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PubMed1997

Proliferation of adult rat hepatocytes by hepatocyte growth factor is potentiated by both phenylephrine and metaproterenol.

We investigated whether or not beta and alpha adrenergic agonists could affect proliferation of adult rat hepatocytes induced by hepatocyte growth factor (HGF) during the early and late phases of primary culture. Adult rat hepatocytes underwent significant DNA synthesis after culture with 5 ng/ml HGF for 3 h at a low cell density (3.3 x 10(4) cells/cm2). Under these culture conditions, the number of nuclei increased significantly during a subsequent 4-h culture period. Hepatocyte DNA synthesis and proliferation induced by 5 ng/ml HGF was reduced at high cell densities near confluence. A beta adrenergic agonist, metaproterenol (10(-7) M), and dibutyryl cAMP significantly potentiated hepatocyte DNA synthesis and proliferation at a concentration as low as 10(-7) M when cultured in combination with 5 ng/ml HGF. Similarly, an alpha-1 adrenergic agonist, phenylephrine (10(-6)-10(-4) M) markedly potentiated HGF-induced hepatocyte DNA synthesis and proliferation. The phenylephrine effect was mimicked by a phorbol ester (10(-6) M), but not by ionomycin (10(-6) M). The mitogenic effects of HGF were almost completely blocked by simultaneous treatment of hepatocytes with genistein (5 x 10(-6) M), U-73122 (10(-6) M), wortmannin (10(-7) M), sphingosine (3 x 10(-6) M) and rapamycin (10 ng/ml). These results demonstrate that HGF can rapidly induce proliferation of adult rat hepatocytes in primary culture. However, this effect is dependent on the initial plating density. The co-mitogenic effects of metaproterenol and phenylephrine may involve both protein kinase A and protein kinase C activation, respectively. The results also suggest that following stimulation with HGF, activation of tyrosine kinase, phosphatidylinositol 3-kinase, phospholipase C and p70 ribosomal protein S6 kinase is essential for hepatocyte proliferation.

Adrenergic beta-Antagonists↗

PubMed1997

Limited utility of the phenylephrine-nitroprusside sigmoid curve method of measuring baroreflex function after myocardial infarction.

BACKGROUND: Conventional testing of baroreflex function with phenylephrine bolus injection measures reflex vagal tone. OBJECTIVE: To evaluate an alternative pharmacological method of baroreflex testing, which might provide more comprehensive evaluation of the baroreflex function in patients with uncomplicated myocardial infarction. METHODS: Forty-eight patients, aged 59 +/- 7 years, were evaluated 5-7 days after myocardial infarction and after 6 weeks of rehabilitation. Baroreflex testing was performed with 10-14 incremental injections of nitroprusside and phenylephrine. The peak heart rate and blood pressure point from each injection were fitted to a four parameter (upper plateau, lower plateau, gain and median blood pressure) sigmoid logistic function. The baroreflex sensitivity (BRS) was also measured by conventional linear analysis of the response of the R-R interval to the initial rise in systolic blood pressure induced by phenylephrine bolus injection. RESULTS: Non-linear curve fitting of four logistic curve parameters was possible for results from 91% of tests; in the remaining tests the upper plateau was held constant at the maximum heart-rate response to allow estimation of the other three parameters. When all four parameters had been estimated, the gain parameter could not be precisely determined (the coefficient of variation of the gain parameter was 85 +/- 10%). The upper (R = 0.72, P < 0.001) and lower plateaux (R = 0.76, P < 0.001) were strongly related to the resting heart rate and weakly related to measures of heart-rate variability. There was also a significant inverse correlation between the lower plateau and the BRS (R = -0.57, P < 0.001). The gain parameter was not related to the BRS or any measure of the heart-rate variability. After 6 weeks' rehabilitation there was a significant decrease in the lower plateau (from 54 +/- 2 to 48 +/- 1 beats/min, P < 0.001), an increase in BRS (from 9.4 +/- 0.8 to 12.1 +/- 0.8 ms/mmHg, P < 0.001) and no change in the other three sigmoid curve parameters. CONCLUSIONS: Non-linear curve fitting of the heart-rate-blood-pressure relationship for patients after myocardial infarction is feasible but technical limitations and the lack of correlation between the gain parameter and other measures of autonomic function suggest that this method has limited usefulness. The lower plateau is related strongly to the BRS; both are vagal measures of cardiac autonomic function.

Aged↗

PubMed1980

Lack of side effects from topically administered 10% phenylephrine eyedrops. A controlled study.

A prospective double-blind study was designed to determine the systemic hypertensive effects of topically administered 10% aqueous buffered phenylephrine hydrochloride vs topically administered 1% aqueous tropicamide, a belladonna alkaloid devoid of vasopressor effect. One hundred persons received phenylephrine, while 50 persons received tropicamide. One drop of coded drug was administered in both eyes of each patient at two-minute intervals over a four-minute period. Blood pressure and pulse rate were measured immediately prior to drop instillation, and 5, 15, and 30 minutes following instillation of the final set of drops. Mean blood pressure and pulse rate dropped from baseline values in both groups at 5, 15, and 30 minutes after drug administration. There was no statistically significant difference between the experimental and control groups with respect to drug effect on either blood pressure or pulse rate throughout the study.

Adolescent↗

PubMed1984

Effect of phenylephrine hydrochloride on conjunctival PO2.

Phenylephrine hydrochloride eyedrops induce vasoconstriction through alpha-adrenergic mechanisms. Ten subjects underwent a 46% reduction in conjunctival PO2 when 2.5% phenylephrine eyedrops were administered. Compared with a control group, this reduction was significant. The induced conjunctival hypoxia lasted about 80 minutes. These findings suggest a number of clinical implications.

Adult↗

PubMed1990

Time course of thymoxamine reversal of phenylephrine-induced mydriasis.

We conducted a randomized, double-masked, paired comparison of 0.1% thymoxamine vs placebo for the reversal of phenylephrine-induced mydriasis. Mydriasis was induced with 2.5% phenylephrine in each eye of 74 subjects (148 eyes). Each subject then received 0.1% thymoxamine in one eye and placebo in the other eye. Pupillary measurements were obtained at regular intervals during the ensuing 8 hours. At all intervals, a greater percentage of thymoxamine-treated eyes returned to baseline pupillary diameters compared with placebo-treated eyes (P less than or equal to .01). For subjects in whom both pupils returned to baseline, thymoxamine-treated eyes returned to baseline in a mean of 2.2 hours, vs 5.2 hours for placebo (P less than .0001). Among thymoxamine-treated eyes, those with light irides responded more rapidly than those with dark irides, returning to baseline in 1.6 vs 2.8 hours, respectively (P = .0046). After constriction to baseline pupillary diameter had been achieved, no patients experienced a rebound dilation.

Adolescent↗

PubMed1995

Cardiac complication from use of cocaine and phenylephrine in nasal septoplasty.

Cocaine hydrochloride is widely used as a topical anesthetic for otolaryngologic surgery. Cardiovascular complications, including myocardial injury, are well-documented side effects of illicit cocaine use. We describe a 23-year-old woman without coronary artery disease who had an acute non-Q-wave myocardial infarction and stunned myocardium after receiving topical phenylephrine hydrochloride and cocaine anesthesia for elective nasal septoplasty. These cases are rare; however, we hope to heighten the awareness of the potential lethal complications of using cocaine, phenylephrine, or the combination of both as topical anesthetics in otolaryngologic practice.

Administration, Topical↗

PubMed2003

Cellular localization of integrin isoforms in phenylephrine-induced hypertrophic cardiac myocytes.

Cardiac hypertrophy is characterized by remodeling of the extracellular matrix (ECM). Integrins are cell-surface molecules that link the ECM to the cellular cytoskeleton where they play roles as signaling molecules and transducers of mechanical force. To clarify the possible roles of integrins in cardiac myocyte hypertrophy, we investigated the cellular localization and expression of ECM proteins and integrins in both normal cardiac myocytes and phenylephrine-induced hypertrophic myocytes. Addition of phenylephrine (PE) to cultured neonatal cardiac myocytes induced sarcomeric organization, increase in cell size, and synthesis of the hypertrophic marker, atrial natriuretic factor (ANF). In particular, fibronectin and collagen underwent dramatic localization changes during PE-induced cardiac hypertrophy. Significant changes were noted in the cellular localization of the respective collagen and fibronectin receptors, integrin alpha1 and alpha5, from diffuse to a sarcomeric banding pattern. Expression levels of integrins were also increased during hypertrophy. Treatment with okadaic acid (OA), an inhibitor of protein phosphatase 2A (PP2A), resulted in inhibition of hypertrophic response. These results suggest that dephosphorylation of integrin beta1 may be important in the induction of cardiac hypertrophy.

Animals↗

PubMedDate not supplied

Comparison of fenoterol, isoproterenol, and isoetharine with phenylephrine aerosol in asthma.

The bronchodilator effect of fenoterol hydrobromide (0.5, 1.25, and 2.5 mg) was compared with either isoproterenol (2.8 mg) or isoetharine (5 mg) with phenylephrine (1.25 mg) in a double-blind placebo-controlled study. When delivered by an intermittent positive-pressure breathing device to 24 nonsmoking young adult asthmatic subjects, fenoterol produced significant improvement in forced expiratory volume at 1 second (FEV1), in maximum midexpiratory flow (FEF25-75%), and in forced expiratory flow at 25 per cent of vital capacity (FEF25%) for 6 to 8 hours, whereas isoproterenol and isoetharine with phenylephrine produced improvement for 1 and 2 hours, respectively. The lowest dosage of fenoterol was as effective as the highest but had fewer adverse effects.

Adolescent↗

PubMed1978

Applications of paired ion high-pressure liquid chromatography to catecholamines and phenylephrine.

Paired ion high-pressure liquid chromatography was useful for separating intact catecholamines (epinephrine, isoproterenol, levodopa, and methyldopa) and phenylephrine from some of their decomposition products. Furthermore, methyldopa was separated from either hydrochlorothiazide of levodopa. Under identical conditions without 1-heptanesulfonic acid (a counterion for paired ion chromatography) in the mobile phase, these separations were not possible. Paired ion chromatography also was tried successfully for the quantitative determinations of isoproterenol, levodopa, methyldopa, and phenylephrine in some dosage forms. The results were compared with the results obtained using some literature methods.

Capsules↗

PubMed1994

Endothelin-1 and phenylephrine-induced activation of the phosphoinositide cycle increases cell injury of cultured cardiomyocytes exposed to hypoxia/reoxygenation.

We explored the effect of glucose-free hypoxia/reoxygenation of cultured neonatal rat ventricular myocytes on endothelin-1 and alpha 1-adrenoceptor induced activity of the phosphoinositide cycle. At the same time the influence of these agonists on depletion of energy-rich phosphates and cellular damage was assessed. Glucose-free hypoxia did not lead to an increase in basal phospholipase C activity. However, endothelin-1 (10(-8) M) and phenylephrine (10(-5) M) evoked activation of phospholipase C was attenuated after 60 min of hypoxia and declined to 38% and 30% respectively of normoxic values after 90 min of hypoxia. During glucose-free hypoxia, phosphatidylinositol 4,5-bisphosphate, the substrate for phospholipase C, but not phosphatidylinositol or phosphatidylinositol 4-monophosphate was seen to decline to 59% of normoxic values which was independent of activation of phospholipase C by agonists. ATP levels decreased after 30 min of hypoxia and declined to 29% relative to normoxic control after 90 min of hypoxia. Total adenine nucleotide levels showed a similar pattern. The presence of 10(-8) M endothelin-1 during hypoxia did not influence the magnitude of ATP depletion. However, after 15 min of reoxygenation, by itself not significantly leading to recovery of ATP levels, ATP levels were decreased by endothelin-1 as compared to hypoxia/reoxygenation without phospholipase C agonist. Cellular damage as determined by lactate dehydrogenase leakage was not observed during 90 min hypoxia. Reoxygenation resulted in a three-fold increase in enzyme release relative to normoxic control. In the presence of endothelin-1 or phenylephrine this reoxygenation-induced damage was respectively 1.7 and 3.0-fold increased. We conclude that the agonist-induced activity of the phosphoinositide cycle is decreased in time during glucose-free hypoxia, partially through a decrease in phosphatidylinositol 4,5-bisphosphate level. However, the remaining activity may give rise to increased cellular damage. As endothelin-1 and alpha 1-adrenergic amines are known to be released during myocardial ischemia, stimulation of the phosphoinositide cycle by these agonists might be an important factor in determining the magnitude of myocardial injury.

Adenine Nucleotides↗

PubMed1996

Endocardial endothelium and myocardial performance in rats: effects of changing extracellular calcium and phenylephrine.

It is known that endocardial endothelium (EE) modulates the performance of its subjacent myocardium. However, one species where these effects have been more difficult to describe is the rat. As the rat is a species which is used to evaluate the contractile effects of various pathologic conditions, a better appreciation of the contractile effects of EE and its modulatory role on the contractile effects of inotropic substances is important. In this study, the contractile effects of increasing extracellular calcium concentrations (0.7 mM to 3.25 mM) and phenylephrine (10(-7) to 10(-4) M) on rat papillary muscles with intact endocardial endothelium (EE on) and after endocardial endothelial removal (EE off) were assessed. At 0.7 mM extracellular calcium concentration, endocardial endothelial removal decreased all measured indices of myocardial performance (P < 0.05 EE on v EE off), except for maximum rate of unloaded muscle shortening (Vmax) which did not change, and decreased time to peak tension development (TTPT) as well as shortening of time to half tension decline from peak tension (RT1/2) shortening. Increasing extracellular calcium concentration from 0.7 mM to 3.25 mM caused all indices of myocardial performance and RT1/2 to increase more in muscles without EE, such that at 2.5 mM extracellular calcium all differences between EE on and EE off had disappeared. The only exception was TTPT which decreased with increasing extracellular calcium concentrations in muscles with EE on but increased in muscles with EE off. Again, at 2.5 mM extracellular calcium concentration differences in TTPT between EE on and EE off had disappeared. Except for minor differences on TTPT, increasing phenylephrine concentrations had similar contractile effects on muscles with EE on and EE off. These results indicate that EE modulates rat myocardial contraction and that these effects are best observed at lower extracellular calcium concentrations (0.7 mM). They also indicate that EE does not appear to significantly modulate the myocardial effects of alpha-adrenergic agonists in the rat.

Animals↗

PubMed2003

Improved pulmonary artery buffering function during phenylephrine-induced pulmonary hypertension.

The goal of this study was to determine the in vivo pulmonary arterial buffering function (BF) during acute and moderate pulmonary hypertension achieved by phenylephrine-induced smooth muscle activation. Pulmonary pressure (Konigsberg P7) and diameter (sonomicrometry) were measured in nine anesthetized sheep. Transit pulmonary arterial hypertension was induced by mechanical occlusion of the pulmonary artery (HP) and by phenylephrine infusion (5 microg/kg/min) (PHE). A viscoelastic Kelvin-Voigt model was used. By increasing the values of the viscous modulus, the pressure-diameter hysteresis area was reduced to a minimum in order to obtain the purely elastic pressure-diameter relationship. The elastic index (E) was calculated as the first derivative of the exponential model of the purely elastic pressure-diameter relationship at the mean pressure point. Systolic, diastolic, mean and pulse pressures were similar during HP and PHE, but significantly higher with regard to control steady state. In HP, E and arterial diameter (both its minimum and maximum values) increased significantly. In contrast, when pulmonary hypertension was induced by VSM activation, E was maintained concomitantly with pulmonary artery vasoconstriction. Pulmonary hypertension produced by occlusion of the pulmonary artery increases elasticity. Smooth muscle activation may offset the deleterious effect of pulmonary hypertension on arterial wall elasticity by reducing E and impeding arterial dilatation and collagen recruitment, maintaining BF during pulmonary hypertension.

Animals↗

PubMed1986

Ocular oxygenation: the effect of phenylephrine on anterior chamber oxygen tension.

Phenylephrine preparations are widely used in medicine for their vasoconstrictive and mydriatic effects. The effect of phenylephrine, a powerful alpha-receptor stimulant, on anterior chamber oxygen tension (Po2) was studied using a polarographic electrode inserted into the mid anterior chamber of cats. A commercial 10% solution was applied topically. A decrease in anterior chamber Po2 was usually observed in 8-24 minutes and declined steadily thereafter. Prior to treatment, the mean anterior chamber Po2 was 26 +/- 3 torr; 1/2 hour after treatment it decreased to 20 +/- 7 torr. After 1 hour it dropped to 13 +/- 8 torr and was further reduced to 11 +/- 6 torr by 2 hours. By 90 minutes, the drug had caused a 58% reduction in anterior chamber oxygen tension. This drop is similar to that reported for epinephrine. It is suggested that the mechanism for most of this decrease is reduced blood flow, mediated by the direct vasoconstrictive effect of the drug in addition to compression of the iris vasculature induced by dilation. The resulting change (reduction) in caliber of the iris arteries produces a parallel change (reduction) in blood volume and flow resulting in a diminished Po2. The clinical implications of this conclusion in disorders where hypoxia is felt to play a causal role such as neovascular glaucoma, diabetes, pregnancy and hyphema in sickle cell disease are explored.

Administration, Topical↗

PubMed1992

Effect of topical phenylephrine on the permeability of the blood-aqueous barrier in man.

The effects of a single instillation of 5% phenylephrine on aqueous flow and the coefficient of protein entry into the anterior chamber, an index of blood-aqueous barrier permeability, were determined in normal human eyes by measuring fluorescein concentrations with a fluorophotometer and aqueous protein concentrations with a laser flare-cell meter. Both parameters showed a concomitant biphasic change. The coefficient of protein entry showed significant increases of 31 and 66% at 1 and 2 h, and a significant decrease of 18% at 3 h. Aqueous flow showed significant increases of 81 and 125% at 1 and 2 h and a significant decrease of 20% at 4 h. It is suggested that a change in the permeability of the blood-aqueous barrier might be related to changes in aqueous flow after topical phenylephrine.

Administration, Topical↗

PubMed1992

Phenylephrine and ATP enhance an amiloride insensitive bicarbonate-dependent alkalinizing mechanism in rat single cardiomyocytes.

To expel the excess protons generated during a cellular acidification and to fully recover basal intracellular pH (pHi), cardiac cells rely on the amiloride-sensitive Na/H antiport. We report that rat single ventricular cardiomyocytes, loaded with the fluorescent pH indicator Snarf-1 and treated with inhibitors of the Na/H antiport, amiloride or its analogues, partially restored their pHi through a bicarbonate-dependent mechanism following an acidosis (imposed by the ammonia-pulse technique). In the presence of ethylisopropylamiloride (10 microM) or amiloride (1 mM) and 25 mM bicarbonate in the extracellular solution, the average time that cells needed to recover half of their pHi, following the removal of 20 mM NH4Cl, was 3.4 min, while the rate of proton efflux was calculated to be 2.0 mM/min. The stilbene derivative, 4-4'-di-isothiocyanostilbene-2,2'-disulphonate (DIDS 200 microM), a known blocker of anion transporters, inhibited this recovery. Both phenylephrine (100 microM, 3 microM propranolol present), an alpha 1-adrenoceptor agonist, and ATP (10 microM), a purinergic agonist, significantly enhanced the rate of proton efflux that was due to this HCO3-dependent alkalinizing mechanism. Phenylephrine and ATP also shortened by three-fold the time that a myocyte needed to recover half of its initial pHi. This bicarbonate-dependent alkalinizing mechanism could provide an additional means by which cardiac cells recover their pHi from acidosis, especially under conditions in which the Na/H antiport is inhibited. Furthermore, catecholamines and ATP, which are released under various pathophysiological conditions often associated with intracellular acidosis, could play an important role in the modulation of pHi under these conditions.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1991

The role of alpha 1-adrenoceptor subtypes in the phasic and tonic responses to phenylephrine in the longitudinal smooth muscle of the rat portal vein.

The purpose of this investigation was to determine whether alpha 1-adrenoceptor subtypes (co)exist in the rat portal vein and, if so, whether they could be functionally associated with the phasic and tonic types of contraction as a response to alpha 1-adrenoceptor stimulation by phenylephrine. A low Ca2+ concentration (0.9 mmol/l) in the Tyrode solution enabled us to quantify changes both in the phasic myogenic activity and in the basal tone of the rat portal vein preparation very precisely. We used both competitive and non-competitive alpha-adrenoceptor antagonists which have been employed successfully by other investigators to discriminate between alpha 1-adrenoceptor subtypes in vascular and other tissues. Schild analysis showed that the competitive alpha-adrenoceptor antagonists prazosin, phentolamine, yohimbine, corynanthine, idazoxan, rauwolscine and 5-methyl-urapidil could not distinguish between the phasic and tonic responses to phenylephrine and/or different alpha 1-adrenoceptor subtypes in the rat portal vein. However, when we compared our pA2 values with those found to be representative indicators according to subclassifications based on the use of selective antagonists in different tissues, the alpha 1-adrenoceptors in the rat portal vein appeared to belong to the alpha 1L- or alpha 1a-subtype. This subclassification was not in accordance with the data obtained with the irreversible alpha-adrenoceptor antagonist chloroethylclonidine. However, the validity of this alkylating agent as a tool for receptor classification was restricted, at least in the rat portal vein, by its effects on receptor reserve.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic alpha-Antagonists↗

PubMed1994

On the mechanism of action of phenylephrine in rat atrial heart muscle.

Both in rat left atrial heart and in aortic smooth muscle preparations, phenylephrine (PE) caused a concentration-dependent increase in force of contraction (FC) in the presence of atenolol (10 mumol/l), which was antagonized by phentolamine, prazosin and WB 4101 in a competitive manner. The pA2 values of the antagonists in the cardiac tissue were 10-20fold lower than those in the rat thoracic aorta. In the spontaneously beating right atrium, PE exerted a positive chronotropic action, which was not significantly antagonized by phentolamine or prazosin. It is therefore assumed that the effects of phenylephrine in the left atrium and in the aorta are mediated by different subtypes of alpha 1-adrenoceptors, whereas the effects in the sino-atrial node are probably unrelated to alpha 1-adrenoceptors. To further elucidate the mechanisms of the positive inotropic effect of PE, action potential configuration and 45Ca2+ fluxes were monitored in the rat left atrium. The increase in FC by PE was associated with an increase in action potential duration (APD) and a reduction in resting membrane potential (RP). In the presence of (-)-devapamil (D888), the effects of PE on APD and RP persisted, whereas the increase in FC was antagonized in a non-competitive manner. Forskolin (300 nmol/l) enhanced the positive inotropic effect of PE. PE exerted a significant increase in 45CA2+ uptake in beating preparations, which was abolished in the presence of (-)D888 (1 mumol/l). In addition to the PE-induced increase in 45Ca2+ uptake, a decrease in 45Ca2+ efflux was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Actin Cytoskeleton↗

PubMed1991

The effect of urapidil on responses to phenylephrine, angiotensin and isoprenaline in man.

Intravenous urapidil, 40 mg bolus followed by an infusion of 18 mg.h-1 for 2 h was administered to 6 female non-patient volunteers. Randomised cumulative dose response curves to angiotensin, phenylephrine and isoprenaline were performed before and commencing 30 min after the start of the infusion of urapidil. Urapidil significantly reduced supine systolic blood pressure, 118.5 mm Hg to 105.3. The diastolic blood pressure was not significantly reduced, heart rate was not affected. Urapidil did not affect the responses to angiotensin or isoprenaline. Urapidil inhibited the pressor response to phenylephrine. The dose required to increase systolic blood pressure by 20 mm Hg increased from 156.9 micrograms.min-1 before to 685 micrograms.min-1 during urapidil; Dose ratio from individual values of 4.58. Urapidil concentrations were not significantly different before and after each agonist infusion. It is concluded that urapidil has alpha 1-adrenoceptor blocking activity in man without any non specific vasodilator action and that it is devoid of beta adrenoceptor blocking action.

Adrenergic alpha-Antagonists↗