which was indicated by bradycardia and suppression of noradrenaline excretion into urine. These results indicate that the inhibition of NO synthase actually decreases production of endogenous NO, and that the hypertension caused by decreases in NO production is due to elevation of total peripheral vascular resistance.

Animals↗
PubMed2004

Two cases of renovascular hypertension and ischemic renal dysfunction: reliable choice of examinations and treatments.

We experienced two aged patients with atherosclerotic renovascular stenosis associated with hypertension and ischemic nephropathy. Both patients exhibited sudden rise in blood pressure (BP) and progressive aggravation of renal dysfunction. In these patients, the use of contrast medium to screen for renal artery stenosis (RAS) ran the risk of further deterioration of renal function. We therefore used magnetic resonance angiography (MRA), which is less conducive to renal damage, to screen for RAS. One-sided RAS was treated by percutaneous transluminal angioplasty of the renal artery (PTRA) and stenting. As a result, BP decreased in both patients. Serum creatinine (Cr) decreased slightly in one patient, whereas, in the other, serum Cr increased transiently and then decreased and stabilized to pre-treatment levels. Thus, although it is unclear whether the combination of PTRA and stenting is among the best treatments for patients with RAS and moderate-to-severe renal dysfunction, PTRA and stenting are clearly of benefit in selected patients. In addition, recent progress in characterizing the pathophysiology of ischemic nephropathy associated with renovascular hypertension has created interest in the therapeutic potential of angiotensin II receptor antagonists, sympatholytic agents, and antioxidants. Therefore, we discuss the therapeutic utility of PTRA and stenting and the above-mentioned medications in patients with RAS and renal dysfunction.

Angioplasty, Balloon↗
PubMed2006

Relief of acute pain in chronic idiopathic gastroparesis with intravenous phentolamine.

OBJECTIVE: To report a case in which complete relief of pain associated with gastroparesis, with promotion of gastric emptying, was achieved with administration of phentolamine. CASE SUMMARY: A 37-year-old opiate-tolerant female with a history of recurrent abdominal pain, gastroparesis, cyclic vomiting syndrome, and migraine headaches was admitted to the emergency department (ED) with severe acute abdominal pain, nausea, and vomiting. The patient had been previously implanted with a permanent gastric electrical stimulator and she was adherent to her prokinetic, antiemetic, analgesic, and migraine prophylactic medications. Pain relief was achieved rapidly and completely in the ED with sympatholysis by administration of intravenous phentolamine 0.5 mg/kg over 60 minutes, with continuous cardiac monitoring. At a 2 month follow-up visit, the patient reported chronic pain relief, and a decrease in opiate doses was maintained by oral administration of clonidine 0.1 mg twice daily. DISCUSSION: Gastroparesis represents a difficult treatment challenge because management of gastric dysmotility and the accompanying severe abdominal pain is often mutually exacerbating and ineffective. Sympatholysis by intravenous phentolamine provided profound and immediate relief of acute gastroparesis-related abdominal pain in our patient. The mechanism of phentolamine is believed to be receptor blockade at alpha-adrenergic receptors and, therefore, inhibition of the peripheral sensitizing effects of circulating norepinephrine. Although action at a peripheral nerve level is presumed, modulation of alpha-adrenoreceptors receptors is also possible at the dorsal root ganglion or at other central nervous system sites. CONCLUSIONS: The dramatic relief of acute pain in gastroparesis by phentolamine observed in this case would warrant investigation of a larger, controlled case series. Patients who respond to intravenous sympatholysis may likewise be candidates for longer term sympathetic modulation with oral sympatholytics.

Abdominal Pain↗
PubMedDate not supplied

Oral phentolamine (Vasomax).

Vasomax is an oral preparation of phentolamine mesilate (Zonagen Pharmaceuticals) currently undergoing worldwide regulatory approval for distribution. Phentolamine is primarily an alpha-adrenergic antagonist with mild sympatholytic action and a beta-adrenergic stimulating action. Over 30 years of clinical experience has shown it to be a strong direct vasodilator on muscular walled vessels, likely based on its inhibitory action on adenosine 5-triphosphate-sensitive potassium channels. This medication is not new, having been marketed in the United States in an oral formulation between 1952 and 1984. Phentolamine initially achieved FDA approval for preoperative use in patients with pheochromocytoma for control of blood pressure and paroxysmal hypertensive episodes. In the past it had been evaluated for hypertension, pulmonary disease, cardiac arrhythmias, angina pectoris and peripheral vascular disease. Unfortunately for most of these indications the clinical responses to oral phentolamine have been variable. The most clinically significant adverse events associated with oral phentolamine in the past were systemic hypotension and vasomotor collapse, severe gastrointestinal side effects especially diarrhea and some complaints of nasal congestion. In this review we will concentrate on phentolamine in a new preparation for on demand treatment of erectile dysfunction of mild to moderate degrees.

Journal Article↗
PubMed1983

Use of clonidine and propranolol as monotherapy in borderline hypertension.

The effect of clonidine (average 0.24 mg/day) and propranolol (average 105 mg/day) on home blood pressure readings in 16 patients with borderline hypertension was investigated in a randomized, double-blind, placebo crossover design. Patients could detect small but significant decreases of blood pressure with both active compounds (-8/-5 with propranolol and -11/-7 with clonidine). The larger mean blood pressure decrease from clonidine vs propranolol was significant (p less than 0.015). Small doses of sympatholytic agents might control the blood pressure in patients with borderline hypertension, and the home blood pressure technique is a convenient tool to detect and monitor such changes. Biochemical predictors of the responsiveness to clonidine were investigated. There was no difference in placebo norepinephrine and renin values between better and lesser responders to clonidine. Plasma norepinephrine fell with clonidine treatment, but with no relationship to the blood pressure response. Plasma norepinephrine response to clonidine might reflect not only the central withdrawal of sympathetic tone, but also, in part, the effect of clonidine on peripheral presynaptic alpha 2-receptors.

Adult↗
PubMed1983

Effects of oxygen breathing on pulmonary vascular input impedance in patients with pulmonary hypertension.

The effect of oxygen breathing on the stiffness of the large pulmonary artery has not been elucidated. We analyzed the proximal pulmonary arterial impedance with a multisensor catheter in ten patients with pulmonary arterial hypertension (PAH), eight patients with pulmonary venous hypertension, and six control subjects. The stiffness of the vessel was quantified by the characteristic impedance (Zo) and compared with the plasma norepinephrine level. Ten minutes of high-oxygen breathing decreased the Zo (from 78 +/- 18 to 57 +/- 14 dynes.sec.cm-5, p less than 0.01) and pulmonary arterial resistance in all the cases with PAH. In this group, norepinephrine also decreased (from 381 +/- 89 to 319 +/- 77 pg/ml, p less than 0.01) following the correction of hypoxemia. Yet, those parameters did not change in the other two groups. These results indicate that in patients with PAH, oxygen breathing can reduce the stiffness of the main pulmonary artery because of the sympatholytic effect.

Biomechanical Phenomena↗
PubMed1994

Angiotensin II-mediated catecholamine release during the pressor response in rats.

Angiotensin II (ANG II)-mediated catecholamine release and its possible contribution to the pressor response was assessed in baroreceptor-denervated rats. Neonatal male Sprague-Dawley rats were injected with the sympatholytic drug, guanethidine monosulphate (50 mg/kg s.c., 6 days/week) for 40 days. Plasma catecholamine concentrations were measured using a 3H-radioenzymatic assay as follows: (a) before and 30 s after the injection of saline or ANG II (79.3 pmol/kg i.v.), at the peak of the pressor response, then 50 s and 80 s thereafter, in guanethidine-treated (GUAN) and saline-injected (SHAM) rats, and (b) before and after adrenalectomy (ADX), following the same time-sequence for ANG II as in (a). Peak pressor responses to graded doses of ANG II (6.6, 26.4, 53.0 and 79.3 pmol/kg i.v.) were measured in GUAN+ADX and ADX rats. Destruction of peripheral sympathetic nerves was confirmed by measurements of plasma noradrenaline (NA), adrenaline (AD) and dopamine (DA) concentrations and by changes in pressor responses and heart rates following i.v. doses of tyramine. ANG II induced significantly (P < 0.05) greater pressor responses in GUAN+ADX rats than in ADX rats, especially after the 53.0 and 79.3 pmol/kg doses. Plasma AD concentrations increased within seconds after the pressor response to ANG II in both GUAN and SHAM rats but there was no change in plasma NA or DA concentrations (P < 0.05). ANG-II-mediated AD release from the adrenal medulla may contribute to the overall pressor action of the peptide. The vasculature became more sensitive to ANG II at a time when NA and DA depletion occurred following sympathectomy and/or adrenalectomy. This heightened sensitivity to ANG II was not due to a decrease in circulating ANG II in sympathectomized rats because even though plasma renin activity fell from 6.54 +/- 0.52 to 3.77 +/- 0.26 ng ANG I/ml per h it remained within the normal range.

Angiotensin II↗
PubMed1999

Effects of chronic bromocriptine (CB-154) treatment on the plasma glucose and insulin secretion response to neurocytoglucopenia in rats.

Neurocytoglucopenia has been reported to increase both parasympathetic and sympathetic tone with a predominant effect on the latter, which accounts for the major effect of plasma hyperglycemia and the inhibition of insulin secretion. The aim of this study was to determine the effects of chronic treatment with bromocriptine (0.4 mg/100 g body wt per day), a potent sympatholytic D(2)-dopaminergic agonist, on hyperglycemia and insulin secretion in response to neurocytoglucopenia induced by 2-deoxy-d-glucose (2DG). After 2 weeks of bromocriptine treatment the animals, freely moving in their cages, were submitted to 2DG administration (50 mg/100 g body wt) via atrial catheter infusion. After 2DG infusion, the plasma prolactin of vehicle-treated (VEH) rats increased rapidly, reaching a peak at 10 min (34.3+/-7.6 ng/ml; P<0.01). In contrast, 2DG infusion failed to induce any significant change in the plasma prolactin levels of bromocriptine-treated (BR) rats. BR rats showed higher resting glucose levels than control rats (8.2+/-0.28 mM (BR) vs 6.0+/-0.18 mM (VEH); P<0.01). However, the hyperglycemic response of BR rats to 2DG injection was 30% lower than that of VEH rats (P<0.05). BR rats also showed a rapid rise in plasma insulin levels reaching a peak at 30 min after 2DG injection (243% higher than basal values; P<0.01). This increased rise in the insulin response to neurocytoglucopenia of BR rats was blocked by previous intravenous injection of atropine methyl nitrate (0.2 mg/100 g body wt). The present results suggest that chronic treatment with bromocriptine determines a strong increase in the parasympathetic tone response to neurocytoglucopenia, which is responsible for the higher stimulation of insulin secretion observed in BR rats. The data also provide further evidence that D(2)-dopaminergic agonist can block neurocytoglucopenia-induced prolactin release.

Animals↗
PubMed1981

Current antidepressant drugs: their clinical use.

Depression is not only a common disorder, but also one that is readily treatable. Antidepressant drugs play a major role in treatment, although concurrent use of electroconvulsive therapy or psychotherapy may be indicated for some patients. Antidepressant drugs have been most specifically beneficial for patients with 'endogenous' depressions, but they should be used whenever this type of depression cannot be definitely ruled out. Besides the older tricyclic antidepressants and monoamine oxidase inhibitors, a new 'second generation' group of drugs is now available. Although these drugs offer no great therapeutic advantages over the older ones, they may prove to have a more acceptable profile of side effects, may act more quickly, and may show less cardiotoxicity with overdoses. Whether one can classify depression pathogenetically according to various biological markers, such as urinary excretion of the norepinephrine metabolite, 3-methoxy-4-hydroxy phenylglycol, is still uncertain. At present, the choice of antidepressant drug for an individual patient is largely empirical. Besides being useful for treating depression, antidepressants may be used for treating enuresis, chronically painful states, obsessive-compulsive-phobic states, acute panic attacks and cataplectic attacks in narcoleptics. Many studies have tried to define a therapeutic range of plasma concentrations of these drugs, so as to afford a better basis for dosing, but routine monitoring of drug plasma concentrations is seldom needed; the primary indication for doing so would be in the patient who has received what should be an adequate dose but who is still unresponsive. The value of maintenance treatment with antidepressants has been clearly established; the pattern it takes is best determined by the natural history of the disorder in individual patients. Most drug interactions with antidepressants are pharmacodynamic in nature and can be managed by adjusting doses. Pharmacokinetic interactions with various sympatholytic antihypertensive drugs, such as guanethidine, methyldopa and clonidine, are rare but may be serious. Patients with depression may be spared a considerable amount of discomfort, morbidity, and possibly mortality, by judicious use of antidepressant drugs and the other treatments currently available.

Anti-Anxiety Agents↗
PubMed1986

The diuretic dilemma and the management of mild hypertension.

Diuretics are used in first-step antihypertensive monotherapy or in combination with adrenergic-inhibiting agents in the majority of hypertensive patients in the United States. A 30-year experience has demonstrated that blood pressure is lowered to as great or greater a degree with diuretics than when many of the presently available antihypertensive drugs, including converting enzyme inhibitors, calcium entry blockers, beta- or alpha-adrenergic inhibitors, or centrally acting sympatholytic agents, are used. Diuretics appear to be especially effective in the elderly and in black patients. All of the major hypertension clinical trials upon which we base our decisions for treatment have employed diuretics as step-1 therapy--with a reduction in morbidity and mortality. In addition, data suggest that more effective treatment of hypertension has contributed to the decrease of over 45% in deaths from cerebrovascular disease and the overall reduction of cardiovascular deaths over the past 15 to 20 years in the United States. The debate concerning the long term safety of diuretic therapy has focused on the USA Multiple Risk Factor Intervention Trial (MRFIT) results and several papers, suggesting that the lipid-raising or potassium-lowering properties of diuretics may produce adverse effects. Suggestions have been made that the use of other drugs without metabolic side effects may result in greater benefit with less risk, especially in the management of mild hypertension where the risk of the disease is not immediate or great. A review of the MRFIT and lipid data from long term studies has failed to establish the 'toxicity' of diuretic agents. In addition, recent studies have not confirmed previous observations that diuretic-induced hypokalaemia increases ventricular ectopy or contributes to sudden death. Although hypokalaemia should be avoided and corrected if it occurs, especially in patients with ischaemic heart disease, in the elderly, in patients with pretreatment ectopy or in patients on low potassium diets, the fear of this metabolic side effect of diuretics should not deter the physician from continuing the use of these agents both as monotherapy in most patients and as second-step therapy with an adrenergic-inhibiting drug.

Arrhythmias, Cardiac↗
PubMed1991

Practical aspects of the use of amiodarone.

Amiodarone is a class III antiarrhythmic drug with sympatholytic properties, which prolongs the refractory period of all cardiac tissues, depresses sinus node automaticity and atrioventricular nodal conduction. It is active on all cardiac arrhythmias, its use being limited by the risk of side effects, mainly extracardiac, which are dependent upon dosage and duration of treatment. The use of an oral loading dose of intravenous infusion to rapidly obtain an efficacious blood concentration may minimise the delay in onset of drug action. Amiodarone progressively accumulates in cardiac muscle and is eliminated slowly, allowing drug free periods (2 days a week) on long term therapy. Pharmacokinetic interaction with digoxin, class I antiarrhythmic drugs and warfarin must be considered during combination therapy, as well as the potentiation of electrophysiological effects when amiodarone is co-administered with combined calcium antagonists and beta-blockers.

Administration, Oral↗
PubMed2005

Sexual dysfunction in male patients with hypertension: influence of antihypertensive drugs.

Evidence suggests that arterial hypertension, in addition to being a cardiovascular and renal risk factor, may also be associated with an impairment of male sexual function. Since other cardiovascular risk factors, especially diabetes mellitus, have also been shown to correlate with impaired sexual function it has been proposed that sexual and especially erectile dysfunction may, at least in part, represent just another manifestation of atherosclerotic vascular disease. In addition to hypertension itself, sexual function in male hypertensive patients may also be affected by antihypertensive drug treatment. Available evidence suggests that centrally acting sympatholytic agents, beta-adrenoceptor antagonists (beta-blockers) and diuretics may have the potential to further impair sexual function. Calcium channel antagonists and ACE inhibitors may be neutral with respect to this endpoint. Preliminary data from several randomised and open studies have suggested that angiotensin II (AT)(1)-receptor antagonists may even be associated with an improvement of sexual function. However, many aspects of the interaction between hypertension, antihypertensive drug treatment and male sexual function remain unclear. Among other factors, the relative contribution of disease labelling both to the higher incidence of sexual dysfunction in hypertensive versus normotensive males and to the negative impact of treatment remains an open question. Furthermore, dose dependence of the observed effects of antihypertensive agents on sexual function, the role of combination therapy and the anticipation of proposed adverse effects of treatment are unresolved issues. Thus, more data from studies of high quality using standardised definitions and procedures are urgently needed to at least partially resolve some of the many open questions.

Antihypertensive Agents↗
PubMed1984

Terazosin: intravenous safety evaluation in rats.

Terazosin, an alpha-adrenergic antagonist, was administered as a 15 mg/ml solution to rats intravenously at a rate of 2 ml/min. Under these conditions the LD50 was 277 mg/kg for males and 293 mg/kg for females. When administered daily for 1 month at dosages of 0, 10, 40 or 150 mg/kg/day, the no-toxic-effect dosage was 40 mg/kg/day. Evidence of toxicity at 150 mg/kg included hypothermia and deaths. Death resulted from acute, exaggerated pharmacologic effects leading to cardiorespiratory failure. Evidence of sympatholytic activity observed at lower dosages included hypoactivity, blepharoptosis, ptyalism and splenic congestion.

Animals↗