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At least 217 records · Page 12Linked to original sources

PubMed1998

Protein kinase C does not mediate phenylephrine-induced down-regulation of Madin-Darby canine kidney cell alpha-1B adrenoceptors.

We examined the down-regulation of alpha-1B adrenoceptors in Madin-Darby canine kidney D1 (MDCK) cells with an emphasis on a possible role of protein kinase C. The alpha-1 adrenoceptor agonist phenylephrine (1-100 microM) concentration-dependently down-regulated alpha-1B adrenoceptors in MDCK cells. Down-regulation by 100 microM phenylephrine was detectable after 2 hr and maximal after 8 to 24 hr. The receptor down-regulation was accompanied by a decrease in phenylephrine-stimulated inositol phosphate formation but not by an altered expression of immunodetectable Gq/11 alpha subunits. Even though alpha-1B adrenoceptor and P2 purinergic receptor stimulation promote prostaglandin E2 formation, receptor down-regulation was not prevented by indomethacin (10 microM) treatment but was partly mimicked by treatment with the purinergic receptor agonists adenosine-5'-O-(3-thio)triphosphate and 2-methylthio-ATP (300 microM each). Phorbol-12-myristate-13-acetate (1-100 nM) concentration-dependently down-regulated MDCK alpha-1B adrenoceptors to a greater extent than did phenylephrine. Three protein kinase C inhibitors, H7 (100 microM), staurosporine (100 nM) and KT5926 (1 microM), markedly attenuated receptor down-regulation promoted by phorbol ester but did not affect that by phenylephrine. Two inhibitors of Ca++/calmodulin protein kinase pathways, KT5926 (1 microM) and W-7 (30 microM), also failed to prevent phenylephrine-induced down-regulation of alpha-1B adrenoceptors. We conclude that agonist-induced down-regulation of MDCK cell alpha-1B adrenoceptors is mimicked by a protein kinase C-activating phorbol ester but that the second messenger kinases protein kinase C and Ca++/calmodulin protein kinase do not mediate agonist-induced down-regulation of the alpha-1B adrenoceptor.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1983

2.5% v 10% phenylephrine in maintaining mydriasis during cataract surgery.

A 10% viscous solution of phenylephrine hydrochloride was more effective than a 2.5% aqueous solution of phenylephrine hydrochloride in maintaining mydriasis during extracapsular cataract surgery. The pupil area after nucleus expression was 57% larger with the stronger phenylephrine concentration. The difference in pupil area was greater in darkly pigmented irides (114%) than in moderately pigmented (70%) or lightly pigmented irides (12%). Mean BP elevations following phenylephrine administration were not higher in the group receiving the 10% solution than in the group receiving the 2.5% solution. In darkly pigmented irides, a 10% viscous solution of phenylephrine hydrochloride is more effective than a 2.5% concentration in maintaining mydriasis during cataract surgery.

Adult↗

PubMed1984

Dissociation of the pressor and cerebral protective effects of phenylephrine.

The relationship between the pressor and cerebral protective effects of the alpha-adrenergic agonist phenylephrine was assessed. Sprague-Dawley rats were anesthetized and underwent right carotid artery ligation and placement of arterial and central venous pressure catheters and EEG electrodes. Following a two-hour recovery, the rats were exposed to hypoxia (4.5% chamber O2). Three groups of rats were infused with phenylephrine hydrochloride at 17, 35, and 88 micrograms/kg/min, respectively. A fourth group received normal saline, and a fifth, no infusion. All rats receiving phenylephrine experienced an initial pressor response to 130, 162, and 180 mm Hg, respectively, compared with control animals (119 mm Hg). Cerebral electrical activity was prolonged with the two lower doses of phenylephrine (24 +/- 3 minutes and 21 +/- 4 minutes, respectively), compared with the control response (13 +/- 1 minutes). High-dose phenylephrine decreased survival time (8 +/- 1 minutes), despite higher BP at the time of brain death.

Animals↗

PubMed2002

Modification of ureteral motility and promotion of urine flow around an intraureteral obstruction by CL-316243, phenylephrine, and furosemide in dogs.

The aim of this study was to evaluate the effects of a beta3-adrenoceptor (AR) agonist (CL-316243), an alpha1-AR agonist (phenylephrine), and a loop diuretic (furosemide) on the spontaneous rhythmic contractions of the isolated canine ureter and on an acute ureteral obstruction produced by inflation of a balloon catheter in anesthetized dogs. In the isolated ureter, CL-316243 concentration dependently reduced both the amplitude and frequency of the rhythmic contractions (pD(2): 7.19 +/- 0.33), whereas phenylephrine significantly enhanced both variables (pD(2): 5.26 +/- 0.09) and furosemide reduced them only slightly. In the acute ureteral obstruction model, the intraureteral pressure (IUP) gradually rose to reach a plateau of 58.9 mm Hg after inflation of a balloon catheter within the lower ureter. Intravenous administration of CL-316243 (0.3 microg/kg) significantly reduced the elevated IUP and the resumed urine flow (UF), leading to a sustained reduction in the IUP. In contrast, the IUP continued to increase above the plateau level for 10 minutes after phenylephrine administration (10 microg/kg) and for 30 minutes after furosemide administration (1,000 microg/kg). In the phenylephrine group, the UF resumed when the IUP reached 75.8 mm Hg, and thereafter the IUP gradually decreased in parallel with the increase in the UF. From these results, we conclude that in dogs, CL-316243 reduces the IUP by allowing the UF to resume as a result of a relaxation of ureter at the obstruction site, whereas with phenylephrine, the reduction in the IUP is secondary to a resumption in the UF resulting from an induced contraction of ureter that causes an increase in hydrostatic pressure above the obstruction site.

Adrenergic alpha-Agonists↗

PubMed1987

Reduction of uterine blood flow by phenylephrine, an alpha-adrenergic agonist, in the day 11 pregnant rat: relationship to potentiation of acetazolamide teratogenesis.

We have demonstrated previously that phenylephrine, a selective postsynaptic alpha-1-adrenergic agonist, significantly potentiates the incidence of acetazolamide-induced right forelimb ectrodactyly in a dose-response manner. As reported herein, phenylephrine also decreases maternal uterine blood flow in a dose-response manner as measured by radioactive microsphere methodology. At the potentiative dose of 12.5 mg/kg phenylephrine decreases uterine blood flow by 86.8% when compared to control. In turn, pretreatment with prazosin, a selective postsynaptic alpha-1-adrenergic antagonist, prevents this large decrease in uterine blood flow and abolishes the potentiation of acetazolamide teratogenesis by phenylephrine. Although the effects of acetazolamide or acetazolamide + phenylephrine on uterine blood flow were not measured the data suggest a correlation between decreased uterine blood flow and potentiation of acetazolamide teratogenesis.

Acetazolamide↗

PubMed1991

Opposite modulation of ouabain cardiotoxicity by hexamethyleneamiloride and phenylephrine.

To see whether the Na/H antiporter plays a role in digitalis cardiotoxicity, we investigated the influence of modulators of Na/H exchange on the toxic effects of ouabain in isolated, paced (0.4 Hz) rat left atria. Ouabain (1 mmol/l) caused a transient positive inotropic effect followed by toxic events, including a complete loss of developed force and a gradual increase in resting force. In the presence of hexamethyleneamiloride (3 and 10 mumol/l), an inhibitor of Na/H exchange, ouabain (1 mmol/l) caused a sustained positive inotropic effect without toxicity. By contrast, phenylephrine (100 mumol/l), an alpha-adrenoceptor agonist reported to stimulate the antiporter, hastened the development of ouabain's toxicity. Neither ouabain, at a subtoxic concentration (650 mumol/l), nor phenylephrine (100 mumol/l) affected diastolic force, but in their combined presence, a substantial contracture developed and twitch contractions disappeared. Phenylephrine (30 or 100 mumol/l) or adrenaline (30 mumol/l), in the presence of a beta-adrenoceptor antagonist, increased the intracellular pH by up to 0.15 pH unit, as measured using ion-selective microelectrodes in quiescent preparations. This effect on pHi was prevented by hexamethyleneamiloride (10 mumol/l). Consistent with phenylephrine's ability to stimulate Na+ influx via the Na/H antiporter, phenylephrine (100 mumol/l) increased intracellular Na+ activity by about 3 mmol/l in ouabain (650 mumol/l)-treated atria. These findings indicate that modulators of Na/H exchange affect the cardiotoxicity of digitalis glycosides and imply that the stimulation of myocardial alpha-adrenoceptors may aggravate digitalis toxicity.

Amiloride↗

PubMed1991

Differential electrophysiologic and inotropic effects of phenylephrine in atrial and ventricular heart muscle preparations from rats.

Stimulation of alpha 1-adrenoceptors evokes a different pattern of inotropic responses in atrial and ventricular heart muscle preparations from rats. The inotropic effects are accompanied by different changes in membrane potential. In an attempt to clarify the question whether or to which extent these events are causally related, the effects of phenylephrine on force of contraction, transmembrane potential, Ca2+ current (ICa) and K+ currents were comparatively studied in either tissue. In atrial preparations, phenylephrine 10 mumol/l caused an increase in force of contraction, a marked prolongation of the action potential duration and a depolarization of the membrane at rest. In the ventricle, however, the addition of phenylephrine 10 mumol/l produced first a decline in force of contraction associated with a hyperpolarization of the membrane and a reduction in the action potential duration. These changes were followed by an increase in force of contraction and a slight prolongation of the action potential, whereas the resting membrane potential remained increased. The hyperpolarization was eliminated in the presence of ouabain 100 mumol/l. In enzymatically isolated atrial and ventricular myocytes, the whole-cell voltage clamp technique was used to study membrane currents on exposure to phenylephrine. Phenylephrine 30 mumol/l did not affect the magnitude of ICa in either cell type. Transient and steady state K+ outward currents, however, were significantly diminished to a similar extent in atrial and in ventricular myocytes. It is concluded that the positive inotropic effect of alpha 1-adrenoceptor stimulation in the rat atrium is related to an increase in action potential duration and a decrease in resting membrane potential due to a decrease in K+ currents.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1994

Ramipril prevents hypersensitivity to phenylephrine in aorta from streptozotocin-induced diabetic rats.

This study investigated the protective effect of the angiotensin converting enzyme inhibitor, ramipril, on endothelium-dependent responses in arteries from control (CON) and streptozotocin-induced (STZ) diabetic rats. Three hypotheses were tested: 1) there is an endothelium-dependent component to the increased alpha-adrenergic responsiveness characteristic of diabetes; 2) endothelium-dependent, acetylcholine-induced relaxation is attenuated in aorta from diabetic rats; and 3) ramipril (3 mg/kg daily in the food, 12-15 weeks) will prevent functional vascular changes in diabetic rats. Vascular function was assessed in aortic rings using standard muscle bath procedures for measurement of isometric force. Sensitivity to phenylephrine was increased in aortic rings from diabetic compared to control values [pD2 values (-log ED50): CON = 6.22 +/- 0.12, STZ = 7.54 +/- 0.11), and removal of the endothelium (-Endo) increased phenylephrine sensitivity (CON-Endo = 7.40 +/- 0.11, STZ-Endo = 8.32 +/- 0.18). The magnitude of the shift in responsiveness following endothelium removal was greatest in control rats. Ramipril treatment (Ram) partially normalized phenylephrine responsiveness in intact (STZ + Ram = 6.55 +/- 0.11) and denuded (STZ-Endo + Ram = 7.75 +/- 0.10) vessels. Vasodilatation to acetylcholine and nitroglycerin was not altered in diabetic rats nor was it affected by ramipril treatment. Diabetes increases contractile sensitivity to phenylephrine but not to vasodilators and chronic ramipril treatment prevents this increase in contractile sensitivity. Ramipril treatment did not alter the hyperglycaemic condition induced by streptozotocin. The changes in phenylephrine sensitivity appear to involve an endothelial and a smooth muscle component.

Acetylcholine↗

PubMed1987

The actions of methacholine, phenylephrine, salbutamol and histamine on mucus secretion from the ferret in-vitro trachea.

Methacholine, phenylephrine and histamine produced highly significant and salbutamol significant increases in the rate of mucus secretion from the ferret trachea. Methacholine, phenylephrine and histamine all produced highly significant increases in the rate of output of lysozyme, but the concentration of lysozyme in the mucus was significantly increased only by phenylephrine. Salbutamol produced no significant change in the output of lysozyme, and the concentration of lysozyme in the mucus was significantly decreased. It is concluded that methacholine, phenylephrine and histamine are potent stimulators of serous cell secretion whereas salbutamol has only a weak secretory action on these cells. Methacholine, histamine and salbutamol probably stimulate secretion from mucous cells as well as from serous cells. The increase in the concentration of lysozyme produced by phenylephrine may be due to stimulation of a fluid reabsorption mechanism.

Albuterol↗

PubMed1984

The effect of subarachnoid epinephrine and phenylephrine on spinal cord blood flow.

Eighteen mongrel dogs were divided into three equal groups. Spinal cord and spinal dural blood flow in the cervical, thoracic and lumbosacral regions were measured using the radioactive microsphere technique. Measurements were taken before and 10 and 40 minutes after lumbar subarachnoid injection of one of the following: physiologic saline; epinephrine 200 micrograms or phenylephrine 5 mg. No significant change in spinal cord blood flow occurred in any of the groups, nor was there any difference between the groups. Dogs receiving subarachnoid phenylephrine did demonstrate a significant reduction of thoracic dural blood flow at ten minutes. Dogs receiving intrathecal epinephrine or phenylephrine demonstrated a significant reduction in lumbo-sacral dural blood flow at ten minutes after injection. The reduction in dural blood flow was still evident at 40 minutes in dogs receiving phenylephrine. Subarachnoid epinephrine (200 micrograms) and phenylephrine (5 mg) do not effect spinal cord blood flow but do produce regional dural vasoconstriction.

Animals↗

PubMed1996

Comparison of glucose 7.5% and 0.75% with or without phenylephrine for tetracaine spinal anaesthesia.

PURPOSE: To investigate whether a marginally hyperbaric tetracaine solution with or without phenylephrine could produce consistent blocks as compared with a conventionally hyperbaric tetracaine solution injected at L3-4 interspace with the patient in the lateral position. METHODS: We studied 120 ASA I or II patients scheduled for elective surgery to the lower limb. Patients were randomly divided into four equal groups to receive spinal anaesthesia using tetracaine 0.5% in glucose 0.75% or 7.5%, with or without phenylephrine 0.125%. Neural block was assessed in a double-blind manner by cold, pinprick, and touch sensation, and a modified Bromage scale after the injection of the study drug. RESULTS: The median (10th, 90th percentiles) peak dermatomal level to pinprick obtained by the solutions in glucose 0.75% was T10 (L1, T5), which was lower than that obtained by the solution in glucose 7.5% extending to T5 (T10, T3) and T5 (T10, T2) with or without phenylephrine, respectively (P < 0.0001). The addition of phenylephrine prolonged the time to two-segment regression but did not change the maximum extent of blocks. CONCLUSIONS: A marginally hyperbaric tetracaine with or without phenylephrine produced consistent blocks with spread restricted to the lower thoracic segments when administered intrathecally at the L3-4 interspace with the patient in the lateral position.

Adult↗

PubMedDate not supplied

Effects of topical phenylephrine on blood flow in the posterior segments of monkey and aged human eyes.

PURPOSE: The aim of this study was to evaluate the effects of topical 5% phenylephrine on circulation in the optic nerve head (ONH) of cynomolgus monkeys and in the central retinal artery (CRA) of aged patients. METHODS: In five monkeys, ONH tissue blood velocity (NB(ONH)), determined using the laser speckle method, and intraocular pressure (IOP), blood pressure (BP), and pulse rate (PR) were measured 2 h after a single unilateral instillation and after a 7-day twice-daily unilateral instillation of phenylephrine. In 20 aged patients (mean age: 70.4 years), the CRA circulation indices were determined by color Doppler imaging (CDI), and IOP, BP, and PR were measured before and after four serial unilateral instillations at 30-min intervals of phenylephrine. RESULTS: In the monkeys, there was no significant change in IOP, BR, or PR, while NB(ONH) decreased 2 h after a single instillation ( P = 0.080) and after a 7-day instillation ( P = 0.043). In theaged patients, IOP in the phenylephrine-treated eyes significantly increased ( P = 0.022), while the CDI indices, BR, and PR did not. In this CDI assessment, the statistical power to detect significant changes (P < 0.05) in the resistive index was estimated as 4.8% of the standard deviation. CONCLUSIONS: Topical phenylephrine decreased the ONH tissue blood velocity in monkeys, suggesting possible risks regarding circulation in the posterior portion of the eye. However, these effects were not observed in the CRA circulation in the patients.

Administration, Topical↗

PubMed1989

Effects of perfusion flow rate, prostaglandin F2 alpha, phenylephrine, and serotonin on isolated, perfused brains of spontaneously hypertensive rats.

Effects of perfusion flow rate and three vasoconstrictors, phenylephrine, prostaglandin F2 alpha (PGF2 alpha) and serotonin, on isolated, perfused brain preparations of spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY) were investigated. The basal perfusion pressure of the cerebral vascular beds at a flow rate of 2.5 ml/min was 48 +/- 3 mm Hg (n = 11) in SHR and 32 +/- 2 mm Hg (n = 12) in WKY (P less than 0.005). The perfusion pressures at all flow rates tested (2.5-6.5 ml/min) in SHR were significantly greater than those in WKY. Concentration-perfusion pressure curves for the vasoconstrictors showed that the brain vascular bed was much more reactive to serotonin compared with phenylephrine and PGF2 alpha. EC50 values (-logM) for serotonin in the perfused brains of SHR and WKY were 7.0 +/- 0.06 (n = 10) and 6.5 +/- 0.06 (n = 11), respectively (P less than 0.01). There were no differences in EC50 values for phenylephrine or PGF2 alpha between SHR and WKY. Exogenous serotonin and phenylephrine caused significantly greater maximal vasoconstrictor responses in SHR compared with WKY, while the pressor response to PGF2 alpha was very weak and no significant difference between SHR and WKY preparations was observed. These results indicate that cerebral vascular beds in SHR exhibit higher cerebrovascular resistance than those in WKY. and that reactivity and sensitivity to serotonin and reactivity to phenylephrine in SHR rats are enhanced to a greater extent compared to WKY.

Animals↗

PubMed1996

Effects of intravenous phenylephrine on blood pressure, nociception, and neural activity in the rostral ventral medulla in rats.

Acute or chronic increases in arterial blood pressure are associated with decreases in nociception. In addition, acute increases in arterial blood pressure inhibit ON cells and excite OFF cells of the rostral ventral medulla (RVM). The current study tested whether the antinociception produced by increases in blood pressure is dependent on changes in the activity of ON and/or OFF cells. Single unit activity of ON or OFF cells was recorded in the RVM during increases in blood pressure produced by intravenous infusion of phenylephrine (1, 2.5, or 10 micrograms/min for 21 min) in lightly anesthetized rats. Nociception was measured using the tail flick test. Phenylephrine dose-dependently increased mean arterial pressure and tail flick latency, but had inconsistent effects on neural activity in the RVM. In a second study, the effects of phenylephrine infusion on tail flick latency was determined before and after saline or lidocaine microinjections into the RVM. Lidocaine had no effect on the ability of phenylephrine to inhibit the tail flick reflex. These data suggest that the RVM, and therefore ON and OFF cells, is not required for phenylephrine-induced antinociception.

Analysis of Variance↗

PubMed1986

Dilute solutions of phenylephrine and pilocarpine in the diagnosis of disordered autonomic innervation of the iris. Observations in normal subjects, and in the syndromes of Horner and Holmes-Adie.

A standardized method of testing irideal sensitivity to 1% phenylephrine and 0.05% pilocarpine is described, and a quantitative basis for pupillary neurotransmitter "supersensitivity" established. In a normal 20-year-old subject the pupillary diameter increases in bright light by no more than 2.1 mm 1 h after ocular application of phenylephrine; this figure should be adjusted for age since "phenylephrine sensitivity" of the iris increases by 0.23 mm per decade. The pupillary diameter, when measured in darkness, has normally decreased by less than or equal to 1.4 mm within 30 min of administration of pilocarpine. Differences in drug-induced diameter alterations between pairs of pupils should not normally exceed 0.7 mm for phenylephrine or 0.4 mm for pilocarpine. Seventy one percent of sympathetically denervated or decentralized (Horner's) pupils and 41% of parasympathetically denervated ("tonic") pupils are abnormally responsive or "supersensitive" to dilute solutions of phenylephrine and pilocarpine respectively. Supersensitivity to these agents is therefore a useful but not invariable diagnostic feature of disturbed irideal innervation.

Adie Syndrome↗

PubMed1994

Cyclosporin A antagonizes phenylephrine, oxytocin and angiotensin effects on glucose metabolism in rat thymus lymphocytes.

Effects of phenylephrine, oxytocin and angiotensin on fructose 2,6-bisphosphate (Fru 2,6-P2) content and glycolytic parameters were studied in incubated thymus lymphocytes. These hormones modified Fru 2,6-P2 content dependent upon the energetic status of the cells. In non-preincubated thymus lymphocytes (with relatively high levels of glycogen and ATP), phenylephrine, oxytocin and angiotensin depressed Fru 2,6-P2 content in a dose-dependent manner. The opposite was found when the cells were preincubated for 2 h without substrates (low levels of ATP and glycogen). Changes in lactate release were less evident, but significant. Phenylephrine did not modify the maximal activities of phosphofructokinase (PFK)-1 or PFK-2. However, both submaximal PFK-1 and PFK-2 activities were inhibited by phenylephrine, and the response to exogenous Fru 2,6-P2 on PFK-1 was also altered. The activities of Fru 1,6-P2 and pyruvate kinase were not modified by phenylephrine or A23187 treatment. Simultaneous presence of Cyclosporin A (CsA), an immunosuppressive drug, antagonizes the alpha-adrenergic effect on Fru 2,6-P2 content. CsA alone did not alter basal levels of ATP, hexose phosphate or Fru 2,6-P2, and its opposing effect to alpha-agonist was dose-dependent. CsA cannot change the positive action of PMA or the negative action of A23187 on Fru 2,6-P2 content. The present data suggest that CsA acts prior to calcium liberation and protein kinase C activation. Different possible molecular models are discussed.

Adenosine Triphosphate↗

PubMed1982

Cyclic AMP-dependent and independent positive inotropic effects of phenylephrine.

To summarize, a large number of studies indicate that the effects of phenylephrine on cardiac contractility are mediated through alpha-adrenoceptors, although not exclusively. There are an equally large number of reports indicating some beta-adrenoceptor stimulant effects of phenylephrine. Of the latter, some are based on the finding of antagonism by beta-receptor antagonists and some on the fact that phenylephrine is capable of elevating cyclic AMP levels, which is primarily a beta-, and not alpha-adrenoceptor effect. Although it is now widely accepted that phenylephrine elevates cyclic AMP levels, the contribution and significance of the elevated nucleotide levels to the overall positive inotropy of phenylephrine appears to be small. Alpha-Adrenoceptors may be involved with calcium, although the precise interaction between calcium and the alpha-adrenoceptor is not clear. Finally, the adrenergic effects seem to depend on the experimental and physiological conditions including calcium ion concentration, thyroid state and driving frequency.

Animals↗

PubMed1994

High-performance liquid chromatographic determination of phenylephrine in human serum using column switching with fluorescence detection.

A method for the determination of total phenylephrine (free plus conjugated) in human serum was developed using column-switching high-performance liquid chromatography (HPLC) with fluorescence detection. After serum was deproteinized with acetonitrile, the conjugated phenylephrine was hydrolyzed with diluted hydrochloric acid. The solution was evaporated to dryness. The reconstituted residue was analyzed with HPLC using a heart-cut technique. Good recoveries of the analytes from spiked human serum samples were obtained with small coefficients of variation. A good linear response was obtained for the concentration range 5-500 ng/ml. The lower limit of quantitation for phenylephrine in human serum was 5 ng/ml. The method was applied to the determination of phenylephrine in human serum after oral administration of phenylephrine hydrochloride.

Chromatography, High Pressure Liquid↗