Disease relevance of L-Phenylephrine

• Pertussis toxin treatment alone significantly reduced the baroreceptor reflex elicited by L-phenylephrine [1].
• Intraventricular injections of galanin-(1-15) significantly inhibited the reflex bradycardia elicited by intravenous L-phenylephrine and thus decreased the baroreceptor sensitivity [2].
• Isolated-perfused rat hearts were allowed to equilibrate for 8 minutes and were then subjected to either 2 minutes of global, normothermic transient ischemia or 2 minutes of 50 mumol/L phenylephrine infusion [3].
• L-phenylephrine, an alpha-1 agonist, induced hypertension, bradycardia and a significant gastric relaxation [4].
• Cardiomyocytes were treated with 100 nmol/L endothelin 1 (ET) and 10 micromol/L phenylephrine (PE) to induce myocardial cell hypertrophy [5].

High impact information on L-Phenylephrine

• The increase in cardiac glycogen synthase phosphorylation induced by DL-isoproterenol, glucagon, and L-phenylephrine was identical, with or without insulin pretreatment; this despite the fact that these three hormones promoted a 3- to 4-fold larger decrease in the enzyme activity ratio with the insulin-treated tissue [6].
• In perfused hearts from normal animals, DL-isoproterenol and glucagon caused an increase in glycogen synthase phosphorylation of 85-100 pmol/unit of enzyme activity, while L-phenylephrine increased the phosphate content by only 20-35 pmol, but all three hormones caused the same degree of inactivation [6].
• The tension responses of ET-free segments of the thoracic aorta to 5 x 10(-6) mmol/L phenylephrine, 60 mmol/L KCl, and cumulative doses of ET-1 were assessed [7].
• Correspondingly, [Ca2+]i responses evoked by 10 micromol/l phenylephrine in hepatocyte doublets shifted from transient to sinusoidal-type [Ca2+]i oscillations and then to a sustained increase in [Ca2+]i, followed by a gradual return to baseline [8].
• The most potent activator of phospholipase C (as measured by inositol phosphate release) was carbachol (muscarinic M1 receptor agonist), followed by L-phenylephrine (alpha 1-adrenergic receptor agonist) in normal oligodendrocytes [9].

Chemical compound and disease context of L-Phenylephrine

• Dose-response curves of inhibitory agents (e.g. WB4101, cholera and pertussis toxins) were determined by comparing the remaining contractility after incubating with the respective drug with a control contraction that was evoked three times (10 mumol/L phenylephrine) and the mean set at 100% [10].

Biological context of L-Phenylephrine

• In perfused diabetic hearts, DL-isoproterenol, glucagon, and L-phenylephrine caused increased phosphorylation of glycogen synthase without affecting the albeit already low activity ratio of the enzyme [6].
• Aged myocytes also had a greater I(to) with an increased rate of activation, but the I(to) inactivation kinetics, steady-state inactivation, and responsiveness to L-phenylephrine, an alpha(1)-adrenergic agonist, were unaltered [11].
• We investigated endothelium-dependent vasodilation induced by acetylcholine (Ach; 10(-8) to 3 x 10(-6) mol/L) in isolated 3-mm aortic rings precontracted with l-phenylephrine (l-Phe; 10(-6) mol/L) [12].
• At concentrations higher than 3 x 10(-4) mol/l, phenylephrine increased the maximum rate of rise of action potential (Vmax) but methoxamine reduced it [13].
• Microinjection of the glutamate receptor antagonist kynurenic acid (2.5 nmol/site) or the GABAergic agonist muscimol (1 nmol/site) into the nucleus tractus solitarii abolished the effects of both L-phenylephrine and chlorophenyl-biguanide on heart rate and renal nerve activity [14].

Anatomical context of L-Phenylephrine

• Conventional measurements of maximum isometric force and dose-response relations for l-phenylephrine in strips of ascending aorta in vitro were followed by radioligand studies on homogenates made from the same strips [15].
• The neurons were selected based upon their spontaneous activity and upon their sensitivity to baroreceptor reflex activation by L-phenylephrine [14].
• RESULTS: Contractile responses to 15 micromol/L phenylephrine in control radial artery segments averaged 44.2% +/- 9.1% of the maximal contractile response to 30 mmol/L KCl [16].
• In vas deferens and kidney, SDZ NVI 085 evoked smooth muscle contraction and vascular constriction and was of similar potency to L-phenylephrine [17].
• After 8 weeks, isolated femoral arteries were mounted on a flow myograph, pressurized at 80 mmHg, and constricted by 40-50% of the lumen internal diameter (i.d.) by L-phenylephrine (1-10 micromol/l) [18].

Associations of L-Phenylephrine with other chemical compounds

• KMD-3213, a novel alpha 1A-adrenoceptor-selective antagonist, caused parallel rightward shifts of the concentration-response curves for l-phenylephrine [19].
• In addition, the alpha-1 adrenergic receptor agonist l-phenylephrine was found to enhance the proliferation of NPCs, whereas an alpha-adrenergic antagonist and selective alpha-1 antagonists significantly inhibited cell proliferation increases induced by l-epinephrine and l-phenylephrine [20].
• Dose-related constrictions of rabbit veins were obtained with L-phenylephrine and the alpha(2)-adrenoceptor agonist dexmedetomidine [21].
• 3. At the start, middle and end of the experiment the bovine endothelial cells were exposed to a PO2 of 142 mmHg (18.9 kPa) and when stimulated by bradykinin the perfusate caused respectively a 70 +/- 4%, 63 +/- 6% and 63 +/- 6% (mean +/- SEM) relaxation of an aortic ring which had been pre-contracted by 10(-6) mol/l phenylephrine [22].
• Papaverine/lidocaine modestly attenuated contraction to 15 micromol/L phenylephrine (32.1% +/- 5.9%; P =.22), but 1000 micromol/L phenoxybenzamine completely abolished radial artery contraction (-7.2% +/- 4.4%; P <.001) [16].

Gene context of L-Phenylephrine

• Moreover, a dominant negative mutant of JNK also significantly prevented the induction of PAI-1 mRNA expression by 100 nmol/l endothelin-1 and 10 micromol/l phenylephrine [23].
• 2. Pretreatment of the endothelium-denuded aortic ring with IL-6 for 3 h caused a significant inhibition of its contraction (58.9 +/- 7.8%, n = 9, P < 0.01) when induced by 10(-6) mol/L phenylephrine [24].
• The baroreceptor reflex was elicited by intravenous injections of different doses of L-phenylephrine before and after the intraventricular administration of galanin peptides [2].
• YJA20379-8 at 2 x 10(-4) g/ml did neither produce any contraction nor relaxation of isolated organs, such as guinea pig ileum, rat fundus, rat uterus and guinea pig vas deferens, and the drug antagonized the contractile responses to several spasmogens, such as acetylcholine, histamine, serotonin, L-phenylephrine, oxytocin and BaCl2 [25].

Analytical, diagnostic and therapeutic context of L-Phenylephrine

• To determine DA-Fp in biological materials, the pretreatment before HPLC was optimized by hydrolysis of its conjugate and suppression of the artifact with l-phenylephrine [26].
• 3. The A7r5 cells were treated with 10 micromol/L phenylephrine or 1 micromol/L isoproterenol for 24 h and changes in gene expression were detected with the DNA microarray [27].
• Iontophoresis of either norepinephrine or the alpha 1-adrenoceptor agonist l-phenylephrine increased the activity of most cells tested whilst the alpha 1-antagonist ergotamine reduced the activity of most cells tested and prevented excitation elicited by VNAB stimulation [28].
• Isometric tension changes, recorded with a pressure transducer, in response to various drugs and electrical stimulation were assessed in an organ chamber, after active muscle tone had been induced by 10 micromol/L phenylephrine [29].
• The increase in hindlimb perfusion pressure to lumbar sympathetic nerve stimulation was significantly smaller in 20- and 24-mo-old rats than in younger animals, whereas vasoconstrictor responses to intraarterial administration of norepinephrine, L-phenylephrine, and methoxamine were reduced only in the 24-mo-old animals [30].

References