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PubMed1985

The effects of alaproclate on the pupillary responses to tyramine, phenylephrine and pilocarpine in depressed patients.

Nine depressed patients were treated with alaproclate, a selective 5-HT uptake inhibitor, for 3 weeks in a dose of 400 mg daily. The pupillary responses to tyramine, phenylephrine, and pilocarpine eye drops were measured on consecutive days before, after 1 week and after 3 weeks of treatment. The tyramine-induced mydriasis was unaffected by alaproclate, suggesting that it does not significantly inhibit the reuptake of noradrenaline. The pilocarpine-induced miosis and the phenylephrine-induced mydriasis were both enhanced after 1 week but not after 3 weeks of treatment. This suggests that alaproclate acutely increases the responsiveness of postsynaptic muscarinic and alpha 1 adrenoceptors.

Alanine↗
PubMed1985

Stimulation of phospholipid turnover by angiotensin II and phenylephrine in proximal convoluted tubules microdissected from mouse nephron.

Angiotensin II and phenylephrine significantly increased phospholipid turnover in cortical tubule suspensions. To further localize this effect we studied the 32P incorporation into phosphatidylcholine (PC) and phosphatidylinositol (PI) in single dissected proximal convoluted tubules of mouse nephron. Both hormones significantly stimulated 32P labeling of PC and PI indicating that the proximal tubule is a target site of angiotensin II and phenylephrine action.

Angiotensin II↗
PubMed1975

Stimulation by phenylephrine of myocardial alpha-adrenoceptors in the left ventricle of the cat.

In the anesthetized cat phenylephrine in doses of 10(-8), 3 x 10(-8) and 10(-7) moles/kg caused an increase of dp/dt(max.) of the left ventricle without altering the heart rate. This cardiostimulating effect was inhibited by the alpha-adrenolytic drug phentolamine (10(-6) moles/kg). The beta-adrenolytic agent prindolol (10(-7) moles/kg), which inhibited the increase of dp/dt(max) evoked by isoprenaline as well as by noradrenaline did not influence the positive inotropic effect of phenylephrine, thus favouring the view that there exist myocardial alpha-adrenoceptors in the ventricle of the cat.

Animals↗
PubMed2001

Effects of norepinephrine and phenylephrine on intestinal oxygen supply and mucosal tissue oxygen tension.

OBJECTIVES: To investigate effects of intravenous norepinephrine (NE) and phenylephrine (PE) on intestinal oxygen supply in an autoperfused, innervated jejunal segment. DESIGN AND SETTING: Prospective, randomized animal study in an animal research laboratory. MATERIALS AND METHODS: In 24 anesthetized and normoventilated pigs a segment of the jejunal mucosa was exposed by midline laparotomy and antimesenteric incision. Mucosal oxygen tension (PO2muc; Clark-type surface oxygen electrodes), microvascular hemoglobin oxygen saturation (HbO2, tissue reflectance spectrophotometry), and microvascular blood flow (perfusion units, PU; laser Doppler velocimetry), systemic hemodynamics, mesenteric-venous acid base and blood gas variables, and systemic acid base and blood gas variables were recorded after a resting period and at 20-min intervals during infusion of NE (0.01, 0.05, 0.1, 0.5, 1, 2 micrograms x kg-1 x min-1; n = 8) or PE (0.1, 0.5, 1, 2, 5, 10 micrograms x kg-1 x min-1; n = 8) and in controls (n = 8) without treatment. RESULTS: NE infusion led to significant tachycardia, an increase in cardiac output, and systemic oxygen delivery and consumption while PE progressively increased mean arterial pressure with only small effects on systemic blood flow. NE or PE infusion did not affect mesenteric venous oxygen tension (baseline: PE 53 +/- 5, NE, 52 +/- 4.2 mmHg), mesenteric oxygen extraction ratio (baseline: PE 0.29 +/- 0.08, NE 0.3 +/- 0.06), jejunal microvascular blood flow (baseline: PE 254 +/- 127, NE 282 +/- 72 PU), PO2muc (baseline: PE 31 +/- 9.1, NE 33 +/- 11 mmHg), and HbO2 (baseline: PE 52 +/- 9.6%, NE 58 +/- 11.6%). CONCLUSION: Despite major differences in systemic hemodynamics jejunal tissue oxygen supply is not affected by progressively increasing intravenous infusion of norepinephrine and phenylephrine.

Animals↗
PubMed2002

Amplification of sumatriptan-induced contractions with phenylephrine, histamine and KCl in the isolated human mesenteric artery: in-vitro evidence for sumatriptan-induced mesenteric ischaemia.

Sumatriptan, a 5-HT(1B/1D/1F) receptor agonist, is used to relieve migraine headache. Sumatriptan contracts some arteries either directly or after modest precontraction with non-serotonergic agonists. Sumatriptan can cause myocardial ischaemia and myocardial infarction. While previous in-vitro studies have shown that sumatriptan has no or only weak contractile activity in human omental arteries, recent clinical studies suggest that sumatriptan may induce mesenteric ischaemia. The aim of this study was to investigate the presence of contractile 5-HT(1B) receptors in the human mesenteric artery and to establish whether the weak sumatriptan-induced contractions are amplified by precontraction with various contractile substances. The study was performed in organ baths using endothelium-denuded isolated human mesenteric arteries. Sumatriptan induced concentration-dependent contractions in some mesenteric arteries [ E(max) 61+/-10% of the maximum contraction induced by 80 mM KCl, pD(2) (-log(10)EC(50)) 6.56+/-0.20, n=9]. In the other mesenteric arteries, sumatriptan induced only very weak ( E(max) <5%) or no contraction ( n=13). GR127935 (3 nM), a selective 5-HT(1B) receptor antagonist, antagonized sumatriptan-induced contractions insurmountably in sumatriptan-sensitive arteries. When the resting tension of the arterial rings was increased moderately by threshold concentrations (EC(10)-EC(20) of maximum contraction induced by 80 mM KCl) with the non-5-HT receptor agonists phenylephrine (10-100 nM), histamine (100 nM-1 microM) or the depolarizing agent KCl (4-10 mM), 5-HT(1B) receptor-mediated responses were amplified in sumatriptan-insensitive arteries (with phenylephrine E(max) 82+/-17%, pD(2) 6.64+/-0.20, n=7; with histamine E(max) 107+/-26%, pD(2) 6.16+/-0.14, n=6; with KCl E(max) 78+/-16%, pD(2) 6.45+/-0.15, n=7). These results show that sumatriptan induced concentration-dependent contractions in sumatriptan-sensitive mesenteric arteries and that 5-HT(1B) receptors were present and active in these vessels. However, in sumatriptan-insensitive arteries, precontraction is required for sumatriptan to induce concentration-dependent contractions. These findings suggest that sumatriptan may induce ischaemia in human mesenteric vasculature directly or in the presence of precontractile risk factors.

Aged↗
PubMed2002

Tetrandrine potentiates caffeine-induced contraction but inhibits phenylephrine-induced contraction in perfused rat mesenteric artery.

Effects of tetrandrine (TET), a bisbenzylisoquinoline alkaloid, on the contractile responses of perfused rat mesenteric arteries to phenylephrine (PE) and caffeine were investigated. TET concentration-dependently (1-30 micro M) attenuated phenylephrine-induced responses but potentiated the contractile responses to caffeine (5-40 mM) in the presence and absence of Ca(2+). Berbamine (BER), a structural analogue of TET, elicited a relatively smaller inhibitory effect on the responses to PE due to Ca(2+) release or Ca(2+) influx. However, both TET and BER elicited a comparable potentiating effect on caffeine-induced contraction. Cyclopiazonic acid (CPA; 10 micro M), a selective sarcoplasmic reticulum Ca(2+)-ATPase pump inhibitor, mimicked the potentiating effect of TET when added 5 min prior to caffeine in Ca(2+)-free medium. However, CPA did not augment and might even inhibit the caffeine-induced response when it was preincubated with the tissue for 25 min prior to the addition of caffeine. We propose that TET elicits differential effects on PE- and caffeine-induced responses in perfused rat mesenteric arterial bed. The inhibitory effect of TET on PE-induced responses is probably due to its direct interactions with alpha-adrenoceptors and PE-sensitive Ca(2+)-channels. The augmentation of caffeine-induced responses by TET, particularly in Ca(2+)-free medium, is likely to be due to its partial inhibition of the sarcoplasmic reticulum Ca(2+)-ATPase pump.

Alkaloids↗
PubMed1999

C2-ceramide attenuates phenylephrine-induced vasoconstriction and elevation in [Ca2+]i in rat aortic smooth muscle.

In the present study, we examined the effects of cell-permeable C2-ceramide on contraction of aortic smooth muscle and intracellular free Ca2+ ([Ca2+]i). C2-ceramide (10(-7) to 10(-4) M) alone did not elicit any significant changes in either basal tension or resting levels of [Ca2+]i in rat aortic smooth muscle. However, C2-ceramide (10(-7) to 10(-4) M) attenuated phenylephrine-induced contractions in isolated rat aortic rings in a concentration-related manner, and inhibited elevations in [Ca2+]i in cultured rat aortic smooth muscle cells induced by phenylephrine. C2-ceramide-induced relaxation was found to be only slightly endothelium-dependent. However, nitric oxide inhibitors (L-NNA, L-NMMA), an inhibitor of prostanoid synthesis (indomethacin), an inhibitor of opiate actions, and several inhibitors of the pharmacologic actions of various vasoactive amines all failed to interfere with the vasorelaxant responses of C2-ceramide. Three different inhibitors of protein kinase C, when used in a wide concentration range, also failed to interfere with the ceramide-induced relaxations. Our results suggest that the sphingomyelin-signaling pathway may play an important regulatory role in arterial wall tone.

Animals↗
PubMed1989

Effect of pregnancy on uterine and carotid artery response to norepinephrine, epinephrine, and phenylephrine in vessels with documented functional endothelium.

The effect of pregnancy on arterial sensitivity to vasoconstrictors is controversial. Some of the controversy may reflect methodologic differences. Vessel reactivity in vitro is altered by both the tension placed on the segment and the presence or absence of functional endothelium. We investigated the effect of pregnancy on guinea pig uterine and carotid arteries to norepinephrine, epinephrine, and phenylephrine. Each vessel segment was stretched to the optimal point along its length-tension curve, and functional endothelium was documented by acetylcholine-stimulated relaxation. A significant dose-response relationship was observed in each vessel for each agent (each p less than 0.0001). Pregnancy was demonstrated to be associated with a significant reduction in both uterine artery response and sensitivity to norepinephrine, epinephrine, and phenylephrine. However, there was no consistent pregnancy-associated effect on carotid artery response and sensitivity.

Animals↗
PubMed1979

Contraindication to the use of ocular phenylephrine in idiopathic orthostatic hypotension.

We studied the effect of topical ocular application of 2.5% phenylephrine ophthalmic solution in patients with idiopathic orthostatic hypotension and in normal subjects. The normal subjects had no pressor effect to the drug. However, the patients with idiopathic orthostatic hypotension, had a marked pressor response. The maximal pressor response in the four patients averaged 44/27 mm Hg. The usual 10% phenylephrine used in practice could have delivered a fourfold greater amount of drug, and presumably would have led to dangerously high blood pressure responses.

Adult↗
PubMed1985

Systemic absorption and cardiovascular effects of phenylephrine eyedrops.

We studied 24 patients undergoing vitreoretinal surgery to compare the systemic absorption and cardiovascular effects of 2.5% aqueous and 10% viscous ophthalmic solutions of phenylephrine hydrochloride. Plasma levels measured in patients receiving two drops of 10% viscous solution were consistently higher ten, 20, and 60 minutes after instillation (P less than .02). Although the mean systolic and diastolic blood pressure was generally higher with the 10% viscous solution, the difference was not statistically significant. Blood pressure was high in several isolated cases. Because maximum plasma levels are achieved within ten to 20 minutes after topical instillation, phenylephrine eyedrops should be administered under close observation so that if an adverse reaction occurs it can be readily treated.

Absorption↗
PubMed1986

Immunohistochemical localization of carbonic anhydrase in submandibular salivary glands of mice and hamsters treated with phenylephrine, testosterone or duct-ligation.

Using the peroxidase antiperoxidase (PAP) technique, the submandibular glands (SMG) from normal mice showed positive carbonic anhydrase (CA) staining in both striated duct (SD) and granular convoluted tubule (GCT) cells, which varied from moderate to strong. In normal hamsters, the GCT showed strong focal staining. Phenylephrine in mice and hamsters resulted in a decrease in CA in GCT cells; staining was much reduced in the GCT segments of the mouse. One hour after a phenylephrine injection into testosterone-treated mice, there was no change in the staining intensity of GCT cells but an increase in cell size. Only a slight decrease in immunostaining occurred in mouse and hamster SD cells. CA staining in duct-ligated glands of mice decreased within 3 days but regenerated duct-like structures at later stages showed moderate staining.

Animals↗
PubMed1989

Role of calcium in the phenylephrine-induced activation of phosphorylase "A" in isolated liver cells.

The ability of phenylephrine to activate phosphorylase in liver cells with variable degrees of Ca2+ loading was studied. Phenylephrine has been found to be capable of stimulating phosphorylase at saturating Ca2+ concentrations that precluded any further action of this ion. Furthermore the degree of activation was proportional to the cellular calcium content. These results allow to conclude that alpha-adrenergic agonists activate phosphorylase by a mechanism apparently unrelated to their ability to mobilize and subsequently increase the cytosolic concentration of free Ca2+.

Animals↗
PubMed1984

Alpha-adrenoceptor-mediated positive inotropic effect of phenylephrine in isolated human ventricular myocardium.

In isolated human ventricular myocardium the alpha-adrenoceptor agonist phenylephrine had a positive inotropic effect in preparations from 9 of 14 patients. This effect was seen in the presence of the beta-adrenoceptor-blocking agent propranolol but was nearly abolished by the alpha-adrenoceptor blocking agent prazosin. In contrast to the beta-adrenoceptor-mediated positive inotropic effect, the effect of phenylephrine was accompanied by a prolongation of the isometric contraction. The results suggest that alpha-adrenoceptors exist in human ventricular myocardium.

Adult↗
PubMed1986

The effects of bepridil, compared with calcium-channel inhibitors and calmodulin antagonists on both spontaneous activity and contractions induced by potassium or phenylephrine in rat portal vein.

Bepridil is known to block calcium channels in some vascular tissues. Recent work has shown that bepridil also antagonises calmodulin. The present study attempted to more fully characterize the vasodilator actions of bepridil by comparing it with the known calcium channel blocking drugs, nifedipine, diltiazem, verapamil and flunarizine, the calmodulin inhibitors, trifluoperazine and W7 and propylmethylenedioxyindene, which is thought to act intracellularly, on rat portal vein. The relative activities of the test drugs were compared on spontaneous activity and on all components of the contractile responses to potassium and phenylephrine. Bepridil inhibited all components of the potassium and phenylephrine responses equally, actions similar to those of the intracellular acting drugs. The exception to this was trifluoperazine which also exerted alpha-adrenoceptor blocking actions. In contrast the calcium channel blocking drugs, with the exception of verapamil, inhibited the tonic component of both spasmogen responses more than the phasic component. Bepridil like the intracellular acting drugs, but unlike the calcium channel blockers, markedly increased the frequency of spontaneous contractions whilst reducing amplitude. It is concluded that the profile of bepridil on rat portal vein more closely resembles that of intracellularly acting drugs than that of classical calcium channel inhibitors.

Animals↗
PubMed1990

Effects of phenylephrine in single isolated smooth muscle cells of rabbit and guinea pig taenia caeci.

Spontaneous transient and evoked outward currents were studied using the whole cell patch-clamp technique with freshly dispersed smooth muscle cells isolated from rabbit and guinea pig taenia caeci. Phenylephrine induced a low amplitude sustained outward current in both tissues. Simultaneously, the frequency and amplitude of spontaneous transient outward currents were increased. However, there were differences between the effects of phenylephrine on the evoked outward currents recorded from smooth muscle cells of rabbit (reduction) and guinea pig (enhancement) taenia caeci.

Animals↗
PubMed1996

Cyclic GMP potentiates phenylephrine but not cyclic ADP-ribose-evoked calcium release from rat lacrimal acinar cells.

In the present study, we describe a role for cyclic GMP (cGMP) in the signalling pathway that leads from alpha-adrenergic receptor activation to intracellular Ca2+ mobilization in rat lacrimal acinar cells. The alpha-adrenergic agonist, phenylephrine, stimulates intracellular Ca2+ release which is blocked by inhibitors of guanylate cyclase and cGMP-dependent protein kinase Ia. The membrane-permeable cGMP analogues, dibutyryl-cGMP and 8-bromo-cGMP, potentiate ( approximately 5-fold) the Ca2+ response to submaximal phenylephrine stimulation. In contrast, the same cGMP analogues have no effect on cyclic ADP-ribose-evoked Ca2+ release from permeabilized lacrimal acinar cells. Collectively, these findings suggest that cGMP, via cGMP-dependent protein kinase I alpha , is required for intracellular Ca2+ release following alpha-adrenergic receptor activation in lacrimal acinar cells.

Acetylcholine↗
PubMed1989

Inotropic effect of phenylephrine and myocardial alpha-adrenergic receptor in newborn and adult animals.

Developmental changes in the myocardial alpha-receptor density were studied using rabbit, rat and dog hearts. In all species studied, alpha-receptor density in the newborn was greater than in the adult. The inotropic effect of phenylephrine was measured using the isolated arterially perfused heart preparation of rabbit and rat. The heart was stimulated electrically at 40/min. In the presence of propranolol, phenylephrine caused a significant positive inotropic effect which was significantly less in the newborn than in the adult. Since alpha-adrenergic stimulation activates protein kinase C, the inotropic effect of protein kinase C activation was studied in the rabbit and rat using phorbol myristate acetate (PMA). PMA caused a negative inotropic effect and the decrease in contractile function in the newborn was greater than in the adult. These data suggest that myocardial alpha-receptor density decreases and the positive inotropic effect of alpha-agonist increases with development. The reasons for this discrepancy remain unclear but there may be developmental differences in the signal transduction processes of alpha-stimulation. The greater negative inotropy of protein kinase C activation in the premature heart may be one of the mechanisms of the reduced inotropy of alpha-agonist in this age group.

Animals↗