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Hypertensive Emergencies and Urgencies
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Maria Lorenza Muiesan, Anna Paini, Claudia Agabiti Rosei, Fabio Bertacchini, Massimo Salvetti
Urapidil is an alpha-blocker with a central sympatholytic effect mediated via stimulation of serotonin 5HT1A receptors in the central nervous system. Intravenous urapidil was suggested to have a potential role in the management of acute stroke, although no studies have specifically investigated the efficacy of urapidil in stroke management. In the Intensive Blood Pressure Reduction in Acute Cerebral Haemorrhage (INTERACT) study, 47% of patients randomized to intensive BP reduction were treated with urapidil (61).
Adrenoceptor Antagonists
Published in Kenneth J. Broadley, Autonomic Pharmacology, 2017
Agents known primarily for their 5-HT receptor antagonist activity also have α-adrenoceptor blocking properties. These include ketanserin which is a selective 5-HT2 antagonist but with substantial α1-adrenoceptor blocking activity that probably accounts for much of its antihypertensive action (Zabludowski et al. 1985). Urapidil is also a 5-HT1A receptor antagonist having α-adrenoceptor blocking properties which may account in part for its blood pressure lowering activity (Fozard & Mir 1987). Urapidil (Table 5.2) is selective for α1-adrenoceptors; it does not cause reflex tachycardia probably because of blockade of central α1-adrenoceptors, a property shared with prazosin and its congeners. The 5-methyl derivative of urapidil is selective for α1A-adrenoceptors (Hanft & Gross 1989)(see Chapter 3).
Systemic and intrathecal pharmacologic treatment
Published in Jacques Corcos, David Ginsberg, Gilles Karsenty, Textbook of the Neurogenic Bladder, 2015
Shachar Aharony, Jacques Corcos
The suggested mechanism of α-blockers in the neurogenic bladder involves decreasing urethral resistance during voiding. A multicenter, placebo-controlled, double-blind trial of urapidil in neurogenic bladder dysfunction demonstrated significant improvement of straining and reduced urinary symptom scores. The results were associated with decreased maximum flow pressure and urethral resistance compared to placebo.97,98
Pharmacological management of malignant hypertension
Published in Expert Opinion on Pharmacotherapy, 2020
Joanna Lewek, Agata Bielecka-Dąbrowa, Marek Maciejewski, Maciej Banach
Urapidil is an antiadrenergic drug that acts through the dilatation of arterioles and thus reduces the total peripheral resistance [15]. It is dedicated to hypertensive emergencies. The initial dosage is 10 to 50 m and it should be slowly injected. Blood lowering is expected within 5 min. Next doses can be repeated if necessary. Continuous infusion is used to maintain an achieved level of blood pressure. The infusion rate depends on the individual patient with the initial infusion rate being 2 mg/min. The maintenance dose is on average 9 mg/hour. The duration of the treatment should not exceed 7 days because, from toxicological point of view, it seems to be safe. Similarly to nicardipine, urapidil should not be used in patients with aortic valve stenosis and additionally with an atriovenous shunt [15].
Clinical study on effect of wrist-ankle acupuncture on incidence of hypertension after intubation during induction of general anesthesia
Published in Clinical and Experimental Hypertension, 2022
Zhe Xu, Xiaoguang Liu, Yanjie Zhou, Huiru Ren, Yuexia Ma, Hongliang Gao, Chunlei Zhang, Wei Hao
During anesthesia, if hypotension occured (decreased by more than 30% of the baseline value for 5 min), the infusion could be accelerated appropriately, and 4 ug of norepinephrine was intravenously injected if necessary. If the HR (heart rate) was <50 beats/min, 0.5 mg atropine was given intravenously. If the SBP (systolic blood pressure) rised more than 30% of the baseline value for more than 5 min, 10 mg of urapidil was given.
A solution to an almost unrecognizable problem: how can we treat a patient before differentiating between hypertensive urgency and emergency?
Published in Expert Opinion on Pharmacotherapy, 2022
Goran Koracevic, Milovan Stojanovic, Miloje Tomasevic, Dragan Simic, Dragan Lovic, Ivan Tasic
It is known that peroral antihypertensives act too slowly and too weakly to decrease very high BP in HTN-Es. On the other hand, IV antihypertensive drugs may lower BP excessively in HTN-U. Therefore, the following approach might be adequate for patients while we are waiting for conclusive acute HMOD results: to decrease BP promptly, but not profoundly. This can be achieved by a slower rate of potent IV drug administration. If the clinical picture indicates a certain HTN-E, but not conclusively, we may proceed to slowly administer an IV antihypertensive to avoid an excessive decrease of BP until we wait for the test to be performed and interpreted. For example, if a patient with very high BP and chest pain with ECG suggestive of non-ST-elevation acute myocardial infarction has to wait for laboratory confirmation of myocardial damage (troponin elevation), it may be wise to administer β blocker IV and/or nitroglycerin in the infusion. The rate of administration should then be (somewhat) slower as opposed to when the acute myocardial infarction is evident.The other reasonable approach can be to give an antihypertensive agent [9,10] which is adequate for many HTN-Es (at a lower than usual rate). Numerous papers suggest nicardipine is a valid antihypertensive drug for patients with very high BP [19–21]. This is confirmed also in a systematic review [22,23]. Nicardipine is indicated in patients with very high BP with acute renal failure, HTN encephalopathy, acute cardiogenic pulmonary edema, acute AoD, eclampsia and severe preeclampsia/hemolysis, elevated liver enzyme levels, and low platelet levels (HELLP) syndrome [10], and stroke [2]. Urapidil is also useful in various indications in patients with very high BP [24,25]. Consequently, urapidil is recommended in various HTN-Es: very high BP with acute renal failure, ACS, acute pulmonary edema [10].