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NTP Toxicology and Carcinogenesis Studies of Phenylephrine Hydrochloride (CAS No. 61-76-7) in F344/N Rats and B6C3F1 Mice (Feed Studies).

Phenylephrine hydrochloride is a sympathomimetic amine recommended for use as a nasal decongestant and as a mydriatic in ophthalmic applications. In 1977, total U.S. human exposure was estimated at 1.9 x 107 g per year. Phenylephrine hydrochloride was nominated for toxicology and carcinogenesis studies because of a lack of previous long-term studies and because two other sympathomimetic agents (soterenol hydrochloride and mesuprine hydrochloride) produced mesovarial leiomyomas in Sprague-Dawley rats. Toxicology and carcinogenesis studies of USP-grade phenylephrine hydrochloride were conducted by administering diets containing the chemical (99% pure) to F344/N rats and B6C3F1 mice of each sex in studies of 14 days, 12 weeks, and 2 years. In the 14-day studies, no toxic effects were seen in rats or mice fed diets containing up to 2,000 ppm phenylephrine hydrochloride. Doses were increased in the 12-week studies, and deaths of male rats and male mice were observed in groups fed diets containing 10,000 or 20,000 ppm; 1/10 male rats in the 5,000-ppm group died. Other than inflammatory eye lesions (considered secondary to the pharmacologic drying action of the chemical), no specific organ toxicity was noted. Body weights decreased as concentrations of phenylephrine hydrochloride in the diet were increased, and feed consumption was lower in dosed rats. Doses of 0, 620, and 1,250 ppm for rats and 0, 1,250, and 2,500 ppm for mice were selected for the 2-year studies because of the decreased body weight gains in animals given higher doses in the 12-week studies. In the 2-year studies, the approximate amount of phenylephrine hydrochloride consumed per day was 24 mg/kg for low dose rats, 50 mg/kg for high dose rats, 133 mg/kg for low dose mice, and 270 mg/kg for high dose mice. Body weight differences in rats appeared to be dose related, and dosed animals were 3%-15% lighter than controls. Body weights of dosed mice averaged 3%-14% lower than those of controls throughout the 2-year studies. Survival of high dose male rats was greater than that of the controls (control, 30/50; low dose, 33/50; high dose, 42/50); differences in survival were not significant for female rats (42/50; 34/50; 36/50), male mice (35/50; 38/50; 43/50), or female mice (37/50; 34/50; 34/50). Few nonneoplastic lesions were related to phenylephrine hydrochloride dosing in rats or mice. Chronic focal inflammation of the liver was observed at increased incidences in dosed rats (male: 2/50; 13/50; 17/50; female:17/50; 28/50; 35/50). Inflammation of the prostate was seen more frequently in dosed than in control males (10/50; 24/50; 24/50). The incidence of focal cellular change in the liver was increased slightly in high dose male mice (0/50; 2/50; 7/50). In male rats, mononuclear cell leukemia (24/50; 9/50; 5/50) and pheochromocytomas of the adrenal gland (14/49; 11/50; 2/50) occurred with negative trends, and the incidences in the high dose group were lower than those in the controls. No increases in neoplasia were seen in dosed male or female rats or mice. Phenylephrine hydrochloride was not mutagenic in four strains of Salmonella typhimurium (TA100, TA1535, TA1537, and TA98) with or without Aroclor 1254-induced liver S9 from male Sprague-Dawley rats or male Syrian hamsters. The results of mutagenicity studies of phenylephrine hydrochloride were equivocal in the mouse lymphoma L5178Y/TK+/- assay in the absence of S9; it was not tested in the presence of S9. Phenylephrine hydrochloride induced sister-chromatid exchanges (SCEs) but not chromosomal aberrations in Chinese hamster ovary cells. The increase in SCEs was seen only in the absence of metabolic activation with S9. An audit of the experimental data was conducted for the 2-year studies of phenylephrine hydrochloride. No data discrepancies were found that influenced the final interpretations. Under the conditions of these 2-year studies, there was no evidence of carcinogenicity of phenylephrine hydrochloride for male B6C3F1 mice given 1,250 or 2,500 ppm in feed. Survival of high dose male rats was greater than of high dose male rats was greater than that of controls, and the incidences of mononuclear cell leukemia and pheochromocytomas were lower in dosed than in control male rats. Inflammation was observed more frequently in the liver and prostate gland of dosed male rats than in controls. Synonyms: benzene methanol,3-hydroxy-a[(methylamino)methyl]hydrochloride (R)-; (-)-meta-hydroxy-a-[(methylamino)methyl]benzyl alcohol hydrochloride; meta-Synephrine hydrochloride; Neo-synephrinereg.

Journal Article↗

Comparative pupil dilation using phenylephrine alone or in combination with tropicamide.

OBJECTIVE: A prevalence survey of actinic and other eye diseases was conducted in Nambour, Queensland, Australia, in 1992. Pupils were dilated with phenylephrine alone for cataract identification because there were concerns that patient discomfort, due to cycloplegia occurring with the usual dilating agents of tropicamide and phenylephrine, may influence future compliance in an associated intervention study. This validation study was undertaken to measure the possible underestimation of cataract prevalence in this community study, which may have occurred because of inadequate dilation from phenylephrine alone. DESIGN: The study design was a repeated measures experimental design. PARTICIPANTS: Forty-seven normal subjects participated in the study. Both eyes were tested. INTERVENTION: Pupil diameter after dilation with three drops of 10% phenylephrine alone was compared with pupil diameter after dilation with three drops of 10% phenylephrine together with three drops of 1% tropicamide. The two regimens were given to the same subjects 1 week apart. Reversal was attempted with thymoxamine hydrochloride 0.5%. MAIN OUTCOME MEASURES: Pupil diameter was assessed using a Neitz cataract camera, and accommodation reserve also was measured. Subjects' subjective appreciation of return of ocular function was assessed by a questionnaire. Repeated measures analysis of variance, paired t test, McNemar's test, and Wilcoxon signed rank test were used to analyze outcomes. RESULTS: Mean maximum pupil size with 10% phenylephrine and 1% tropicamide was significantly larger than pupil size after the use of 10% phenylephrine alone (F1,19 = 18.99, P = 0.0003). However, there was no significant difference between the two dilation regimens when comparing the proportion of subjects who dilated to 6 mm or more (McNemar's X(2)1 = 2.7, P > 0.1). Compared with 10% phenylephrine and 1% tropicamide, pupil diameters were significantly smaller (t46 = 16.77, P = 0.0001), and accommodation reserve greater (t46 = 4.14, P = 0.0001), 40 minutes after reversal with thymoxamine in the group dilated with 10% phenylephrine alone. CONCLUSION: Pupil dilation with 10% phenylephrine alone, if allowed at least 40 minutes to act, will be as satisfactory for the identification of cataracts in a normal population as 10% phenylephrine and 1% tropicamide and is more acceptable because of reduced problems with glare and accommodation.

Accommodation, Ocular↗

Fetal and maternal effects of phenylephrine and ephedrine during spinal anesthesia for cesarean delivery.

BACKGROUND: In our routine practice, we observed a reduced incidence of fetal acidosis (umbilical artery pH < 7.20) at cesarean delivery during spinal anesthesia when a combination of phenylephrine and ephedrine was used as first line vasopressor therapy, compared with using ephedrine alone. METHODS: The study was randomized and double blind. It compared phenylephrine 100 microg/ml (phenylephrine group), ephedrine 3 mg/ml (ephedrine group), and phenylephrine 50 microg/ml combined with ephedrine 1.5 mg/ml (combination group), given by infusion, to maintain maternal systolic arterial pressure at baseline during spinal anesthesia for elective cesarean delivery. RESULTS: Fetal acidosis was less frequent in the phenylephrine group (1 of 48) (P = 0.004) and less frequent in the combination group (1 of 47) (P = 0.005) than in the ephedrine group (10 of 48). The mean systolic arterial pressure was similar for the three groups: Phenylephrine group median 98% (IQR 94-103) of baseline, ephedrine group 100% (96-106) and combination group 101% (97-108) (P = 0.11). The mean heart rate was higher in the ephedrine group (median 107% [IQR 99-118] of baseline) than in the phenylephrine group (88% [82-98]) (P < 0.0001), or the combination group (96% [86-102]) (P < 0.0001). Nausea and vomiting were less frequent in the phenylephrine group (nausea 17%, vomiting 0%) than in the ephedrine group (nausea 66%, vomiting 36%) (P < 0.0001), or the combination group (nausea 55%, vomiting 18%) (P < 0.0001). CONCLUSIONS: Giving phenylephrine alone by infusion at cesarean delivery was associated with a lower incidence of fetal acidosis and maternal nausea and vomiting than giving ephedrine alone. There was no advantage to combining phenylephrine and ephedrine because it increased nausea and vomiting, and it did not further improve fetal blood gas values, compared with giving phenylephrine alone.

Acidosis↗

Signals mediating stimulation of cardiomyocyte glucose transport by the alpha-adrenergic agonist phenylephrine.

Phenylephrine, a potent stimulator of cardiomyocyte glucose transport (GT), caused a rapid rise in cytosolic Ca2+ by 30%. Agents inducing a similar Ca2+ response did not stimulate (angiotension II, vasopressin) or inhibited GT by 20% (elevated extracellular Ca2+). Stimulation of GT by phorbol myristate acetate was additive to both phases of phenylephrine's effect (4 min, 60 min). Phenylephrine had no influence on the adenosine 3', 5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP) levels. Agents raising cAMP (isoproterenol) or cGMP (e.g., nitroprusside) did not stimulate GT. Wortmannin (inhibitor of 1-phosphatidylinositol 3-kinase) suppressed the action of insulin on GT but not that of phenylephrine. In contrast, the Na+/H+ exchange inhibitor amiloride (which blocks phenylephrine-induced cytosolic alkalinization or even lowers cellular pH) depressed the effect of phenylephrine by 50%, whereas insulin-stimulated GT was little affected. However, raising extracellular pH up to 8.4 failed to increase GT. Lowering pH to 6.8 decreased phenylephrine's effect by 40% whereas insulin-dependent GT was not significantly altered. Clorgyline, tranylcypromine (monoamine oxidase inhibitors), and added catalase suppressed the slow phase of phenylephrine's action, whereas amiloride also affected the fast phase. We conclude that 1) stimulation of cardiomyocyte GT by phenylephrine does not involve cAMP, cGMP, or 1-phosphatidylinositol 3-kinase; 2) protein kinase C activation cannot explain the full extent of stimulation; 3) Ca2+ release or cytosolic alkalinization may be required but is not sufficient to trigger phenylephrine's action, and 4) the slow phase of stimulation is mediated by the monoamine oxidase-dependent degradation of phenylephrine and by the resulting H2O2 formation.

Adrenergic alpha-Agonists↗

Phenylephrine-induced hypertension does not improve outcome after closed head trauma in rats.

UNLABELLED: Phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) is reported to increase cerebral perfusion pressure and collateral flow to ischemic areas of the brain in a rat model of focal cerebral ischemia. In the present study, we examined whether phenylephrine-induced hypertension of similar magnitude and duration was beneficial in a rat model of closed head trauma (CHT). Forty-eight rats were randomized into four experimental conditions: CHT at time 0 min (yes/no), plus phenylephrine-induced hypertension (increase of 30-35 mm Hg for 15 min) at 65 min (yes/no). CHT was delivered using a weight-drop device (0.5 J). Outcome measures were neurological severity score (NSS) at 1, 4, and 24 h, and brain tissue specific gravity (microgravimetry) and injury volume (2,3,5-triphenyltetrazoium chloride) at 24 h. After CHT, NSS at 24 h (median +/- range) and brain tissue specific gravity (mean +/- SD, injured hemisphere) were 7+/-2 and 1.033+/-0.007 without phenylephrine and 8+/-2 and 1.035+/-0.005 with phenylephrine (P = 0.43), respectively. Tissue injury volume (mean +/- SD) was 335+/-92 mm3 without phenylephrine and 357+/-154 mm3 with phenylephrine (P > 0.62). The results of our study indicate that postinjury treatment with 15 min of phenylephrine-induced hypertension does not attenuate brain edema, reduce tissue injury volume, or improve neurological outcome after CHT in rats. IMPLICATIONS: Phenylephrine-induced hypertension is reported to increase cerebral perfusion pressure and blood flow in a rat model of focal cerebral ischemia. In our study, phenylephrine-induced hypertension did not decrease brain edema or tissue injury volume or improve neurological outcome in a rat model of closed head trauma.

Animals↗

Losartan reduces phenylephrine constrictor response in aortic rings from spontaneously hypertensive rats. Role of nitric oxide and angiotensin II type 2 receptors.

Nitric oxide seems to be involved in the mechanisms underlying the antihypertensive and renal responses of losartan in spontaneously hypertensive rats (SHR). We investigated the contribution of nitric oxide to the effect of this angiotensin II (Ang II) type 1 (AT1) receptor antagonist on the constrictor response of phenylephrine in aortic rings from SHR. Furthermore, since it has been suggested that Ang II could bind to unblocked AT2 receptors, during administration of an AT1 receptor antagonist, we also studied the effect of the AT2 receptor antagonist PD 123319 on the contractile response to phenylephrine in aortic rings from SHR. To this end, we studied dose-response curves of phenylephrine (10(-9) to 10(-5) mol/L) in the presence and absence of losartan (10(-9), 10(-7), and 10(-5) mol/L) in SHR aortic rings. Preincubation with losartan reduced the constrictor response to phenylephrine but not to KCl (10 to 120 mmol/L) in a dose-dependent manner. On the other hand, the presence of captopril (10(-5) mol/L) in the incubation medium did not alter the response to phenylephrine, even at the dose of 10(-3) mol/L. The reduced response to phenylephrine in the presence of losartan was abolished in both endothelium-denuded rings and rings treated with a nitric oxide synthesis inhibitor. A similar situation was observed in PD 123319-pretreated rings, in which the effect of losartan on the contractile response to phenylephrine was reversed. Losartan was not able to stimulate the production of aortic cGMP compared with the control group. Likewise, losartan did not modify the relaxing responses to either acetylcholine or sodium nitroprusside in phenylephrine-preconstricted aortic rings. Furthermore, losartan did not alter isometric tension in aortic rings in either basal or phenylephrine-preconstricted conditions. These data demonstrate that Ang II potentiates the vasoconstriction induced by phenylephrine through the stimulation of AT1 receptors. Moreover, AT2 receptors and nitric oxide appear to be involved in this effect.

Angiotensin Receptor Antagonists↗

Studies on the alpha-andrenergic activation of hepatic glucose output. II. Investigation of the roles of adenosine 3':5'-monophosphate and adenosine 3':5'-monophosphate-dependent protein kinase in the actions of phenylephrine in isolated hepatocytes.

The effects of the alpha-adrenergic agonist phenylephrine on the levels of adenosine 3':5'-monophosphate (cAMP) and the activity of the cAMP-dependent protein kinase in isolated rat liver parenchymal cells were studied. Cyclic AMP was very slightly (5 to 13%) increased in cells incubated with phenylephrine at a concentration (10(-5) M) which was maximally effective on glycogenolysis and gluconeogenesis. However, the increase was significant only at 5 min. Cyclic AMP levels with 10(-5) M phenylephrine measured at this time were reduced by the beta-adrenergic antagonist propranolol, but were unaffected by the alpha-blocker phenoxybenzamine, indicating that the elevation was due to weak beta activity of the agonist. When doses of glucagon, epinephrine, and phenylephrine which produced the same stimulation of glycogenolysis or gluconeogenesis were added to the same batches of cells, there were marked rises in cAMP with glucagon, minimal increases with epinephrine, and little or no changes with phenylephrine, indicating that the two catecholamine stimulated these processes largely by mechanisms not involving cAMP accumulation. DEAE-cellulose chromatography of homogenates of liver cells revealed two major peaks of cAMP-dependent protein kinase activity. These eluted at similar salt concentrations as the type I and II isozymes from rat heart. Optimal conditions for preservation of hormone effects on the activity of the enzyme in the cells were determined. High concentrations of phenylephrine (10(-5) M and 10(-4) M) produced a small increase (10 tp 16%) in the activity ratio (-cAMP/+cAMP) of the enzyme. This was abolished by propranolol, but not by phenoxybenzamine, indicating that it was due to weak beta activity of the agonist. The increase in the activity ratio of the kinase with 10(-5) M phenylephrine was much smaller than that produced by a glycogenolytically equivalent dose of glucagon. The changes in protein kinase induced by phenylephrine and the blockers and by glucagon were thus consistent with those in cAMP. Theophylline and 1-methyl-3-isobutylxanthine, which inhibit cAMP phosphodiesterase, potentiated the effects of phenylephrine on glycogenolysis and gluconeogenesis. The potentiations were blocked by phenoxybenzamine, but not by propranolol. Methylisobutylxanthine increased the levels of cAMP and enhanced the activation of protein kinase in cells incubated with phenylephrine. These effects were diminished or abolished by propanolol, but were unaffected by phenoxybenzamine. It is concluded from these data that alpha-adrenergic activation of glycogenolysis and gluconeogenesis in isolated rat liver parenchymal cells occurs by mechanisms not involving an increase in total cellular cAMP or activation of the cAMP-dependent protein kinase. The results also show that phosphodiesterase inhibitors potentiate alpha-adrenergic actions in hepatocytes mainly by a mechanism(s) not involving a rise in cAMP.

Adrenergic alpha-Agonists↗

Improving the ocular absorption of phenylephrine.

An oxazolidine prodrug of phenylephrine and the base form of phenylephrine were synthesized, suspended in sesame oil, and tested for mydriatic activity against phenylephrine HCl. The HCl salt was formulated as a viscous aqueous solution and as a sesame oil suspension. A dosing volume of 10 microliter was instilled into rabbit eyes and the pupillary diameter was measured over time. A 0.045 M prodrug suspension was judged equal in mydriatic activity to a 0.45 M viscous solution of phenylephrine HCl with the exception that the time of maximum response occurred 60 min earlier with the prodrug. When phenylephrine base was suspended in sesame oil at 0.045, 0.12, and 0.45 M, the mydriatic activity was also greater than equimolar suspensions of phenylephrine HCl. The pH of tear fluids was also measured over time and found to rise 1.1, 0.70, and 0.30 pH units for 0.45, 0.12, and 0.045 M suspensions of the base form but remain unchanged when phenylephrine HCl was instilled in the rabbit eye. The greater activity associated with the base form of phenylephrine was judged a result of the change in pH to favour the absorption of phenylephrine. This latter approach should be applicable to either weak acids or weak bases with pKa values outside of the normal pH range (7-8) of the tears and in concentrations greater than 0.045 M suspended in a non-aqueous vehicle.

Absorption↗

Effect of alpha 1-adrenoceptor stimulation with methoxamine and phenylephrine on spontaneously beating rabbit sino-atrial node cells.

Effects of methoxamine and phenylephrine on the action potential and the membrane currents in spontaneously beating rabbit sino-atrial node cells were examined by means of a two-microelectrode voltage-clamp technique. Both methoxamine and phenylephrine (10(-4) mol/l) prolonged the cycle length (CL) and the action potential duration (APD), significantly. 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. Both agents depolarized the maximum diastolic potential (MDP). These changes in the action potential parameters occurred in a concentration-dependent manner. In the presence of phentolamine (10(-5) mol/l), methoxamine (3 x 10(-4) mol/l) did not modify the action potential parameters. Also, phenylephrine did not affect them during exposure to phentolamine (10(-5) mol/l) and pindolol (10(-7) mol/l). In voltage-clamp experiments, at 10(-3) mol/l both methoxamine and phenylephrine slightly increased the slow inward current (Isi), but decreased the time-dependent outward current (Ik). The steady-state activation variable of Ik (p infinity) was unaffected by these agents. The hyperpolarization-activated current (Ih) was suppressed in the presence of methoxamine, but enhanced in the presence of phenylephrine. An additional application of pindolol (10(-7) mol/l) during exposure to phenylephrine (10(-3) mol/l) depressed the action potential amplitude (APA) and Vmax, and prolonged CL slightly. Under the same condition, all the membrane currents (Isi, Ik and Ih) were decreased. In addition, the time courses of decay for Isi were not modified in the absence and the presence of phenylephrine (10(-3) mol/l) and phenylephrine plus pindolol (10(-7) mol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

An analysis of the inhibitory effects of prazosin on the phenylephrine response curves of the rat aorta.

On the endothelium-intact rat aorta some studies have shown prazosin to cause nonparallel rightward shifts of alpha 1-adrenoceptor agonist response curves. The aim of the present study was to analyze the inhibitory effect of prazosin on the phenylephrine responses of the endothelium-intact and endothelium-denuded rat aorta. Firstly I used phenoxybenzamine treatment to characterize the phenylephrine responses. The KA values for phenylephrine were 0.13-0.18 microM and 0.07-0.16 microM in the endothelium-intact and endothelium-denuded rat aorta, respectively. In order to produce maximal responses of the endothelium-intact or--denuded preparation, phenylephrine had to occupy 95-99% of the alpha 1-adrenoceptors. Secondly I compared the inhibitory effects of phentolamine and prazosin on the endothelium-intact rat aorta. Phentolamine at 0.1 and 1 microM caused parallel rightward shifts of phenylephrine response curves with no effect on phenylephrine maximal responses (phentolamine pA2 = 7.9). The inhibitory effects of phentolamine were readily reversible. Prazosin at 0.1-10 nM caused nonparallel rightward shifts of the phenylephrine response curves with a depression of the maximal response. These inhibitory effects of prazosin were either irreversible or only very slowly reversible in drug-free solution and slowly reversible in the presence of phentolamine. Ninety min was required for the inhibitory effect of prazosin to reach equilibrium whereas phentolamine was at equilibrium after 45 min. Finally I have characterized the inhibitory actions of prazosin on the endothelium-denuded rat aorta. Prazosin caused parallel rightward shifts of phenylephrine response curves with no effect on phenylephrine maximal responses. The inhibitory effects of prazosin were at equilibrium after 45 min and were readily reversible.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The positive inotropic effect of phenylephrine in the presence of propranolol. Increase in time to peak force and in relaxation time without increase in c-AMP.

The effects of phenylephrine on the shape of the contraction curve and on the cyclic adenosine 3',5'-monophosphate (c-AMP) content were studied in electrically driven (frequency 0.2 Hz) cat papillary muscles. All experiments were done in the presence of 1 micron propranolol in order to minimize interference from beta-adrenoceptors. 1. Phenylephrine increased the force of contraction in a concentration-dependent manner. Maximal effects (about 200% of control) occurred at 30 micron phenylephrine. 2. The positive inotropic effect (PIE) of phenylephrine was antagonized by phentolamine. Phentolamine, 5 micron, produced a parallel shift of the concentration-response curve for the PIE of phenylephrine by about two log units to the right. 3. The PIE of 30 micron phenylephrine occurred without any detectable increase in the c-AMP levels of the preparations. 4. The PIE of 30 micron phenylephrine developed about three times more slowly than the PIE of an equieffective concentration of isoprenaline. 5. The PIE of phenylephrine was accompanied by significant, concentration-dependent increases in both time to peak force and relaxation time. 6. It is concluded that the PIE of phenylephrine in the presence of propranolol is mediated mainly by a stimulation of alpha-adrenoceptors. It is unlikely to be related to an increase in c-AMP. With respect to time course and influence on the shape of the contraction curve it is qualitatively different from the effects of beta-adrenoceptor stimulation. These data are taken to support the hypothesis that the mechanical effects of alpha- and beta-adrenoceptor stimulating agents on the heart are produced by different mechanisms.

Adrenergic beta-Antagonists↗

Effect of adrenergic antagonists during phenylephrine stimulation of the mandibular gland of red kangaroos, Macropus rufus.

Intracarotid infusions of l-phenylephrine at 1.0 nmol.kg(-1).min(-1) or(.)10 nmol.kg(-1).min(-1) were accompanied by increases in salivary protein, urea, magnesium and bicarbonate, and by decreases in osmolality, hydrogen ion activity, sodium, potassium and chloride relative to cholinergically stimulated saliva. Intravenous infusions of phenylephrine at the same dose rates had much less effect on salivary composition with the differences between the routes of administration being greatest for the higher dose rate. Propranolol administered with phenylephrine via the carotid artery, at an antagonist:agonist ratio of 10:1, was much more effective in blocking the phenylephrine-induced changes in salivary composition than equimolar infusion of phentolamine with phenylephrine. Simultaneous intracarotid infusions of either a beta(1)-antagonist (CGP20712A) or a beta(2)-antagonist (ICI118551) with phenylephrine showed that ICI118551 was more potent than CGP20712A at preventing the changes in salivary composition associated with phenylephrine administration. It was concluded that alpha(1)-adrenoreceptors were not present in functionally significant numbers in the gland and that the effect of phenylephrine on the kangaroo mandibular was mediated by beta-adrenoreceptors predominantly of the beta(2)-subtype. As the phenylephrine dose rates in the kangaroos were comparable with those used to determine alpha-adrenergic responses of eutherian salivary glands and as both propranolol and phentolamine appeared to have minor beta-sympathomimetic activity, at least one subtype of beta-adrenoreceptors in macropods may not be identical to its eutherian counterpart.

Adrenergic alpha-Agonists↗

Phenylephrine induces endogenous noradrenaline release in the rat vas deferens through nitric oxide synthase pathway.

We have previously observed that in the rat vas deferens nitric oxide synthase pathway potentiated phenylephrine-induced contractility raising the possibility of a facilitatory role on neurotransmission by nitric oxide. To confirm this hypothesis we studied the effect of phenylephrine on the concentration response curves obtained in preparations from reserpine-treated rats in the absence and presence of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA). The endogenous noradrenaline released by normal preparations (without reserpine) was measured in the perfusion fluid of preparations stimulated with phenylephrine, in the absence and presence of L-NMMA, L-NMMA + the nitric oxide donor 3-morpholinosydnonimine hydrochloride (SIN-1), the alpha1-adrenoceptor antagonist prazosin and the blocker of noradrenaline carrier desipramine. The phenylephrine-induced noradrenaline release in a calcium-free medium was also measured. L-NMMA decreased the Emax of phenylephrine concentration response curves obtained in preparations from normal (reserpine-untreated) but not from reserpine-treated rats. In the perfusion fluid of preparations incubated with phenylephrine, a concentration-dependent increase of noradrenaline was observed which was reversed by L-NMMA and restored when SIN-1 was added together with the nitric oxide synthase inhibitor. The concentration-dependent phenylephrine-induced noradrenaline increase was not modified by desipramine but was abolished by 10 microM prazosin. In calcium-free medium, phenylephrine failed to increase the noradrenaline concentration. These results suggest that in the rat vas deferens, nitric oxide pathway potentiates the phenylephrine-induced contractility through a mechanism which involves calcium-dependent release of endogenous noradrenaline and seems to depend, at least partially on the activation of alpha1-adrenoceptors.

Adrenergic Uptake Inhibitors↗

Role of PKCalpha and PKCiota in phenylephrine-induced contraction of rat corpora cavernosa.

Constriction of the penile vasculature prevents erection and is largely mediated by physiological agonists. We hypothesized that protein kinase C (PKC) may act as a regulator of penile vascular tone. Studies were designed to identify PKC isoforms present and to investigate their roles in phenylephrine-induced muscle contraction in the isolated rat corpora cavernosa. We demonstrated the presence of PKCalpha, beta, gamma, epsilon, delta, eta, and iota in rat corpora cavernosa and a subcellular distribution, which favored a membrane association for PKCalpha, beta, delta, and iota. Phenylephrine (3 microM) generated an active stress of 9.6 +/- 1.5 mN/mm2 and was associated with a significant increase of PKCalpha and PKCiota immunoreactivity in the particulate fraction. The amount of PKCalpha and PKCiota in the particulate fraction rose by 36 +/- 4.4 and 51 +/- 2.2% with phenylephrine stimulation. Furthermore, the phenylephrine concentration-response curve was potentiated in the presence of phorbol 12-myristate13-acetate (PMA) (0.1 microM), a PKC activator (EC50: phenylephrine 1.0 +/- 0.8 microM vs phenylephrine + PMA 0.3 +/- 0.1 microM) and inhibited in the presence of chelerythrine chloride (30 microM), a PKC inhibitor (EC50: phenylephrine 1.0 +/- 0.8 microM vs phenylephrine + chelerythrine chloride 5.7 +/- 2.4 microM). Based on these results, we suggest a potential role for PKCalpha and PKCiota in phenylephrine-induced smooth muscle tone of the rat cavernosum.

Adrenergic alpha-2 Receptor Agonists↗

Allergic contact dermatitis from phenylephrine in eyedrops.

Phenylephrine is widely used as an ophthalmic drug. However, there are only very few reports on allergic contact dermatitis induced by phenylephrine. In addition, little is known on cross reactivity patterns between the sympathomimetics phenylephrine, epinephrine and ephedrine which share a similar chemical structure. We report on a man who developed allergic contact dermatitis to Neosynerphin POS eyedrops containing phenylephrine hydrochloride. Cross reactivity between phenylephrine, epinephrine and ephedrine was studied by patch testing. Patch tests were performed with the European standard, an ophthalmics and preservatives series, Neosynerphin POS eyedrops, phenylephrine hydrochloride 10% aq., epinephrine and ephedrine (both 1.0 % aq.). Test sites were read after 48, 72 and 168 hours according to the recommendations of the ICDRG. Neosynerphin POS and phenylephrine hydrochloride 10 % aq. gave positive reactions, whereas epinephrine and ephedrine tested negative. Although phenylephrine is an epinephrine analog delayed type hypersensitivity to phenylephrine did not result in cross reactivity with chemically related epinephrine and ephedrine.

Cross Reactions↗

Influence of phenylephrine bolus administration on left ventricular filling dynamics in patients with coronary artery disease and patients with valvular aortic stenosis.

BACKGROUND: Left ventricular diastolic function is known to be impaired in patients with coronary artery disease and patients with valvular aortic stenosis. Phenylephrine is frequently administered as an intravenous bolus in these patients perioperatively to increase coronary perfusion pressure. Although this is common practice, there is no information about the effect of phenylephrine bolus administration on left ventricular filling dynamics. METHODS: Twenty patients with coronary artery disease (group 1), 15 patients with valvular aortic stenosis (group 2), and 10 subjects without cardiovascular disease (group 3, control) entered the study. Left ventricular filling was evaluated using transesophageal pulsed Doppler echocardiography before and after phenylephrine injection given to patients whose mean blood pressure has decreased by more than 20% (and was not higher than 90 mmHg). We recorded the transmitral blood flow velocity curve and measured peak early and peak atrial flow velocity, acceleration and deceleration time of the early flow velocity peak, and mitral valve diameter. We calculated the ratio of peak early to peak atrial flow velocity (PE/PA), acceleration and deceleration rate of the early flow peak, and peak filling rate. RESULTS: Phenylephrine effectively restored arterial pressure in all three groups. However, in group 1, phenylephrine administration resulted in a reduction of PE/PA, acceleration rate of the early flow peak, and peak filling rate from 1.25 (mean) to 0.75 (P < 0.001), 411 to 276 cm/s2 (P < 0.001), and 439 to 305 ml/s (P < 0.001), respectively. In contrast, in group 2, intravenous phenylephrine increased PE/PA, acceleration rate of the early flow peak, and peak filling rate from 0.76 to 0.97 (P < 0.001), 365 to 503 cm/s2 (P < 0.05), and 321 to 388 ml/s (P < 0.01), respectively. In the control subjects, phenylephrine caused a transient reduction of PE/PA and peak filling rate from 1.71 to 1.39 (P < 0.001) and 618 to 524 ml.s-1 (P < 0.001), respectively. CONCLUSIONS: Phenylephrine bolus administration causes an alteration of left ventricular filling in coronary artery disease patients that seems to be more marked than that seen in normal subjects. In patients with aortic stenosis no deleterious effects were observed in response to phenylephrine.

Adult↗

Mechanism of neurotransmitter release elicited by the preferential alpha 1-adrenergic receptor agonist phenylephrine in superfused superior cervical ganglion cells in culture.

Phenylephrine increased [3H]norepinephrine efflux and accumulation of cyclic AMP in cultured rat superior cervical ganglion cells superfused with Tyrode's solution. The purpose of this study was to determine the mechanism and relationship between these two events. Electrical stimulation (1-2 Hz), potassium chloride (50 mM), and the preferential alpha 1-adrenergic receptor agonist phenylephrine (1-100 microM) increased fractional tritium efflux, whereas methoxamine, cirazoline, and amidephrine were relatively ineffective. Phenylephrine, but not methoxamine and cirazoline, also increased cyclic AMP accumulation. Phenylephrine-induced tritium efflux was not altered by alpha- and beta-adrenergic receptor antagonists or by removal of extracellular calcium. Phenylephrine-induced cyclic AMP accumulation was blocked by the beta-adrenergic receptor antagonists propranolol and atenolol. Forskolin (10 microM) and the nonhydrolyzable cyclic AMP analogue 8-(4-chlorophenylthio)cyclic AMP (100 microM) had minimal effect on tritium efflux. However, phenylephrine-evoked increase in tritium efflux was dose dependently attenuated by the neuronal uptake blocker cocaine, and phenylephrine dose-dependently inhibited the incorporation of [3H]norepinephrine into neuronal stores. We conclude that the increase in tritium efflux induced by phenylephrine is independent of cyclic AMP accumulation and appears to be mediated by uptake of phenylephrine via the neuronal carrier-mediated amine transport process, which in turn promotes efflux of the adrenergic transmitter from its storage sites.

Adrenergic alpha-Agonists↗

Whether phenylephrine exerts inotropic effects through alpha- or beta-adrenoceptors depends upon the relative receptor populations.

Phenylephrine produced concentration-related positive inotropic responses in isolated left atria and papillary muscles of guinea-pigs and rats. In rat tissues, these responses were unaffected by propranolol but antagonized by prazosin and therefore mediated via alpha 1-adrenoceptors. The alpha 1-adrenoceptor agonist methoxamine also exerted positive inotropic effects in these rat tissues. The maximum alpha-adrenoceptor-mediated effect of methoxamine (relative to the isoprenaline maximum) was greater than that of phenylephrine in left atria (in the presence of propranolol), whereas in papillary muscles phenylephrine exerted the greater maximum. In guinea-pig papillary muscles, the response to phenylephrine was unaffected by prazosin but was antagonized by propranolol and therefore caused by stimulation of beta-adrenoceptors. Methoxamine had no effect in guinea-pig papillary muscles. Guinea-pig left atria produced biphasic concentration-response curves for phenylephrine, the lower portion being antagonized by phentolamine and was therefore alpha-adrenoceptor-mediated, while the upper portion was antagonized by propranolol and therefore beta-adrenoceptor-mediated. Methoxamine exerted a small inotropic response, the maximum of which was similar to that of the first component of the phenylephrine response. Phenylephrine was a partial agonist for the cardiac beta-adrenoceptor. The density of rat ventricular alpha-adrenoceptors was 4 times greater than beta-adrenoceptor density, as measured by [3H]-prazosin and [3H]-dihydroalprenolol binding. This explains why the responses of rat papillary muscles were alpha-adrenoceptor-mediated. In contrast, the density of beta-adrenoceptor binding sites in guinea-pig ventricles was 6 times greater than the alpha-adrenoceptor density. This explains why the phenylephrine responses were beta-adrenoceptor-mediated in guinea-pig papillary muscles. In the left atria of guinea-pigs, which displayed both alpha- and beta-adrenoceptor-mediated responses, the densities of alpha- and beta-adrenoceptor binding sites were similar. Thus, phenylephrine exerts positive inotropic effects through alpha- or beta-adrenoceptors depending upon their relative densities.

Animals↗