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PubMed2004

Inhibition of phenylephrine-induced cardiac hypertrophy by docosahexaenoic acid.

Many of the cardiovascular benefits of fish oil result from the antiarrhythmic actions of the n-3 polyunsaturated lipids docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). The beneficial effects of DHA/EPA in patients with coronary artery disease and myocardial infarction may also result from modulation of the myocardial hypertrophic response. Hypertrophy was assessed in neonatal cardiomyocytes exposed to phenylephrine (PE) by measuring cell surface area, total protein synthesis ((14)C leucine incorporation), and the organization of sarcomeric alpha-actinin and by monitoring expression of atrial natriuretic factor (ANF). We report that PE induced a twofold increase in cell surface area and protein synthesis in cardiomyocytes. The hypertrophied cardiomyocytes also exhibited increased expression of ANF in perinuclear regions and organization of sarcomeric alpha-actinin into classical z-bands. Treatment of cardiomyocytes with 5 microM DHA effectively prevented PE-induced hypertrophy as shown by inhibition of surface area expansion and protein synthesis, inhibition of ANF expression, and prevention of alpha-actinin organization into z-bands. DHA treatment prevented PE-induced activation of Ras and Raf-1 kinase. The upstream inhibition of Ras --> Raf-1 effectively prevented translocation and nuclear localization of phosphorylated extracellularly regulated kinase 1 and 2 (Erk1/2). These effects consequently led to inhibition of nuclear translocation, and hence, activation of the downstream signaling enzyme p90 ribosomal S6 kinase (p90(rsk)). These results indicate that PE-induced cardiac hypertrophy can be minimized by DHA. Our results suggest that inhibition of Ras --> Raf-1 --> Erk1/2 --> p90(rsk) --> hypertrophy is one possible pathway by which DHA can inhibit cardiac hypertrophy. In vivo studies are needed to confirm these in vitro effects of DHA.

Animals↗

PubMed1977

Selective GLC determination of epinephrine, isoproterenol, and phenylephrine in pharmaceutical dosage forms.

A simple, specific GLC analytical procedure for the quantitation of epinephrine, isoproterenol, and phenylephrine in commercial tablets, powders, inhalation solutions, ophthalmic and nasal drops, and injectable preparations is presented. Samples are taken to dryness where required, the dried residue is reacted with an appropriate trimethylsilylating reagent, and the derivatives are eluted from a methyl silicone column using temperature programming. Quantitation of the flame-ionization detector signal is achieved relative to the dibenzyl succinate internal standard by an electric integrator. The results obtained by applying the method to the analysis of each of the three drugs in several simulated decomposed mixtures were in good agreement with theoretical values, even at impurity levels of up to 80% by weight. When applied to commercial formulations, the procedure was feasible for tablets, powders, and solutions at drug concentrations of 0.2% or greater. The commonly incorporated buffering and antioxidant excipients did not interfere.

Chemical Phenomena↗

PubMed1980

Simultaneous GLC analysis of salicylamide, phenylpropanolamine hydrochloride, caffeine, chlorpheniramine maleate, phenylephrine hydrochloride, and pyrilamine maleate in capsule preparations.

A GLC method is described for the quantitative determination of salicylamide, phenylpropanolamine hydrochloride, caffeine, chlorpheniramine maleate, phenylephrine hydrochloride, and pyrilamine maleate. The sample was dissolved in ethanol, and an aliquot of the solution was brought to dryness and treated with 0.1 ml of 4-(dimethyl-amino)pyridine in pyridine-acetic anhydride (1:1). The components were isolated and measured by applying 1 microliter of the reaction mixture to a chromatograph equipped with a flame-ionization detector and fitted with 8% OV-101 glass columns. The accuracy was good. Dicyclohexylphthalate was used as the internal standard.

Aminopyridines↗

PubMed1984

Determination of the structure of a synthetic impurity in guaifenesin: modification of a high-performance liquid chromatographic method for phenylephrine hydrochloride, phenylpropanolamine hydrochloride, guaifenesin, and sodium benzoate in dosage forms.

An impurity present in all commercial guaifenesin-containing dosage forms examined was isolated and identified as 2-(2-methoxyphenoxy) 1,3-propanediol (VI). The eluant of a previously developed stability-indicating liquid chromatographic method for phenylephrine hydrochloride (I), phenylpropanolamine hydrochloride (II), and guaifenesin (III) was modified to yield a better separation between phenylpropanolamine and the impurity. The method was expanded to include sodium benzoate (IV), a preservative found in some liquid formulations.

Benzoates↗

PubMed2004

Phenylephrine-induced neurogenic prostatitis facilitates the promotion of PIN-like lesions in rats.

BACKGROUND: Atypical prostate hyperplasia, resembling PIN lesions in men, together with chronic inflammatory exudates, have been reported after chronic administration of phenylephrine (PE). The present study aims to characterize the evolution of the expression of typical leukocyte markers immunohistochemically as correlated to the promotion of PIN lesions. METHODS: Adolescent rats received injections of PE (subcutaneously) (10 mg/kg BW/per day) and were euthanized 3, 8 hr, 1, 3, 7, 14 days thereafter. The dissected prostates were fixed in formalin, and paraffin embedded sections were cut and immunoreacted. RESULTS: PE exerted a time related bi-phasic effect on the rat prostate. A first inflammatory reaction phase took place at 3-8 hr post injection characterized by vascular dilatation, congestion, edema, and massive leukocytic infiltrate, mainly of ED1+ cells. At 24 hr, the amount of ED1+ cells decreased approaching the equivalent values of ED2+, CD8+ cells, and mastocytes. Their values remained relatively high for the rest of the experimental period. A second phase of proliferative changes, consisting of healing fibrosis as well as dysplastic epithelial lesions, similar to human PIN lesions, appeared on the 7th day. CONCLUSIONS: Neuro-immune interactions promote prostatic fibrosis and dysplastic changes; these being preceded by an acute and transient inflammatory reaction.

Adrenergic alpha-Agonists↗

PubMed1997

Regulation of phospholipases C and D in rat ventricular myocytes: stimulation by endothelin-1, bradykinin and phenylephrine.

The physiological activator of protein kinase C (PKC), diacylglycerol, is formed by hydrolysis of phosphoinositides (PI) by phospholipase C (PLC) or phosphatidylcholine by phospholipase D (PLD). We have measured activation of these phospholipases by endothelin-1 (ET-1), bradykinin (BK), or phenylephrine (PE) in ventricular myocytes cultured from neonatal rat. The stimulation of PI hydrolysis after 10 min by 0.1 microM ET-1 (about 12-fold) was much greater than for BK or PE (each about four-fold), and did not correlate with translocation of nPKC delta or nPKC epsilon (Clerk A. Bogoyevitch MA. Andersson MB. Sugden PH, 1994. J Biol Chem 269: 32848-32857: Clerk A, Gillespie-Brown J, Fuller SJ, Sugden PH, 1996. Biochem J 317: 109-118). However, ET-1 and BK stimulated a similar rapid increase in [3H]InsP, formation (< 30 s), which was much greater than that seen with PE. This early phase correlated with PKC translocation. Acute or chronic exposure to 12-O-tetradecanoylphorbol-13-acetate (TPA) or treatment with Ro-31-8220 showed that the stimulation of PI hydrolysis by PE, but not ET-1 or BK, was inhibited by activation of PKC. Furthermore, ET-1 and BK heterologously desensitized the stimulation of PI hydrolysis by PE, ET-1 or BK homologously uncoupled their own receptors from [3H]InsP3 formation, but there was no evidence of heterologous desensitization with these two agonists. Anomalously, chronic exposure to TPA increased the stimulation of PI hydrolysis by BK, but this probably resulted from an increase in BK receptor density. PLD was also rapidly activated by TPA. ET-1, BK or PE. Experiments with Ro-31-8220 showed that the stimulation of PLD by ET-1 and BK was mediated through activation of PKC. We discuss the characteristics of the activation of PI hydrolysis and PLD by ET-1, BK, and PE with respect to the translocation of PKC.

Adrenergic alpha-Agonists↗

PubMed2001

Altered contractions to endothelin-1, phenylephrine, potassium chloride and relaxations to acetylcholine at various stages of renal hypertension in the rat.

This study is aimed at investigating the contraction and relaxation responses in the thoracic and abdominal aortae at various stages of hypertension. Hypertension in the rats was produced by aortic banding and the responses in the abdominal and thoracic aortic rings were studied 2 and 8 weeks after aortic banding. Contractile responses to phenylephrine ( 10(-6)M), KCl (80 mM) or to endothelin-1 ( 10(-12)to 10(-6)M) and the relaxation responses to acetylcholine ( 10(-7)to 10(-5)M) were similar in the thoracic and abdominal rings of normotensive rats. The intact thoracic rings from 2 week aortic-banded hypertensive rats (ABHR) showed attenuated responses to all the contractile agents used. However, the relaxation to acetylcholine was not altered. In the rings from 8 week ABHR, the responses to contractile agents were not significantly altered but the acetylcholine-induced relaxations were significantly attenuated. The endothelial-derived relaxing factors might act to antagonize the vasoconstrictive responses during the onset of hypertension but might be disabled, as the endothelial dysfunction becomes predominant after 8 weeks of hypertension. The results thus suggest that the contractile and relaxant responses are differentially altered during different stages of hypertension.

Acetylcholine↗

PubMed1982

alpha-Adrenoceptors mediating the positive inotropic effect of phenylephrine in the right ventricular muscle of the monkey (Macaca fuscata).

The property of adrenoceptors mediating the positive inotropic effect (PIE) in the ventricular muscle of the Japanese monkey (Macaca fuscata) was investigated by the use of phenylephrine (PE) and adrenoceptor antagonists. The intrinsic activity (0.6) and the pD2-value (5.41) for PE were comparable to those in other mammalian species. The beta-adrenoceptor antagonist, pindolol (3 x 10(-8) mol/l) shifted only the upper part of the concentration-response curve (CRC) for PE to the right; the pD2-value for PE was not significantly affected by pindolol. On the other hand, phentolamine (10(-6) mol/l) shifted the lower part of the CRC for PE more than the upper part. In the presence of both pindolol and phentolamine the curve was shifted to the right in a parallel manner. The time required for twitch relaxation was negatively correlated to the degree of PIE of PE in the presence of phentolamine but not pindolol. These results indicate that both beta- and alpha-adrenoceptors mediate the positive inotropic action in the ventricular muscle of the Japanese monkey and that in contrast to the action via beta-adrenoceptors the action via alpha-adrenoceptors is not accompanied by the "relaxant effect".

Animals↗

PubMed1984

Regulation of oxygen consumption in perfused rat liver: decrease by alpha-sympathetic nerve stimulation and increase by the alpha-agonist phenylephrine.

In livers perfused with Krebs-Henseleit bicarbonate buffer containing bovine red cells, 5 mM glucose and 2 mM lactate, electrical stimulation round the hepatic artery and the portal vein caused via alpha-receptors a decrease in oxygen consumption and portal flow, an increase in glucose output and a switch from lactate uptake to output. In livers perfused with erythrocyte- and substrate-free buffer both in a volume- or pressure-constant system stimulation of the liver nerves resulted in similar changes. Infusion of the alpha-agonist phenylephrine mimicked the metabolic and hemodynamic nerve effects, but led to an increase in oxygen uptake. The converse effects of alpha-sympathetic nerve stimulation and alpha-agonist infusion on oxygen consumption indicate either a different mode of action or a complex mechanism with opposing metabolic and hemodynamic components.

Animals↗

PubMed1993

Potentiating effect of phenylephrine on isoproterenol activation of thyroxine type II deiodinase in the pineal gland of adult rats.

In the present study we show, for the first time, that phenylephrine (PHE), an alpha-adrenergic receptor agonist, potentiates the effect of isoproterenol (ISO), a beta-adrenergic agonist, in activating pineal type II5'-deiodinase (5'-D) activity. The potentiating effect of PHE was observed only at doses of ISO which induce submaximal activation of the enzyme. However, at doses which lead to maximal activation of the enzyme, PHE was ineffective. The results suggest that not only beta-, but also alpha-adrenergic receptors, are involved in the sympathetic noradrenergic regulation of pineal 5'-D activity in the adult rat.

Animals↗

PubMed1994

Effects of isoprenaline, phenylephrine on heart and influence of nifedipine on these effects.

In a perfused isovolumetrically contracting rat heart model, the effects of isoprenaline (IPN) and phenylephrine (PE) on myocardial contraction and relaxation were investigated, and the influence of nifedipine on these effects was studied. Both IPN and PE increased the myocardial contraction and improved its relaxation, but some differences existed. Nifedipine (10 nmol/L) substantially inhibited the PE-mediated inotropic effect, but in case of IPN-mediated inotropic ones, it did not. It was assumed that there may be various types of slow channels, one was activated by IPN, and the other, by PE.

Animals↗

PubMed1990

Halothane anaesthesia does not modify the cardiovascular response to phenylephrine in man.

Conflicting results exist regarding the ability of halothane to alter the vascular response to alpha 1 adrenergic agonists in animals. Because data from humans are lacking, we studied the haemodynamic response to phenylephrine (PHE) in eight patients about to undergo coronary artery bypass surgery before and during halothane anaesthesia. After obtaining baseline measurements in patients while awake, the responses to PHE infusion at 30, 40, and 50 micrograms.min-1 were determined. New baseline measurements were made following stabilisation during anaesthesia with halothane, one per cent inspired in oxygen, prior to surgical incision. Then the responses to identical PHE doses were measured again. Halothane did not influence the cardiovascular response to PHE: there was no dose-response shift for any cardiovascular variable. No arrhythmias or signs of ischaemia were observed. We conclude that one per cent halothane anaesthesia does not attenuate PHE-induced vasoconstriction in man.

Anesthesia, Inhalation↗

PubMed1992

Does propranolol alter the vascular response to phenylephrine before or during halothane anaesthesia in patients with coronary artery disease?

Preoperative beta-adrenergic blockade with propranolol, by allowing unopposed alpha-adrenergic stimulation in response to stress, has been suggested as a factor contributing to hypertension following coronary artery bypass surgery (CABG). Thus, one might expect to find an exaggerated haemodynamic response to phenylephrine (PHE), an alpha 1 agonist. To study this, the cardiovascular response to PHE infusion at 30, 40, and 50 microgram.min-1 prior to and during halothane anaesthesia was measured before surgical stimulation during elective CABG in patients taking chronic propranolol therapy and compared with that of patients not taking any cardiovascular medications. Chronic propranolol therapy did not alter the haemodynamic response to PHE, before or during halothane anaesthesia, and the incidence of postoperative hypertension requiring vasodilator therapy was the same for both groups.

Anesthesia, Inhalation↗

PubMed2001

Desflurane, compared to halothane, augments phenylephrine-induced contraction in isolated rat aorta smooth muscle.

PURPOSE: The mechanism responsible for the mediation of hypertension in response to increased desflurane levels is unclear. This study compared the effect of desflurane and halothane on phenylephrine (PE)-induced contraction in rat aorta ring and the effect of desflurane in the presence and absence of nitric oxide (NO) synthase activity. METHODS: Endothelium-free rat aorta rings were exposed serially to 10(-7) M, 10(-6) M and 10(-5) M PE alone and subsequently in the presence of 2 MAC desflurane and halothane. Secondly, endothelium-free preparations were exposed to 10(-6) M PE serially in the presence of 0, 1, 2 and 3 MAC desflurane and halothane. Thirdly, using an endothelium-intact preparation, the effect of desflurane on PE-induced contraction was examined, in the presence or absence of NG-nitro-L-arginine (L-NNA), an inhibitor of constitutive and inducible NO synthase. RESULTS: Contraction amplitudes secondary to 10(-6) and 10(-5) M PE in endothelium-free preparations were increased by 74% and 36% respectively (P <0.05) in the presence of 2 MAC desflurane compared to controls. In endothelium-free preparations, contraction amplitudes secondary to 10(-6) M PE were increased in the presence of 1 and 2 MAC desflurane by 32% and 18% respectively (P <0.05) and reduced by 16% in the presence of 3 MAC halothane (P <0.05). In endothelium-intact preparations an expected absolute increase in contraction amplitude occurred in the presence of L-NNA but the desflurane effect was detectable both in the presence and absence of L-NNA. CONCLUSION: Our results suggest that desflurane may have a local vasoconstrictive effect independent of endothelium and NO synthase activity. The mechanism remains to be determined.

Anesthetics, Inhalation↗

PubMed2000

[Primary cesarean section. Use of phenylephrine during anesthesia in a patient with hypertrophic obstructive cardiomyopathy].

We report on anaesthesia management for elective Caesarean section in a parturient woman with hypertrophic obstructive cardiomyopathy (HOCM). Special considerations for anaesthesia are associated with this condition. Women with HOCM need a closed diagnostic and therapeutic follow-up during pregnancy. Anaesthesiologists have to be aware of the cardiac peculiarities. Special risks may arise from endogenous catecholamine release during labour or from therapy with beta-adrenergic drugs for treatment of blood pressure drops or suppression of uterine contractions. Epidural anaesthesia is an appropriate anaesthesia method for Caesarean section, also in patients with HOCM. Adequate hemodynamic monitoring is essential. Phenylephrine is a pure alpha-adrenergic vasoconstrictor without inotropic effects. It is suitable for therapy of blood pressure drops induced by peripheral vasodilation.

Adult↗

PubMed2005

The phenylephrine blood pressure clamp in pharmacologic magnetic resonance imaging: reduction of systemic confounds and improved detectability of drug-induced BOLD signal changes.

RATIONALE: Peripheral physiologic changes accompany many central pharmacologic manipulations and can interact with brain activity and cerebral perfusion in complex ways. This considerably complicates the interpretation of drug-induced brain activity changes. OBJECTIVES: To evaluate a method whereby drug-induced blood pressure (BP) changes are prevented. METHODS: A continuously adjusted infusion of the peripheral vasoconstrictor phenylephrine (PEP) was used to counter-regulate BP changes elicited by application of the dopamine receptor agonist apomorphine (APO) in the rat. Central effects of APO were measured using pharmacologic magnetic resonance imaging (phMRI) with blood oxygenation level dependent (BOLD) contrast at a field strength of 7 T. RESULTS: Compared to a NOPEP control group, the PEP blood pressure clamp successfully prevented BP changes and improved the detectability of central APO effects. Moreover, APO-induced central changes no longer correlated with BP time courses. CONCLUSIONS: The method is suitable for isolating central drug effects from peripherally originating (BP) confounds in high-field functional magnetic resonance imaging (fMRI) studies. It may also be useful in fMRI studies of autonomic regulation, cognition, and emotion if the experimental manipulation entails BP changes.

Analysis of Variance↗

PubMed1999

Changes of intracellular calcium concentrations by phenylephrine in renal arterial smooth muscle cells.

In smooth muscle cells isolated from swine renal interlobar arteries, phenylephrine (PE) at concentrations of 1-10 microM produced biphasic increases of the intracellular calcium concentration. An early transient rise was followed by a maintained plateau. The maintained component was sensitive to extracellular calcium, in contrast to the early transient, which was still observed in nominally calcium-free solution. Nifedipine (1 microM) and NiCl2 (100 microM) only weakly affected the calcium signal, suggesting that voltage-sensitive calcium channels play only a minor role in the PE-induced changes in intracellular calcium. Thapsigargin (0.5 microM) elevated the intracellular calcium concentration and depressed both the early transient and the maintained component of the PE response. In calciumfree medium PE induced a transient rise of the intracellular calcium concentration with a depressed plateau. Readmission of calcium elevated the intracellular calcium concentration above the baseline. Both components of the PE-induced calcium signal were completely abolished when the cells were pretreated with the phospholipase C (PLC) inhibitor U73122 (2 microM). LaCl3 (100 microM, 1 mM), an inhibitor of calcium-release-activated current (ICRAC), had no effect on the PE-induced calcium signal. GdCl3 (50 microM), SKF 96365 (10 microM) and flufenamic acid (100 microM), reported to inhibit nonselective cation channels, blocked or transiently reduced the maintained calcium signal. Several protein kinase inhibitors such as genistein (10 microM), H7 (50 microM), H89 (1 microM) and bisindolylmaleimide (0.2 microM) reduced the maintained calcium signal. We conclude that the initial transient spike of the PE-induced calcium signal is due to release of calcium from inositol 1,4,5-trisphosphate-sensitive calcium stores evoked by alpha 1-adrenoceptor-coupled stimulation of PLC and that the maintained component is due to capacitative calcium entry, which is modulated by protein kinases.

Adrenergic alpha-Agonists↗

PubMed1983

Effects of trimazosin and prazosin on blood pressure and on pressor responses to phenylephrine in rats.

As part of an ongoing investigation into the cardiovascular properties of trimazosin, 99 male Sprague-Dawley rats were anesthetized and cannulas were placed in jugular veins for administration of drugs. The rats were injected with phenylephrine and then treated with either solvent, diazoxide, prazosin, or trimazosin. Blood pressure and heart rate were measured by a pressure transducer and a biotachometer, respectively; both were recorded continuously. Preliminary results indicate that trimazosin was less potent but more efficacious in lowering blood pressure than was prazosin and caused less blockade of the alpha-1-adrenoceptors even when its hypotensive effect exceeded that of prazosin. The differences in hypotensive potency and in alpha-1-receptor blockade are consistent with the fact that trimazosin has less affinity than does prazosin for alpha-1-receptors in vitro. The greater efficacy of trimazosin, compared to prazosin, is further evidence that in addition to alpha-1-receptor blockade, another mechanism contributes to the hypotensive effect of trimazosin. This mechanism has yet to be elucidated.

Animals↗