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Biochemical and Pharmacological Rationales in Radiotracer Design
Published in Lelio G. Colombetti, Principles of Radiopharmacology, 2019
Raymond E. Counsell, Nancy Korn
The antiarrhythmic properties of propranolol have been demonstrated using a wide variety of experimentally induced arrhythmias,54,55 as well as in clinically occurring arrhythmias.56,57 However, the undesirable effects associated with beta adrenergic receptor blockade58,59 have stimulated interest in an analog of propranolol that is devoid of significant beta-adrenergic blocking activity. A dimethyl quaternary derivative of propranolol (Pranolium®, Figure 5), was synthesized which met these qualifications.60 Preliminary tissue-distribution studies using 14C-pranolium in dogs with ouabain-in-duced arrhythmias showed conversion of the arrhythmia which appeared related to selective concentration of radioactivity in the myocardium.61 At 2 hr post administration of 14C-pranolium to dogs, heart to blood ratios were 26 to 38, which increased to 70 to 108 by 4 hr. Similiar studies using Rhesus monkeys, however, showed no selective accumulation in the myocardium even though reversal of the arrhythmia took place. This apparent species difference is similar to that noted previously in the radioiodinated bretylium analog, NM-154.
Control Of Parathyroid Function By Dopamine
Published in M.D. Francesco Amenta, Peripheral Dopamine Pathophysiology, 2019
E. M. Brown, C. J. Chen, H. B. Niznik, E. L. Fogel, D. Hawkins
The parathyroid gland has been of particular interest to investigators studying the control of hormonal secretion because of the unusual, inverse relationship between the extracellular and intracellular Ca+ + concentrations, on the one hand, and PTH release, on the other. In addition to Ca+ +, however, it has recently been recognized that a variety of other factors also modulate PTH release.4 For example, beta-adrenergic catecholamines and prostaglandins of the E series stimulate PTH release, while alpha-adrenergic catecholamines and PGF2α inhibit PTH release. In the course of screening a number of pharmacological agents, we noted that dopamine was a potent secretagogue for PTH in vitro in dispersed bovine parathyroid cells (Figure 2),5 an observation confirmed by other investigators.6 This effect did not appear to be mediated by the beta-adrenergic receptor, since it was not blocked by beta-adrenergic antagonists. The stimulation of PTH release by dopamine (DA), however, was stereospecifically inhibited by the dopaminergic antagonist, flupenthixol.5 Conversely, is-oproterenol-stimulated PTH release was inhibited by propranolol but not by flupenthixol.5 Subsequent in vivo studies in cattle confirmed that DA raises circulating levels of immu-noreactive PTH,7 and that this effect was partially inhibited by pimozide, but not by propranolol.
Cardiovascular responses in pathological situations
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
Hypertension can be controlled with the ‘ACD’ regime: ACE inhibitors/ARBs, Ca2+ channel blockers and diuretics. Beta adrenergic receptor blockers can be added, but are not considered first-line antihypertensive drugs.
Beta-blocker carteolol and oxprenolol produce cutaneous analgesia in response to needle pinpricks in the rat
Published in Neurological Research, 2023
There are limitations to this study. Firstly, in an equipotent basis (ED25, ED50, and, ED75), the duration of blockade induced by carteolol was longer than that induced by oxprenolol or bupivacaine, but it does not appear to be a consistent relationship between the beta-blocker potency and total recovery time. Secondly, prolonged vasoconstriction can cause ischemic damage and this should be considered. Thirdly, Beta-adrenergic receptor antagonists rapidly reach the central nervous system and therefore some of the observed effects may also occur systemically (eg. acting centrally) rather than locally [35,36]. To prevent the central effect of drugs, the 6 stings were performed in the demarcated area immediately after the CTMPs were evoked outside the wheal. Lastly, we did not estimate whether beta-blockers induced neurotoxicity or systemic toxicity. Beta-blockers as FDA-approved drugs were used to treat congestive heart failure and tachycardia [1]. Over the past 10 years, there have been increasing reports of topical beta-blockers for various skin diseases [31]. However, the toxicities should be examined before the use of Beta-blockers as an infiltrative anesthetic.
Prolonged coma resulting from massive levothyroxine overdose and the utility of N-terminal prohormone brain natriuretic peptide (NT-proBNP)
Published in Clinical Toxicology, 2019
Ophelia Wong, Anselm Wong, Shaun Greene, Andis Graudins
Treatment of thyrotoxicosis and toxicity after levothyroxine overdose is similar. Thyroid storm is treated using principles highlighted by Idrose [7]:Supportive care – management of dehydration, fever, cardiac monitoring and glucose.Inhibition of new thyroid hormone synthesis, e.g., propylthiouracil or methimazole.Inhibition of thyroid hormone release, e.g., iodine with Lugol solution.Beta adrenergic receptor blockade, e.g., propranolol.Preventing peripheral conversion of T4 to T3, e.g., steroids, propranolol and propylthiouracil.Treat the underlying cause.
Age-dependent sympathetic neural responses to ß1 selective beta-blockade in untreated hypertension-related tachycardia
Published in Blood Pressure, 2018
Dagmara Hering, Wiesława Kucharska, Marzena Chrostowska, Krzysztof Narkiewicz
This study is the first to demonstrate the effects of highly β1 cardioselective beta-adrenergic receptor antagonist betaxolol on sympathetic CV profile in males with untreated hypertension and ambulatory tachycardia. The major novel findings are that (1) the autonomic neural responses to betaxolol are age-dependent in untreated hypertension-related tachycardia; (2) chronic treatment with betaxolol reduces sympathetic drive to the heart but not to the peripheral vessels in younger adults; and (3) the paradoxical reduction in MSNA achieved with betaxolol occurs despite lowering of HR and BP in older males. Our study also revealed three other new findings to indicate (1) age-related difference in hemodynamic and sympathetic profile in hypertension-related tachycardia; (2) lowering HR with betaxolol bore no association with an inhibition of MSNA; and (3) betaxolol improves the dynamics of HRV in younger, but not in older subjects with untreated hypertension and tachycardia. Betaxolol was well tolerated and no drug-related side effects were noted in the study cohort.