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Management of RSD
Published in Hooshang Hooshmand, Chronic Pain, 2018
Guanethidine causes expulsion of norepinephrine at the nerve ending. The half–life of guanethidine is quite prolonged. A single injection of guanethidine has a 50% excretion rate of 2 to 3 days through the kidneys.248 The duration of regional block with guanethidine has been reported from days up to months.12,48,74,127,128,144,200,253
Control of blood vessels: extrinsic control by nerves and hormones
Published in Neil Herring, David J. Paterson, Levick's Introduction to Cardiovascular Physiology, 2018
Neil Herring, David J. Paterson
Vesicle release, or exocytosis, is triggered by a rise in cytosolic [Ca2+] as the action potential activates axonal N-type Ca2+ channels. The Ca2+ activates a protein on the vesicle membrane, synaptobrevin. If the vesicle is close to the surface membrane, the synaptobrevin binds to the membrane protein syntaxin. This ‘docking’ process allows the two membranes to fuse and release the vesicle contents. Guanethidine blocks exocytosis by acting as a local anaesthetic on sympathetic terminals, and was formerly used to treat hypertension. Conversely, amphetamines have a sympathomimetic effect because they displace NAd from the vesicle into the cytosol, from where it escapes into the extracellular fluid.
Drugs Affecting Storage and Release from Sympathetic Neurones
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
The effective blood pressure lowering action of the neurone blockers and protection from pressor reflexes made them the drugs of choice for the treatment of all grades of hypertension in the early 1970s. However, because of the incidence of undesirable side-effects, their use is now restricted to severe hypertension which fails to respond to the newer agents and to patients who have tolerated the drugs for many years. Guanethidine does not cross the blood-brain barrier and does not cause CNS side-effects. The neurone blockers, however, do have a range of unwanted effects arising from sympathetic blockade, including diarrhoea, ejaculation failure, postural hypotension and lasitude due to poor muscle blood flow. They produce sodium and water retention leading to oedema which may be corrected by concurrent use of a diuretic. The thiazide diuretics usefully potentiate the antihypertensive activity and thus allow the dosage of the neurone blocker to be reduced with a consequent reduction of the side-effects. Drug interactions with other agents acting on the noradrenergic neurone are abundant, as discussed above.
An algorithm for Botulinum toxin A injection for upper eyelid retraction associated with thyroid eye disease: long-term results
Published in Orbit, 2021
Gamze Ozturk Karabulut, Korhan Fazil, Basak Saracoglu Yilmaz, Can Ozturker, Zehra Karaağaç Günaydın, Muhittin Taskapili, Pelin Kaynak
In the active stage of the disease conservative treatment is the mainstay to overcome corneal exposure symptoms such as tearing, grittiness, and pain. Surgical approaches during fibrotic stage include recession of levator muscle aponeurosis, Müller’s muscle or both,33–35 excision of Müller’s muscle,34 introducing a spacer to lengthen LPS,36 myotomies, and blepharotomies.37,38 Several nonsurgical approaches have been reported during active and fibrotic stage due to quick onset and reversibility. Topical administration of adrenergic blocker guanethidine to overcome sympathetic effects was poorly tolerated due to side effects such as vasodilatation and irritation.39,40 The hyaluronic acid gel injected at the level of eyelid retractors to lengthen them and to add weight on the tarsus in TED have been reported.31,41,42 Injection of fillers in the lower eyelid also lengthens the lower eyelid retractors, elevates the lower eyelid and reduces inferior scleral show.43 Periocular,44 subconjunctival,45–47 fornix,48 and peri-levator palpebra superioris49 injection of triamcinolone resulted in favorable results especially in the early active phases of TED.
What are the considerations for anti-hypertensive treatment in patients with Parkinson’s disease?
Published in Expert Opinion on Pharmacotherapy, 2020
In the treatment of AH in PD antihypertensives containing moxonidine, alpha-methyldopa or reserpine [2,18,23] are contraindicated. Verapamil, diltiazem, amlodipine and nifedipine should not be combined with levodopa. Amlodipine was reported to induce Parkinson symptoms [24], not confirmed in several studies [25,26]. On the other hand some molecules used as antihypertensives are discussed as disease-modifying drugs [25,26] Negative influence on the PD results from preparations containing reserpine [2,18]. Combinations of guanethidine with dopaminergic agents often results in arrhythmias [18]. The effect of molsidomine is reinforced in combination with levodopa [18,23].
Dopamine β hydroxylase as a potential drug target to combat hypertension
Published in Expert Opinion on Investigational Drugs, 2020
Sanjay Kumar Dey, Manisha Saini, Pankaj Prabhakar, Suman Kundu
Immediately after the discovery of NA as the key player in regulating SNS, centrally acting SNS inhibitors including methyldopa and clonidine, antagonistic drugs obstructing sympathetic neurones such as guanethidine, β-adrenoceptor blockers like propranolol, and α-adrenoceptor blockers were developed [56]. Combination of antiadrenergic drugs with either diuretics or vasodilators became next generation antihypertensives [57]. Some of these β1 selective β-blockers like metoprolol can be used in diabetics or even chronic obstructive pulmonary disorders (COPD) [58,59] and asthmatic patients [60].