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PubMedDate not supplied

Effect of desipramine on propranolol-induced diminution of noradrenaline release by nerve stimulation.

In atria from rats killed 1 h after either chronic parenteral (daily subcutaneous injections of 5 mg/kg/day for 15 days) or prolonged oral administration of (-)-propranolol (1 mg/ml ad libitum during 15 days) there was a 50% decrease in the overflow of [3H]noradrenaline ([3H]NA) elicited by cardioaccelerans nerve stimulation at 2 Hz, as previously reported for the in vitro exposure of guinea pig atria to propranolol. The chronotropic responses to nerve stimulation and to isoprenaline were also significantly reduced. On the other hand, 40 h after the last injection of propranolol, the overflow of [3H]NA induced by stimulation was still reduced to 50% of the control values, whereas no blockage to nerve stimulation or to isoprenaline was observed. Neither the basal output of [3H]NA nor the tissue levels of the endogenous transmitter were modified by any of the treatment schedules applied. In a separate set of experiments performed in isolated guinea pig atria stimulated at 4 Hz during 1 min, the in vitro exposure to 0.5 microM desipramine prevented the 30% decrease in the overflow of [3H]NA caused by 0.1 microM (-)-propranolol. Desipramine, by itself, did not modify the overflow of the transmitter. It is concluded that propranolol, both in vitro and after chronic in vivo treatments, reduces the overflow of [3H]NA in response to nerve stimulation. The fact that the in vitro effect of the beta-blocker is antagonized by desipramine suggests that propranolol may have to be taken up by the nerve terminals in order to exert its presynaptic inhibition on the release of noradrenaline.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Time course of blood pressure changes after intravenous administration of propranolol or furosemide in hypertensive patients.

The time course of changes in supine and standing blood pressures, heart rate, plasma renin activity, and plasma noradrenaline concentration after intravenous administration of propranolol (0.20 mg . kg-1, with a maximum of 15 mg) or furosemide (40 mg) was studied for a period of 8 h in hypertensive patients. Twenty minutes after intravenous injection of propranolol or furosemide, supine blood pressure was unchanged. Thereafter, blood pressure started to decrease gradually. Maximum reduction was obtained after 4-5 h. Twenty minutes after administration of propranolol, heart rate and plasma renin activity were reduced, and remained so during the following 8 h. Supine plasma noradrenaline concentration did not change significantly after propranolol, but standing levels, showed a tendency to increase as blood pressure fell. Twenty minutes after administration of furosemide, plasma renin activity was increased and remained elevated during the following 8 h. Heart rate and plasma noradrenaline concentration were unchanged after 20 min, but both increased gradually as blood pressure started to fall. The results show that intravenous administration of both propranolol and furosemide leads to a delayed reduction of blood pressure. The increase in total peripheral resistance, which prevents blood pressure from falling acutely after intravenous injection of propranolol, is not reflected in an acute rise in plasma noradrenaline. The delayed hypotensive response does not seem to be due to a return of sympathetic activity to pretreatment levels, since plasma noradrenaline concentration shows a tendency to rise as blood pressure falls.

Adult↗
PubMed1985

Clinical effects of low-dose captopril plus a thiazide diuretic on mild to moderate essential hypertension: a multicenter double-blind comparison with propranolol. Captopril Research Group of Japan.

A total of 270 patients with mild to moderate essential hypertension were evaluated in a multicenter double-blind randomized study that compared the effect of captopril plus a thiazide diuretic with that of propranolol plus a diuretic. All patients were previously uncontrolled with diuretics alone. Following a 4-week placebo control period, during which diuretic was not withdrawn, the patients were treated either with 37.5-75 mg/day of captopril (n = 133) or with 60-120 mg/day of propranolol (n = 137) for 12 weeks, the diuretic being continued in both groups. Blood pressure in both groups was significantly reduced after 2 weeks of treatment. Reduction in systolic but not diastolic blood pressure after 10 and 12 weeks of treatment was significantly greater in the captopril group than in the propranolol group (p less than 0.05). Treatment was considered to be effective in 77% of the captopril patients and in 61% of the propranolol group. The difference was significant (p less than 0.05). Side effects occurred in 6 of the 133 patients (4.5%) treated with captopril and in 16 of the 137 patients (11.7%) treated with propranolol. The difference between the two groups was significant (p less than 0.05). There were few significant changes in laboratory data in either group. The serious side effects previously reported with higher doses of captopril were not observed. The results indicate that low-dose captopril plus a diuretic is more efficacious than propranolol plus a diuretic in mild to moderate essential hypertension previously uncontrolled with a diuretic alone.

Adult↗
PubMed1987

Effects of metoprolol, alone and in combination with lidocaine, on ventricular fibrillation threshold: comparison with atenolol, propranolol, and pindolol.

Metoprolol and other beta-adrenergic blocking drugs are known to exert cardioprotective effects that include significant reduction in occurrence of ventricular fibrillation (VF) following myocardial ischemia and infarction. To help determine the mechanism of these cardioprotective effects, this study evaluated the effect of equipotent beta-blocking doses of metoprolol and three other beta-blockers with differing ancillary properties on ventricular fibrillation threshold (VFT) in the normal canine heart. Metoprolol tartrate (1.0 mg/kg i.v.), atenolol (0.3 mg/kg i.v.), propranolol hydrochloride (0.3 mg/kg i.v.), pindolol (0.03 mg/kg i.v.), or saline control (0.9% NaCl solution; vehicle) was given, alone and in combination with lidocaine (L), to groups of six pentobarbital (32.5 mg/kg i.v.) anesthetized mongrel dogs after control VFT and control isoproterenol-induced (ISO) positive chronotropic effects had been determined. The D- (membrane stabilizing, non-beta blocking) and L- (beta blocking) isomers of propranolol also were administered to separate groups of six anesthetized dogs in a dose of 0.3 mg/kg i.v. Blood samples (venous) were taken before drug or vehicle administration, 10 min after drug/vehicle administration and at half-hour intervals thereafter during experimentation. ISO responses and VFT were determined 5 and 15 min, respectively, after drug/vehicle administration and at half-hour intervals for a total experimental period of 165 min. VF was induced with a train of pulses (5 s, 100 Hz, 3-ms duration, 250-omega resistance) applied by bipolar platinum electrodes to a paced heart (200 beats/min). Voltage (V) was increased every 60 sec (0.25-V increments between 0-3.5 V and 0.5-V increments greater than 3.5 V) until VF occurred. Metoprolol increased VFT significantly (p less than 0.05) and maximally (max delta V = 2.3 +/- 0.7 V) at 135 min postdrug when the ISO-induced increase in heart rate was inhibited (%I ISO) by less than 53%. Max delta V was not significantly increased following i.v. administration of atenolol (0.8 +/- 0.6 V), pindolol (0.1 +/- 0.1 V), or saline (0.1 +/- 0.1 V). Max delta V was 0.5 +/- 0.2 in the D-propranolol-treated group and 0.5 +/- 0.3 in the L-propranolol-treated group. These values did not differ from max delta V obtained in the propranolol-treated group (0.6 +/- 0.4 V). Changes in VFT for all groups were, over time, negatively correlated with %I ISO and were not dependent on membrane stabilizing effect (metoprolol, propranolol (D,DL), pindolol), intrinsic sympathomimetic activity (pindolol), or cardioselectivity (metoprolol, atenolol).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1990

Effects of propranolol on premature action potentials in canine Purkinje and ventricular muscle.

We compared the effects of a low (0.09 microgram/ml) concentration of propranolol expected to produce only beta-adrenoceptor blockade and a high concentration (0.9 microgram/ml) expected to produce additional direct local anesthetic-like electrophysiological effects on basic and premature action potentials. Both isolated dog cardiac Purkinje and ventricular muscle fibers were examined using conventional microelectrode techniques. The low concentration of propranolol produced no significant electrophysiological change in either fiber type. The high concentration of propranolol shortened the action potential duration and refractoriness while decreasing the maximal upstroke velocity (Vmax) in both Purkinje and ventricular muscle fibers at a constant basic cycle length. In Purkinje fibers, the high concentration also slowed the kinetics of restitution of the action potential duration (tau c from 124.6 +/- 6.5 to 201.4 +/- 16.0 ms, p less than 0.01, n = 7), slowed the recovery kinetics of Vmax, and shifted the early portion of the normalized restitution curve toward longer action potential duration values in both fiber types. The range of premature action potential durations, defined as the difference between action potential durations during the first 100 ms of restitution, was decreased by the high concentration of propranolol in both Purkinje and ventricular muscle fibers by 39.5% and 33.9%, respectively. These findings indicate that (a) low concentrations of propranolol produced no direct electrophysiological effect, and (b) high concentrations of propranolol produced several potential antiarrhythmic effects in addition to the previously reported effects on Vmax and the action potential duration.

Action Potentials↗
PubMed1991

The pharmacokinetic and pharmacodynamic interaction between lacidipine and propranolol in healthy volunteers.

The pharmacokinetic and pharmacodynamic profiles of lacidipine, a 1,4-dihydropyridine calcium antagonist, and the beta-adrenoceptor blocker propranolol were determined alone and in combination in 24 healthy male volunteers. One group (I) of 12 subjects received a single oral dose of 4 mg lacidipine on two separate occasions, which was taken together with a single oral dose of either 160 mg propranolol or placebo; a second group (II) of 12 subjects received propranolol on two occasions, taken with either lacidipine or placebo. Propranolol significantly decreased the maximum plasma concentration (Cmax) and area under the plasma concentration-time curve (AUC) of lacidipine (by 38% and 42%, respectively) whereas lacidipine significantly increased the Cmax and AUC of propranolol (by 35% and 26%, respectively); neither the time to maximum plasma concentration (tmax) nor the terminal half-life (t 1/2) were affected. With regard to the pharmacodynamics, in Group I, there was a greater reduction in supine systolic blood pressure (6 mm Hg) and diastolic blood pressure (4 mm Hg) compared to the reduction produced by lacidipine alone, and pulse rate was approximately 5 beats/min less. In Group II, a significantly greater reduction (6 mm Hg) in supine systolic blood pressure compared to the reduction produced by propranolol alone occurred, but there was no marked difference in supine diastolic blood pressure and pulse rate. In conclusion, a modest pharmacokinetic and pharmacodynamic interaction is evident and should be evaluated further in patients with hypertension.

Administration, Oral↗
PubMed1991

Myocardial adaptation to chronic propranolol therapy in diabetic rats.

The myocardial adaptation to chronic beta-adrenergic blockade was explored in diabetic and control female Wistar rats. Propranolol was administered by intraperitoneal injection, 30 mg/kg every 12 h. Treatment began 2 months after streptozotocin injection and at a comparable time in controls. Diabetes reduced the heart rate by 90 beats/min; propranolol decreased the heart rate by 30 beats/min further in diabetic rats. Propranolol reduced the heart rate by 100 beats/min in controls. Study of isolated ventricular papillary muscle showed qualitatively similar effects of propranolol in control and diabetic animals. Diabetes resulted in prolonged contraction duration and decreased shortening velocity; both developed tension and peak shortening were unchanged. In contrast, propranolol resulted in prolonged contraction duration but no change in shortening velocity; both developed tension and peak shortening were increased. The shortening of isometric relaxation in response to norepinephrine was exaggerated with propranolol therapy in control but not diabetic rats. These findings indicate that the myocardial adaptation to chronic beta-blockade results in increased developed tension and increased extent of muscle shortening in vitro, and differs qualitatively from the adaptation to diabetes.

Animals↗
PubMed1992

Cardiac microdialysis measurement of extracellular adenine nucleotide breakdown products during regional ischemia and reperfusion in canine heart: protective effect of propranolol against reperfusion injury.

Using cardiac microdialysis, we studied release of the adenine nucleotide breakdown products (ANBP) adenosine (ADS), inosine (INS), and hypoxanthine (HYP) into the interstitium of canine myocardium during 20- and 40-min occlusion of the anterior descending coronary artery and reperfusion. Dialysate ANBP concentrations reached maximum values not at the end of ischemia but in the first 10 min of reperfusion. The effect was more pronounced after 20-min ischemia. Further reperfusion led to an ANBP decrease that was more prolonged after 40-min ischemia. Pretreatment with DL-propranolol (0.5 mg/kg, intravenously, i.v.) given 40 min before coronary occlusion had no effect on adenine nucleotide catabolism rate during 20- and 40-min ischemia, but it facilitated washout of ANBP from ischemic zone immediately after the start of reperfusion. A similar effect was elicited by a D-stereoisomer of propranolol with no beta-adrenoceptor blocking activity. Results suggest that the reperfusion injury and probably the no-reflow phenomenon were the cause of enhanced adenine nucleotide catabolism at the beginning of reperfusion and prolonged ANBP washout from the ischemic zone. Reduction of reperfusion injury by propranolol could be related to the membrane stabilizing and antioxidant activity of this agent. Examination of DL-propranolol kinetics in arterial and coronary venous blood plasma showed that drug accumulation in the myocardium was almost maximum at the start of ischemia; therefore, the efficiency of cardio-protection with DL-propranolol was not limited by pharmacokinetic causes. Insertion of an additional microdialysis probe in the myocardium allowed monitoring of extracellular propranolol concentrations.

Adenine Nucleotides↗
PubMed1994

Cardiodepressant actions of combined diltiazem and propranolol in dogs.

The cardiovascular actions of combined intravenous (i.v.) diltiazem and propranolol were studied in barbiturate-anesthetized dogs. When given alone, diltiazem increased cardiac output (CO) and P-R interval duration (P-R) while decreasing mean arterial pressure (MAP), heart rate (HR), and systemic vascular resistance (SVR). Propranolol alone decreased CO and HR while increasing SVR. With the same i.v. doses, combined infusion of diltiazem and propranolol rapidly resulted in depression of CO to levels similar to those achieved with propranolol beta-adrenoceptor blockade alone. The combination decreased MAP to levels achieved with diltiazem-induced calcium channel blockade. P-R increased beyond the durations produced by either drug given alone. Pharmacokinetic interactions were not apparent, although slight increases in propranolol plasma concentrations were observed during combined drug infusions. These studies support clinical observations that the cardiovascular effects resulting from a combination of diltiazem and propranolol may be attributed to the characteristic cardiovascular actions of each individual drug.

Animals↗
PubMed2000

Effects of prolonged propranolol treatment on left ventricular remodeling and oxidative stress after myocardial infarction in rats.

Mechanisms determining the benefit of beta blockade in patients with heart failure remain incompletely understood but are assumed consequent to prevention of deleterious effects of catecholamines. Recent studies have demonstrated that oxidative stress in congestive heart failure may be related to increased catecholamine levels. The aim of this study was to examine effects of long-term treatment with propranolol on progression of left ventricular (LV) dysfunction, remodeling and oxidative stress on an experimental model of chronic heart failure. Six weeks after myocardial infarction by coronary ligation, Wistar rats were randomized to two groups: 10 weeks of therapy with propranolol (50 mg/kg/day in drinking water) and no treatment (infarcted controls). A third group was sham-operated rats without treatment. Animals were anesthetized for hemodynamic measurements, and hearts were then removed for histologic analysis, papillary muscle contractility study, and oxidative stress measurements using thiobarbituric acid reactive substance (TBARS) determination. Control infarcted rats demonstrated significant alterations of hemodynamic parameters and remodeling with increase of heart weight/body weight, of right ventricular lateral wall thickness, of LV circumference, LV septal area/body weight, and LV papillary muscle weight/body weight as compared with sham. In propranolol-treated rats, hypertrophy of the LV septum, papillary muscle, and right ventricle were similar to those of the infarcted control. Myocardial oxidative stress was significantly increased in control infarcted rats compared with sham, and propranolol prevented such oxidative stress increase. Papillary muscle isometric tension parameters were not significantly different among groups. Propranolol treatment prevented isoprenaline-induced spontaneous papillary muscle activity in vitro. Oxidative stress is increased in the rat model of heart failure secondary to coronary ligation. Long-term treatment with propranolol in vivo does not modify the compensatory process of hypertrophy but completely abolishes the oxidative stress increase and reduces the increased cardiac sensitivity to catecholamine-induced arrhythmias observed in this experimental model of heart failure.

Animals↗
PubMed1985

Assessment of blood collection systems for the high performance liquid chromatography measurement of propranolol.

The effect of blood collection devices on the high performance liquid chromatography (HPLC) measurement of propranolol was assessed. Blood was collected from hypertensive patients treated with propranolol for at least 7 days. Two venipunctures (opposite arm technique) were performed on each patient using the reference (syringe/silanized, ethylene diamintetraacetate tubes) procedure and the Vacutainer Brand Tubes (lavender-, royal blue-, green-, and red-stoppered) that were free of tris(2-butoxyethyl) phosphate. Propranolol concentrations were determined utilizing a published HPLC procedure. This study showed that in the four evacuated tubes, propranolol concentrations in serum or plasma were highly correlated to those of the reference procedure (correlation coefficients, 0.986 to 0.997; and slope, 0.912 to 1.013). Mean propranolol concentrations of the red-stoppered tube serum were lower (7.5%) than that of the reference syringe (0.01 less than p less than 0.05). Thus, lavender-, royal blue-, green-, and red-stoppered tubes would be acceptable for propranolol monitoring.

Blood Specimen Collection↗
PubMed1994

Evaluation of dosage-release formulations on inhibition of drug clearance: effect of sustained- and immediate-release verapamil on propranolol pharmacokinetic parameters.

Limited information exists regarding the influence of dosage-release formulation on inhibition of drug metabolism. Therefore, the purpose of this study was to evaluate the effect of immediate-release (IR) and sustained-release (SR) verapamil on the pharmacokinetic parameters of propranolol in 12 healthy men. IR propranolol, 160 mg, was administered alone (Phase A) and following either IR verapamil, 80 mg t.i.d., (Phase B) or SR verapamil, 240 mg q.d., (Phase C) in a randomized crossover fashion. Of the 12 subjects enrolled, only seven were able to be analyzed secondary to assay interference. Oral clearances for L-propranolol for Phases A, B, and C were 198 +/- 70, 156 +/- 76, and 143 +/- 85 L/h, respectively. Oral clearances for D-propranolol for Phases A, B, and C were 203 +/- 96, 172 +/- 96, and 152 +/- 102 L/h, respectively. No significant differences were observed. However, when the verapamil groups (Phase B and C) were combined and compared to Phase A, a significant decrease in clearance for propranolol isomers was observed. In conclusion, due to the unexpected low numbers of patients evaluated, no significant differences in oral clearance were observed among the three treatment phases. However, there is a trend suggesting that SR verapamil had the greatest effect on propranolol clearance, which may warrant caution when changing from one formulation to another.

Adult↗
PubMed1999

Lack of effect of propranolol in the prevention of large oesophageal varices in patients with cirrhosis: a randomized trial. French-Speaking Club for the Study of Portal Hypertension.

OBJECTIVE: Beta-blockers have been shown to reduce portal pressure in patients with cirrhosis and limit the development of portosystemic shunts in portal hypertensive animals. Thus, a randomized double-blind trial was conducted to evaluate propranolol in the prevention of the development of large oesophageal varices in patients with cirrhosis without varices or with small varices. METHODS: One hundred and two patients received long-acting propranolol (160 mg/day) and 104 patients received a placebo. At inclusion, there was no significant difference between the two groups in terms of clinical characteristics or biochemical tests. At 2 years, the size of varices was estimated on video recordings. RESULTS: One-third of the patients were lost to follow-up, and 95%/97% of the remaining patients were compliant in the propranolol and placebo groups, respectively. At 2 years, the proportion of patients with large varices was 31% in the propranolol group and 14% in the placebo group (P< 0.05). Three and four patients bled in the propranolol and placebo groups, respectively, and nine and ten died, respectively. CONCLUSION: This trial suggests that propranolol administration cannot be recommended for the prevention of the development of large oesophageal varices in patients with cirrhosis; thus other studies are needed in selected subgroups of patients.

Adrenergic beta-Antagonists↗
PubMed2003

Short-term selection for the interaction between S-propranolol and ethanol in mice.

BACKGROUND: We have previously demonstrated that there is an interaction between S-propranolol, a beta-adrenergic blocking agent, and ethanol on the hypnotic sensitivity of inbred short- and long-sleep mice (ISS and ILS). We found that the interaction was due to an additive hypothermic effect of ethanol and S-propranolol that markedly decreased the disappearance rate of ethanol. There was no discernible effect of S-propranolol on the hypnotic actions of ethanol as evidenced by the waking blood ethanol levels. Because ISS mice were more sensitive to this effect than were ILS mice, it seemed that there was a genetic effect to the response. Therefore, we carried out a short-term breeding project to determine whether the response could be selectively bred. METHODS: We used the heterogeneous stock of mice from the Institute for Behavioral Genetics to carry out the selection study. The index for selection was the difference in sleep time between the same animal treated with propranolol and ethanol versus treatment with saline and ethanol at least 1 week apart. RESULTS: In four generations, we were able to achieve separation between mice with a large difference in sleep time (high line) from those with a smaller difference in sleep (low line) time. There was no difference between the average blood ethanol at awakening in the high line versus the low line. The effect was not due to a difference in rate of propranolol metabolism between the two lines. Sleep time with ethanol alone was not different between the high and low lines. CONCLUSIONS: The magnitude of the interaction between ethanol and S-propranolol is controlled by alleles with polymorphisms present in the HS stock of mice. The response is most likely due to a difference in the mechanisms of thermogenesis controlled by the beta-adrenergic receptors in muscle and fat. Because there were no sleep time differences between the high and low lines given ethanol alone, central nervous system sensitivity to ethanol is not a correlated response to the selection.

Animals↗
PubMed2004

The antihypertensive efficacy and safety of a chronotherapeutic formulation of propranolol in patients with hypertension.

This study evaluated the antihypertensive efficacy and tolerability of a chronotherapeutic formulation of propranolol designed for nighttime dosing (propranolol controlled release [CR]). A total of 434 patients with mild-to-moderate hypertension were randomized to placebo or to one of four doses of propranolol CR (80, 120, 160, or 640 mg/d). At baseline, the mean morning blood pressures were similar in each treatment group and averaged 152/101 mm Hg. After 8 weeks of treatment, morning diastolic blood pressure, the primary efficacy measurement, was significantly reduced from baseline in placebo (-6.98 mm Hg) and all propranolol groups (p<0.001). The decreases ranged from 10.1 mm Hg in the 80-mg/d group to 11.0 mm Hg in the 120-mg/d group and were significantly larger than placebo in the 120-, 160-, and 640-mg/d groups (p<0.05). Blood pressure measured in the evening (trough) demonstrated similar antihypertensive efficacy. Heart rate and rate-pressure product were reduced in a dose-related manner by propranolol CR. The formulation was well tolerated with only fatigue and dizziness being reported more frequently than in the placebo group. Propranolol CR is an effective antihypertensive formulation that may reduce blood pressure during the morning period of maximum cardiovascular risk.

Adult↗
PubMed1975

Plasma levels and beta-adrenoceptor blockade with acebutolol, practolol and propranolol in man.

1 The degree of beta-adrenoceptor blockade of isoprenaline-induced tachycardia has been determined in three healthy volunteers after the administration of single oral doses of acebutolol, practolol or propranolol. 2 Plasma levels of these drugs were determined either colorimetrically (acebutolol and practolol) or fluorimetrically (propranolol). The colorimetric assay of acebutolol in plasma is fully described but the other drugs were assayed by published methods. 3 The degree of beta-adrenoceptor blockade and the plasma level for acebutolol and practolol were well correlated, whereas in the case of propranolol correlation was poor, due in part to the presence in plasma of active metabolites not detected by the fluorimetric assay. The plasma levels of practolol and propranolol are in agreement with those previously reported. 4 The maximum cardiac beta-adrenoceptor blockade achieved in this study with the respective single oral doses of acebutolol (300 mg), practolol (400 mg) or propranolol (40 mg) were similar in each of the three subjects. Therefore the beta-adrenoceptor blocking potencies of these drugs against isoprenaline-induced tachycardia are inversely related to these doses; indicating that propranolol is 7-8 times more potent than acebutolol and the latter slightly more potent than practolol.

Acebutolol↗
PubMed1978

Plasma protein binding of propranolol and isoprenaline in hyperthyroidism and hypothyroidism.

1. The possibility that thyroid disease might result in alterations in the plasma proteins binding of drugs has been investigated by studying the binding of propranolol and isoprenaline in patients with hyperthyroidism and hypothyroidism. 2. Plasma protein binding of propranolol and isoprenaline has been measured in seven hyperthyroid patients and ten hypothyroid patients. Plasma binding was estimated by equilibrium dialysis at 37 degree C using triatiated propranolol and isoprenaline, both when the patients had thyroid dysfunction and again when they were euthyroid. 3. In the hyperthyroid group, mean propranolol binding varied from 86 +/- 1.7% when hyperthyroid to 88.4 +/- 0.8% when euthyroid. The comparable isoprenaline figures were 65.1 +/- 3.2% and 68.1 +/- 1.4% respectively. Neither difference was significant. 4. Isoprenaline binding was significantly lower (64.3 +/- 1.6%) when patients were hypothyroid than when they became euthyroid (68.8 +/- 1.2%). Propranolol binding was not altered by hypothyroidism. 5. It is concluded that clinically important alterations in free drug concentrations of propranolol or isoprenaline do not occur in hyperthyroidism or hypothyroidism.

Adult↗
PubMed1978

Effect of propranolol on sympathetic nervous activity in hydrallazine-treated hypertensive patients.

1 The effect of propranolol was examined on a) blood pressure and heart rate responses due to i.v. hydrallazine b) modification of these cardiovascular parameters during cold pressor test c) urinary catecholamine excretion rate. 2 Intravenous hydrallazine reduced significantly mean blood pressure by 15.2 mm Hg and increased heart rate by 24.9 beats/min. Propranolol reduced significantly mean blood pressure by 19.0 mm Hg and heart rate by 14.1 beats/min. Hydrallazine plus propranolol caused a significant reduction of mean blood pressure (by 37.7 mm Hg) but this was not accompanied by a significant fall in heart rate (by 3.3 beats/min). 3 During the control period, cold pressor test increased mean blood pressure by 16.0 mm Hg. Heart rate was increased by 12.5 beats/min in four patients. However, there was a reduction in heart rate (5.5 beats/min) in two other patients. During the propranolol period, cold pressor test-induced increase of mean blood pressure was not reduced but propranolol blocked the increase of heart rate. 4 Urinary catecholamine excretion rate was increased during hydrallazine administration. This excretion was not modified by propranolol.

Adult↗