Our library of drug research abstracts drawn from the medical literature is updated on a regular schedule, and you can be assured that new propranolol research articles will be listed here shortly after becoming available to us.
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Medical research on propranolol
Regulation of sympathetic nerve activity by l-carnosine in mammalian white adipose tissue.
Neurosci Lett. 2008 Jun 14;
Shen J, Yao JF, Tanida M, Nagai K
Previously, we showed that l-carnosine, a bioactive dipeptide, influences the sympathetic nerve activity innervating kidney and brown adipose tissue. Because the autonomic nervous system plays an important role in the regulation of lipid metabolism, we investigated the in vivo effects of l-carnosine on the sympathetic nerve activity innervating white adipose tissue (SNA-WAT) and lipolysis. We found that intraperitoneal (ip) administration of l-carnosine at doses of 100ng/rat and 10mug/rat elevated and suppressed SNA-WAT, respectively. The effect of lower dose of l-carnosine (100ng/rat) was eliminated by pretreatment with diphenhydramine hydrochloride, a histamine H(1) receptor antagonist. In contrast, the effect of higher dose of l-carnosine (10mug/rat) was suppressed by thioperamide maleate salt, a histamine H(3) receptor antagonist. Moreover, ip administration of 100ng and 10mug of l-carnosine increased and decreased the levels of plasma free fatty acids (FFAs), respectively. The changes of plasma FFAs resulting from the exposure to 100ng and 10mug of l-carnosine were diminished by the beta-adrenergic receptor blocker propranolol hydrochloride and the muscarinic receptor blocker atropine sulfate, respectively; and eliminated by the corresponding histamine receptor antagonists, which eliminated the changes in SNA-WAT. Our results suggest that low doses of l-carnosine may regulate the lipolytic processes in adipose tissue through facilitation of the sympathetic nervous system, which is driven by histamine neurons through the H(1) receptor, and that the beta(3)-receptor may be involved in this enhanced lipolytic response. High doses of l-carnosine, on the other hand, may lower lipolysis by suppressing sympathetic nerve activity via the H(3) receptor, and the muscarinic receptor may be related to this response.
Endocrine arterial hypertension: therapeutic approach in clinical practice.
Minerva Endocrinol. 2008 Jul 3;
Mazza A, Armigliato M, Zamboni S, Rempelou P, Rubello D, Pessina AC, Casiglia E
This review describes the therapeutic approach of endocrine arterial hypertension in clinical practice. In mineralocorticoid-related hypertension, adrenalectomy is the treatment of choice for aldosterone-producing adenomas and monolateral primary aldosteronism, whereas pharmacologic blood pressure (BP) control is indicated for the other forms of primary aldosteronism such as bilateral adrenal hyperplasia. Spironolactone is the drug of choice, but intolerable side effects limit its use; amiloride or eplerenone are a valid alternative. If BP remains uncontrolled, angiotensin converting enzyme inhibitors (ACE-I), angiotensin II receptor antagonists (AII-RA) and calcium channel blockers (CCB) may be added. Hypertension accompanying Cushing's syndrome can be approached with surgery, but antihypertensive treatment both pre- and postoperative is required as well. Eplerenone, AII-RA and ACE-I are indicated, while peroxisome proliferator activated receptor gamma-agonists may help for the insulin resistance syndrome. Drugs that suppress steroidogenesis should be used with care because of their serious side effects. Subjects with catecholamine-dependent hypertension due to a neuroendocrine neoplasm need to undergo preoperative alpha-adrenergic blockade with phenoxybenzamine or doxazozine. When adequate alpha-adrenergic blockade is achieved, beta-adrenergic blockade with low dose propranolol may be added. If target BP is not achieved, CCB and/or metyrosine are indicated. Laparoscopic adrenalectomy is the procedure of choice for solitary intra-adrenal neoplasms
Rare association of antisynthetase syndrome and Kennedy's disease.
Clin Rheumatol. 2008 Jul 1;
Szabo N, Lukacs S, Gunasekera W, Danko K
Antisynthetase syndrome is a type of Idiopathic Inflammatory Myopathy (IIM) associated with anti-Jo1 antibody. Kennedy's disease or X-linked spinal and bulbar muscular atrophy (SBMA) is a rare neuromuscular disease. We describe the case report of a 53-year-old man who presented with proximal muscle weakness and a history of bilateral hand tremor. Initial physical examination demonstrated "mechanic's hands", Raynaud's phenomenon, having elevated creatine kinase and lactate dehydrogenase levels and anti-Jo1 antibody positivity. His muscle biopsy demonstrated inflammatory infiltrate characteristic of IIM. Considering these findings, we reached the diagnosis of antisynthetase syndrome and commenced immunosuppressive therapy. On follow-up examination, he had developed dysphagia, and his tremor had worsened. His electroneurogram result was characteristic of Kennedy's disease, and the genetic test result showed an allele with 44 CAG repeat expansion in the androgen receptor gene of the X chromosome. This confirmed that in addition to antisynthetase syndrome, he also had Kennedy's disease. This patient now receives immunology and neurology follow-up. His symptoms have improved with low dose corticosteroids, propranolol for tremor, vitamin B supplementation, and physiotherapy. This article presents a rare case report of a patient with concurrent antisynthetase syndrome and Kennedy's disease, both of which lead to elevated creatine kinase levels and muscle weakness, thus, underpinning the importance of careful follow-up of patients with IIM and maintaining an open mind to other diagnoses when faced with refractory and/or new symptoms.
Frequency of respiratory disorders and bradycardia in essential tremor - consideration of treatment.
Parkinsonism Relat Disord. 1998 Jun; 4(1): 7-10
Dhand A, Birdi S, Rajput AH
Essential tremor (ET) is a common movement disorder and the prevalence rate increases with age. The most frequently prescribed and perhaps the most effective drugs for symptomatic treatment of ET are beta-blocking drugs such as propranolol. Some beta blockers are contraindicated in respiratory disorders (RD) and in cardiac conditions such as bradycardia, the frequency of which is unknown in ET patients. We studied RD and bradycardia (BPM
J Obstet Gynaecol Res. 2008 Jun; 34(3): 354-8
Kashanian M, Fekrat M, Zarrin Z, Ansari NS
Objective: The comparison between the effect of oxytocin alone or in combination with propranolol on labor. Methods: A double blind randomized controlled trial was performed on 150 nulliparas with a gestational age of 39-41 weeks of pregnancy and a Bishop score of
Vascul Pharmacol. 2008 Jun 8;
Nakazawa T, Sato A, Mori A, Saito M, Sakamoto K, Nakahara T, Ishii K
We investigated the effects of epinephrine and dopamine on retinal blood vessels in streptozotocin (STZ, 80 mg/kg, i.p.)-treated rats and age-matched control rats to determine whether diabetes mellitus alters the retinal vascular responses to circulating catecholamines. Experiments were performed 6-8 weeks after treatment with STZ or the vehicle. The fundus images were captured with the digital fundus camera system for small animals we developed and diameters of retinal blood vessels contained in the digital images were measured. Epinephrine increased the diameters of retinal blood vessels, but the vasodilator responses were reduced in diabetic rats. Dopamine produced a biphasic retinal vascular response with an initial vasoconstriction followed by a vasodilation. The vasoconstrictor effects of dopamine on retinal arterioles were enhanced in diabetic rats, whereas the difference between the two groups was abolished by treatment with propranolol. The vasodilator effect of isoproterenol, but not of the activator of adenylyl cyclase colforsin, on retinal blood vessels was reduced in diabetic rats. No difference in vasoconstriction of retinal blood vessels to phenylephrine between non-diabetic and diabetic rats was observed. The vasodilator responses of retinal blood vessels to 1,1-dimethyl-4-phenylpiperazinium, a ganglionic nicotinic receptor agonist, were also attenuated in diabetic rats. These results suggest that diabetes mellitus alters the retinal vascular responses to circulating catecholamines and the impairment of vasodilator responses mediated by beta-adrenoceptors contributes to the alteration.
Lacosamide, the new anticonvulsant, effectively reduces harmaline-induced tremors in rats.
Eur J Pharmacol. 2008 Jun 14;
Stöhr T, Lekieffre D, Freitag J
The present study aimed at evaluating the efficacy of lacosamide (0.3 to 30 mg/kg), a new anticonvulsant drug, in a model of essential tremor in comparison to the reference compounds propranolol and primidone. We observed a high tremorlytic effect of lacosamide reducing the intensity of tremors following harmaline administration in a dose-dependent manner. The higher dose also modified the latency and intensity of tremor at onset. The effect of lacosamide was equal or even superior to propranolol and primidone indicating that lacosamide may be a new antitremorgenic drug that merits further clinical investigation.
Rev Med Chil. 2008 Mar; 136(3): 356-8
Díaz N R, Silva G D
We report a 36 year-old pregnant woman who presented with acute pulmonary edema in the absence of preexisting cardiac disease. On admission she was on sinus rhythm and her blood pressure was mildly elevated. No cardiac abnormalities were detected by color Doppler echocardiography and no ischemic changes were seen on the electrocardiogram. Cardiac enzymes were normal. Thyroid function tests were diagnostic for hyperthyroidism. She was treated with propylthiouracil and propranolol and discharged in good conditions seven days after admission. This case emphasizes the need to consider hyperthyroidism as the cause of unexplained pulmonary edema in young patients with no history of heart disease who present with heart failure.
Increase in the vascular residence time of propranolol-loaded nanoparticles coated with heparin.
J Nanosci Nanotechnol. 2008 May; 8(5): 2369-76
Socha M, Lamprecht A, El Ghazouani F, Emond E, Maincent P, Barré J, Hoffman M, Ubrich N
Propranolol-HCI incorporated nanoparticles prepared with a blend of a polyester and a polycationic polymer and coated or not with a low molecular weight heparin by electrostatic interactions were prepared by emulsification followed by solvent evaporation. The mean diameter was 388 and 357 nm for coated and uncoated nanoparticles, respectively, and the entrapment efficiency ranged from 20 to 32%. Coated nanoparticles were negatively-charged, whereas uncoated nanoparticles displayed a positive zeta potential (+30 mV). After intravenous administration to rabbits of propranolol-HCI solution and propranolol-loaded nanoparticles coated or not with heparin, pharmacokinetic data revealed that coated nanoparticles exhibited a prolonged blood residence time. It can be concluded that the hydrophilic layer of heparin at the surface of nanoparticles conferred stealth properties which probably reduce the phagocytosis process and avoid immediate uptake by the mononuclear phagocytic system.
Eur J Pharmacol. 2008 May 24;
Floreani M, Quintieri L, Varani K, Dorigo MT, Dorigo P
This in vitro study was designed to investigate whether carteolol, a non-conventional partial agonists of beta(1)-adrenoceptors, relaxes phenylephrine-constricted rat aorta through activation of the low-affinity state of beta(1)-adrenoceptors or antagonist effect at alpha(1)-adrenoceptors. Carteolol-induced complete concentration-dependent relaxation of phenylephrine-contracted aorta (pD(2)=3.65+/-0.04), this effect not being modified by endothelium removal and not antagonised by NO-synthase inhibitor N(G)-nitro-l-arginine methyl ester (100 microM) or cyclo-oxygenase inhibitor indomethacin (10 microM). The effect of carteolol was unaffected by the non-selective beta-adrenoceptor antagonist propranolol (1 microM), or the beta(2)-adrenoceptor selective antagonist (+/-)-1-[2,3-(dihydro-7-methyl-1H-inden-4-yl)oxy]-3-[(1-methylethyl)amino]-2-butanol (ICI 118,551, 1 microM). Increasing concentrations of carteolol produced a parallel rightward shift of the concentration-response curves for phenylephrine-induced contraction, exhibiting a pK(B) of 4.28+/-0.07. Carteolol affinity for alpha(1)-adrenoceptors was evaluated by means of competition experiments carried out in BHK-21 cell membranes expressing rat recombinant alpha(1D)-adrenoceptor, the alpha(1)-adrenoceptor subtype mainly present in rat aorta. Carteolol competed monophasically with [(3)H]prazosin, exhibiting a pK(i) value (3.39+/-0.31) similar to its pD(2) and not very far from its pK(B). In conclusion, this study indicates that carteolol relaxes phenylephrine-contracted aorta through its alpha(1)-adrenoceptor antagonist properties, excluding the possibility that the relaxant effect is due to the activation of beta-adrenoceptors, particularly of the low-affinity state of beta(1)-adrenoceptors, by the drug.