Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The cardioselectivities of five beta-adrenoceptor antagonists were compared. Six normal subjects received, in a double-blind random order, 200 mg acebutolol, 50 mg atenolol, 10 mg betaxolol, 100 mg metoprolol, 80 mg propranolol, and placebo. All beta-adrenoceptor antagonists produced a similar reduction in exercise tachycardia. Isoprenaline infusions in incremental doses were given. Dose-response curves were constructed and the doses of isoprenaline required to increase heart rate by 25 beats/min (I25), forearm blood flow by 3 ml/100 ml/min (IF3), and finger tremor by 200% (IT200), and decrease diastolic blood pressure by 25 mm Hg (ID25), after each treatment were compared. After propranolol, I25, ID25, IF3, and IT200 were greater (p less than 0.02) than after atenolol, betaxolol, and metoprolol; I25, ID25, and IT200 were greater than after acebutolol. After acebutolol I25, ID25, and IF3 were greater than after atenolol and betaxolol; IT200 was greater than after betaxolol. Atenolol and betaxolol caused less reduction in the isoprenaline-induced changes in blood glucose, plasma potassium, lactate, renin activity, and serum insulin than propranolol. Acebutolol caused less attenuation of blood glucose and plasma lactate, and metoprolol less attenuation of plasma renin activity, than propranolol. It is concluded that acebutolol, atenolol, betaxolol, and metoprolol cause less blockade of beta 2-adrenoceptors than propranolol, and atenolol and betaxolol are more cardioselective than acebutolol.
J Cardiovasc Pharmacol 1987 Aug
PMID:A comparison of the cardioselectivity of five beta-adrenoceptor blocking drugs. 244 Nov 75

A double-blind controlled, randomized, parallel, multicenter 12-week study was conducted to compare the antihypertensive efficacy of lisinopril with that of metoprolol in treatment of moderate to severe hypertension. Initially, 118 patients were recruited on lisinopril and 61 on metoprolol; and for the purpose of efficacy analysis at week 8, 115 patients on lisinopril and 60 on metoprolol were included. The doses of lisinopril or metoprolol were 40-80 mg/day and 100-200 mg/day, respectively. At week 4, the pretreatment diastolic blood pressure of 111 mm Hg was decreased to 97 mm Hg (p less than 0.01) with lisinopril: metoprolol decreased the diastolic blood pressure from 110 to 99 mm Hg (p less than 0.01). Similar decreases were noted at week 8; however, the drop in blood pressure with lisinopril was not significantly different from that with metoprolol. Systolic blood pressure also demonstrated a decrease of about 18 mm Hg with lisinopril and 12 mm Hg with metoprolol (p less than 0.01). This larger decrease in systolic blood pressure with lisinopril was statistically significant at week 4 (p less than 0.05). These decreases in systolic blood pressures were maintained at week 8, again with statistical significance (p less than 0.01). Of the 118 lisinopril-treated patients, four were discontinued from lisinopril therapy because of headache, dizziness, rash, flushing, or lymphadenopathy. Four patients out of 61 (9.8%) were discontinued from metoprolol therapy because of fatigue, somnolence, asthenia, weight gain, flatulence, tremor, or bronchospasm. In conclusion, lisinopril 40-80 mg once daily is as effective as metoprolol 100-200 mg once daily in reducing diastolic blood pressure in patients with moderate to severe hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1987
PMID:Evaluation of antihypertensive efficacy of lisinopril compared to metoprolol in moderate to severe hypertension. 244 53

Several mechanisms have been suggested for the absence of reflex tachycardia in response to the hypotensive effect of the selective alpha 1-adrenoceptor antagonist indoramin, including, in animals, membrane-stabilising activity, prolongation of repolarisation time, and reduction in baroreflex sensitivity. The present study investigated the effect of acute and chronic oral administration of indoramin (50 mg daily for 8 days) on baroreflex sensitivity in six healthy male volunteers. Baroreflex function was measured by determining the relationship between systolic blood pressure (SBP) and R-R interval following intravenous administration of phenylephrine. Indoramin shifted (p less than 0.05) the phenylephrine dose-response curve to the right on days 1 and 8 compared with placebo. Baroreflex sensitivity [R-R (ms)/SBP (mm Hg)] was reduced (p less than 0.05) by indoramin on day 1 compared with placebo (18.3 +/- 1.3 vs. 11.2 +/- 2.2 ms/mm Hg), and on day 8 compared with pretreatment values (18.3 +/- 2.8 vs. 10.8 +/- 1.8 ms/mm Hg). Acute but not chronic administration of indoramin caused (p less than 0.05) sedation; tremor tended to increase with chronic administration. It is suggested that depression of baroreflex sensitivity by indoramin may explain, in part, the lack of reflex tachycardia associated with its antihypertensive effect.
J Cardiovasc Pharmacol 1988 Mar
PMID:Effect of acute and chronic indoramin administration on baroreflex function and tremor in humans. 245 20

The effects of three different nonselective beta-blockers on central and peripheral hemodynamics as well as on pulmonary function were compared in 13 healthy subjects (19-37 years). The subjects were given carvedilol 50 mg, pindolol 10 mg, propranolol 80 mg, and placebo orally twice daily for 1 week in a double-blind, crossover, randomized manner. Heart rate, blood pressure, arterial calf blood flow (venous occlusion strain gauge plethysmography), and pulmonary function (flow-volume spirometry) were measured at the first and at the last trial day. Heart rate and blood pressure were lower on carvedilol and propranolol than on pindolol and placebo; the maximal bradycardiac effect was 13 and 17 beats/min and hypotensive effect 9/10 mm Hg and 10/7 mm Hg on carvedilol and propranolol, respectively. Both carvedilol and pindolol increased arterial flow by about 40% (p less than 0.05 and p less than 0.01, respectively) and reduced peripheral resistance by about 34% (p less than 0.05 and p less than 0.01, respectively), the effect persisting after 1 week of treatment. None of the medications had any noteworthy effects on pulmonary function. Two subjects complained of tremor on pindolol. We conclude that carvedilol and pindolol possess distinct vasodilatory properties. Carvedilol had a stronger hypotensive effect than pindolol and was well tolerated.
J Cardiovasc Pharmacol 1987
PMID:Vasodilatory effects of carvedilol and pindolol. 245 73

The selectivity of single oral doses of xamoterol, 200 mg, prenalterol, 50 mg, and salbutamol, 8 mg, was compared in eight healthy male volunteers by measuring their effects on sleeping heart rate, supine heart rate, blood pressure, forearm blood flow, finger tremor, and exercise heart rate in the presence and absence of the specific beta 2-adrenoceptor antagonist ICI 118,551, 25 mg. Xamoterol, 200 mg, increased sleeping heart rate and systolic blood pressure, decreased exercise heart rate, and had no effect on diastolic blood pressure, forearm blood flow, or finger tremor. The concurrent administration of ICI 118,551, 25 mg, did not alter these results. Supine heart rate was increased by xamoterol and did not differ from that for xamoterol with ICI 118,551. Prenalterol, 50 mg, increased sleeping heart rate, supine heart rate, systolic blood pressure, forearm blood flow, and finger tremor, decreased diastolic blood pressure, and had no effect on exercise tachycardia. The concurrent administration of ICI 118,551 with prenalterol reduced the increase in sleeping heart rate, supine heart rate, and forearm blood flow, and reduced the fall in diastolic blood pressure caused by prenalterol alone. The increase in finger tremor following prenalterol with ICI 118,551 tended to be less than that following prenalterol. Salbutamol, 8 mg, increased sleeping heart rate, supine heart rate, systolic blood pressure, forearm blood flow, finger tremor, and exercise heart rate, and caused a fall in diastolic blood pressure. When salbutamol, 8 mg, was administered with ICI 118,551, 25 mg, the only changes detected were a small initial increase in finger tremor and a small rise in diastolic blood pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
J Cardiovasc Pharmacol 1988 May
PMID:The selectivity of xamoterol, prenalterol, and salbutamol as assessed by their effects in the presence and absence of ICI 118,551. 245 40

A method is described for studying platelet function in human whole blood immediately after venepuncture in order to evaluate the antithrombotic potential of new pharmacological agents. In this method, platelet aggregation is quantified by measuring the fall in single platelet count, by using a whole blood platelet counter. We have investigated the platelet aggregation inhibitory effects of the new positive inotropic agents pimobendan and UD CG 212 (reported to be Ca++ sensitisers and phosphodiesterase inhibitors), alone and in combination with dipyridamole. Venous blood was drawn directly into prewarmed (37 degrees C) plastic syringes containing anticoagulants (3.2% trisodium citrate solution) plus a platelet aggregation inhibitor. Spontaneous platelet aggregation (SPA) was studied by roller mixing aliquots of blood in the collecting syringes for 6 min at 37 degrees C. Collagen induced platelet aggregation was studied by incubating aliquots of blood with 1 microgram/ml collagen on a shaking water bath for 3 min. In the absence of an inhibitor, there was a 50% fall in single platelet count due to SPA and a 65% fall was induced by collagen. Both SPA and collagen induced aggregation responses were inhibited by pimobendan (0.5-10 microM) and UD CG 212 (0.5-10 microM), in a dose dependent manner. A combination of 10 microM dipyridamole with 2 microM pimobendan or UD CG 212 was markedly a more effective inhibitor of platelet aggregation than a high dose of either inhibitor alone. It is suggested that the present method is simple and rapid, with minimal sample processing, and therefore the results may be protected from serious artifacts.(ABSTRACT TRUNCATED AT 250 WORDS)
Cardiovasc Res 1989 Mar
PMID:Platelet aggregation inhibitory effects of the new positive inotropic agents pimobendan and UD CG 212 in whole blood. 259 Sep 3

The cardiovascular and behavioral actions of cimetidine, injected into the lateral ventricle, were studied in conscious, freely moving rats. Cimetidine produced a dose-dependent pressor response accompanied by decreases in heart rate and increases in pulse pressure. At doses of 25-100 micrograms, cimetidine produced sedation; however, when 200 micrograms was injected, tremor was observed in all animals. If cimetidine was administered twice within 30 min to the same animal, tachyphylaxis in response to any of these actions was never evident. Although histamine produced similar pressor actions when administered intraventricularly, these effects were always subject to tachyphylaxis. The actions of cimetidine were not altered by central pretreatment with the H1 antagonist chlorpheniramine. A possible hypothesis of the central mechanism by which cimetidine produces these effects is discussed.
J Cardiovasc Pharmacol
PMID:Cardiovascular and behavioral actions of centrally administered cimetidine. 620 9

Previous studies have suggested that racial differences may exist in beta-adrenoceptor-mediated responsiveness. However, no clear conclusions can be drawn based on these studies because of the confounding effect of the parasympathetic nervous system on responses to isoproterenol bolus doses. In this study, we blocked the effects of the parasympathetic nervous system with atropine, to determine whether racial differences exist in sensitivity to beta-adrenoreceptor stimulation and blockade. Sixteen healthy black and white men participated in the study. Atropine was administered before all studies to induce parasympathetic blockade. Isoproterenol sensitivity studies and treadmill exercise were then performed in the with and without beta-adrenoceptor blockade by propranolol. Responses measured included heart rate (HR), blood pressure (BP), and tremor. The average isoproterenol dose producing a 25-beat/min increase in HR was more than twofold higher in blacks than in whites (3.4 +/- 1.2 vs. 1.6 +/- 0.4 micrograms, respectively, p < 0.05). There were no racial differences in response to beta-adrenoreceptor blockade. Our results showed that during parasympathetic blockade blacks were less sensitive to the chronotropic effects of isoproterenol than whites. We conclude that these response differences are due to greater beta-adrenoceptor sensitivity in whites than in blacks.
J Cardiovasc Pharmacol 1995 Jan
PMID:Racial differences in beta-adrenoceptor-mediated responsiveness. 772 60

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
J Cardiovasc Pharmacol 1996
PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99

Beta-adrenergic-blocking drugs (BABs) have a firm place in the therapy of cardiovascular conditions including angina and hypertension. Although all BABs are competitive inhibitors of beta-receptors, they may differ in their additional pharmacodynamics, i.e., beta1-(cardio)selectivity, partial agonistic activity (PAA), and pharmacokinetic properties. Understanding these additional properties would allow the physician to choose the more appropriate agent for some patients or for specific situations. beta1-Selective BABs may be of potential importance in patients with obstructive airway disease, peripheral vascular disease, and hyperlipidemia and in diabetic patients receiving antidiabetic drugs. These BABs may better control the increased blood pressure in response to hypoglycemia, exercise, or cigarette smoking. Nonselective BABs may be preferably used to decrease epinephrine-induced hypokalemia or to prevent myocardial infarction, and in certain circumstances (i.e., migraine, anxiety, thyrotoxicosis or essential tremor). BABs with PAA may theoretically cause a lesser degree of cardiodepression (reduction of heart rate at rest, cardiac output, and AV conduction), bronchospasm, and peripheral vasoconstriction and minor effects on plasma lipids. Withdrawal syndrome may be absent after BABs with PAA. The pharmacokinetic properties of the BABs such as absorption, bioavailability, elimination half-life, liver metabolization, interindividual variability, as well as pharmacological interactions depend on their hydrophilic/lipophilic ratio. The development of new BABs continues. It has been possible to incorporate into a drug molecule combinations of PAA, preferred beta1-blockade, and beta2-agonist activity. Even if these new agents cause less adverse effects (e.g., vasoconstriction, bronchospasm), their clinical significance remains to be established.
J Cardiovasc Pharmacol 1990
PMID:Optimization of beta-blockers' pharmacology. 1152 10


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