Atropine sulfate monohydrate

Atropine is a competitive antagonist of muscarinic acetylcholine receptor with IC50 values of 2.22±0.60nM, 4.32±1.63nM, 4.16±1.04nM, 2.38±1.07nM and 3.39±1.16nM for M1, M2, M3, M4 and M5, respectively [1].

Atropine is an antimuscarinic agent and has shown the pharmacological effects because of binding to muscarinic acetylcholine receptors. Atropine, the orthosteric antagonist, has been reported to compete with [3H]-NMS for all muscarinic subtypes with a potency consistent with the high affinities at the mAChR subtypes. The Ki values are 1.27±0.36nM, 3.24±1.16nM, 2.21±0.53nM, 0.77±0.43nM and 2.84±0.84nM, respectively [1, 2, 3].

References:
[1] Lebois EP1, Bridges TM, Lewis LM, Dawson ES, Kane AS, Xiang Z, Jadhav SB, Yin H, Kennedy JP, Meiler J, Niswender CM, Jones CK, Conn PJ, Weaver CD, Lindsley CW. Discovery and characterization of novel subtype-selective allosteric agonists for the investigation of M(1) receptor function in the central nervous system.ACS Chem Neurosci. 2010;1(2):104-121.
[2] BUSCH H, ALLEN H, ANDERSON DC.Effects of atropine and carbachol on labeling of protein fractions of mouse pancreas in vitro.J Pharmacol Exp Ther. 1959 Nov; 127:200-4.
[3] Feron O1, Smith TW, Michel T, Kelly RA.Dynamic targeting of the agonist-stimulated m2 muscarinic acetylcholine receptor to caveolae in cardiac myocytes. J Biol Chem. 1997 Jul 11; 272(28):17744-8.

Acetylcholine-Atropine Interactions: Paradoxical Effects on Atrial Fibrillation Inducibility.[Pubmed:28328743]

J Cardiovasc Pharmacol. 2017 Jun;69(6):369-373.

Atropine (ATr) is well known as a cholinergic antagonist, however, at low concentrations ATr could paradoxically accentuate the parasympathetic actions of acetylcholine (ACh). In 22 pentobarbital anesthetized dogs, via a left and right thoracotomy, a leak-proof barrier was attached to isolate the atrial appendages (AAs) from the rest of the atria. In group 1 (Ach+ATr+Ach), ACh, 100 mM, was placed on the AA followed by the application of ATr, 2 mg/mL. The average atrial fibrillation (AF) duration was 17 +/- 7 minutes. After ATr was applied to the AA and ACh again tested, the AF duration was markedly attenuated (2 +/- 2 minutes, P < 0.05). In group 2 (ATr+Ach), ATr was initially applied to the AA followed by the application of ACh, 100 mM. There was no significant difference in AF duration (16 +/- 4 minutes vs. 18 +/- 2 minutes, P = NS). The inhibitory effect of ATr on induced HR reduction (electrical stimulation of the anterior right ganglionated plexi and vagal nerves) was similar between groups 1 and 2. These observations suggest that when ATr is initially administered it attaches to the allosteric site of the muscarinic ACh receptor (M2) leaving the orthosteric site free to be occupied by ACh. The M3 receptor that controls HR slowing does not show the same allosteric properties.

Topical Atropine in the Control of Myopia.[Pubmed:28293653]

Med Hypothesis Discov Innov Ophthalmol. 2016 Fall;5(3):78-88.

Atropine has been used for more than a century to arrest myopia progression. Compelling evidence of its protective effect has been reported in well-designed clinical studies, mainly performed during the last two decades. However, its exact mechanism of action has not been determined. Experimental findings have shown that the mechanism is not related to accommodation, as was thought for decades. A review of the published literature revealed a significant amount of evidence supporting its safety and efficacy at a concentration of 1.0%, and at lower concentrations (as low as 0.01%).

Ventricular repolarization duration and dispersion adaptation after atropine induced rapid heart rate increase in healthy adults.[Pubmed:28347481]

J Electrocardiol. 2017 Jul - Aug;50(4):424-432.

BACKGROUND: Proper adaptation of ventricular repolarization (VR) to rapid heart rate (HR) increase is crucial for cardiac electro-mechanical function. The pattern and temporal aspects of this adaptation and its components (duration and dispersion) during normal conduction are, however, incompletely known in humans and were the topic of this study. METHODS & RESULTS: The VR duration (QT & QTpeak) and dispersion (Tamplitude, Tarea & ventricular gradient; VG) responses were studied by continuous vectorcardiogram after a bolus injection of atropine 0.04mg/kg b.w. in 31 healthy young adults (16 men). The primary measure (T90 End) was the time to reach 90% change from baseline to end value 300s later. Mean (SD) of T90 End was 23 (9) s for a 41% RR decrease, 130 (35) s for a 16% QTend decrease and 110 (36) s for a 19% QTpeak decrease; the response was single-exponential for these measures. For 35-43% decreases of Tamplitude, Tarea & VG, mean (SD) of T90 End were 21 (10), 38 (20) and 40 (23) s and the response pattern was double-exponential with varying overshoot. CONCLUSIONS: VR duration and dispersion responses to a very rapid HR increase during normal conduction differed substantially. In contrast to the well-known single-exponential delay in VR duration adaptation the responses of VR dispersion measures were double-exponential and much more rapid. We describe a new and completely non-invasive phenotypic characterization of different components of VR adaptation.

Prophylactic Atropine Administration Prevents Vasovagal Response Induced by Cryoballoon Ablation in Patients with Atrial Fibrillation.[Pubmed:28295425]

Pacing Clin Electrophysiol. 2017 May;40(5):551-558.

BACKGROUND: Cryoballoon (CB) ablation of pulmonary vein ostia often induces a vagal response. This prospective study was designed to assess the effectiveness of prophylactic intravenous administration of atropine on hemodynamic impairment induced by CB ablation in patients with atrial fibrillation. METHODS: Twenty-five patients with paroxysmal atrial fibrillation undergoing CB ablation were prospectively enrolled and assigned to one of two groups. First 12 patients (trial group) were administered 1 mg of atropine before deflation of the CB, while the following 13 patients (control group) were given atropine only after the onset of the hemodynamic variation (decrease in heart rate and/or blood pressure). Treatment was considered effective when the hemodynamic variations were restored. RESULTS: In the trial group, three patients with transient hypotension did not require supportive care throughout the procedures, and one patient with hypotension required supportive care. In the control group, hypotension, bradycardia, and mixed bradycardia with hypotension requiring supportive care occurred in six, three, and three patients, respectively. Overall, the rate of marked vagal responses was significantly lower when prophylactic atropine was administrated (4/12 patients vs 12/13 patients, respectively; P < 0.01). CONCLUSIONS: Atropine is significantly effective in the prevention of all types of vasovagal responses induced by CB ablation in patients with atrial fibrillation.

Atropine sulfate monohydrate (Atropine sulfate hydrate) is a broad-spectrum and competitive muscarinic acetylcholine receptor (mAChR) antagonist with anti-myopia effect.

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