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PubMed2006

Effects of epinephrine, norepinephrine, and phenylephrine on microcirculatory blood flow in the gastrointestinal tract in sepsis.

OBJECTIVE: The use of vasopressors for treatment of hypotension in sepsis may have adverse effects on microcirculatory blood flow in the gastrointestinal tract. The aim of this study was to measure the effects of three vasopressors, commonly used in clinical practice, on microcirculatory blood flow in multiple abdominal organs in sepsis. DESIGN: Random order, cross-over design. SETTING: University laboratory. SUBJECTS: Eight sedated and mechanically ventilated pigs. INTERVENTIONS: Pigs were exposed to fecal peritonitis-induced septic shock. Mesenteric artery flow was measured using ultrasound transit time flowmetry. Microcirculatory flow was measured in gastric, jejunal, and colon mucosa; jejunal muscularis; and pancreas, liver, and kidney using multiple-channel laser Doppler flowmetry. Each animal received a continuous intravenous infusion of epinephrine, norepinephrine, and phenylephrine in a dose increasing mean arterial pressure by 20%. The animals were allowed to recover for 60 mins after each drug before the next was started. MEASUREMENTS AND MAIN RESULTS: During infusion of epinephrine (0.8 +/- 0.2 mug/kg/hr), mean arterial pressure increased from 66 +/- 5 to 83 +/- 5 mm Hg and cardiac index increased by 43 +/- 9%. Norepinephrine (0.7 +/- 0.3 mug/kg/hr) increased mean arterial pressure from 70 +/- 4 to 87 +/- 5 mm Hg and cardiac index by 41 +/- 8%. Both agents caused a significant reduction in superior mesenteric artery flow (11 +/- 4%, p < .05, and 26 +/- 6%, p < .01, respectively) and in microcirculatory blood flow in the jejunal mucosa (21 +/- 5%, p < .01, and 23 +/- 3%, p < .01, respectively) and in the pancreas (16 +/- 3%, p < .05, and 8 +/- 3%, not significant, respectively). Infusion of phenylephrine (3.1 +/- 1.0 mug/kg/min) increased mean arterial pressure from 69 +/- 5 to 85 +/- 6 mm Hg but had no effects on systemic, regional, or microcirculatory flow except for a 30% increase in jejunal muscularis flow (p < .01). CONCLUSIONS: Administration of the vasopressors phenylephrine, epinephrine, and norepinephrine failed to increase microcirculatory blood flow in most abdominal organs despite increased perfusion pressure and-in the case of epinephrine and norepinephrine-increased systemic blood flow. In fact, norepinephrine and epinephrine appeared to divert blood flow away from the mesenteric circulation and decrease microcirculatory blood flow in the jejunal mucosa and pancreas. Phenylephrine, on the other hand, appeared to increase blood pressure without affecting quantitative blood flow or distribution of blood flow.

Analysis of Variance↗

PubMed2005

Increased contractile response to phenylephrine in detrusor of patients with bladder outlet obstruction: effect of the alpha1A and alpha1D-adrenergic receptor antagonist tamsulosin.

PURPOSE: Alpha1-adrenergic receptor (alpha1-AR) antagonists are effective for treating patients with lower urinary tract symptoms associated with bladder outlet obstruction (BOO). In humans up-regulation of alpha1-AR function in the detrusor in patients with BOO has been suggested but to our knowledge it is not yet confirmed. We investigated the effect of phenylephrine, an alpha1-AR agonist, on isometric tension in small detrusor muscle biopsies from patients with lower urinary tract symptoms and BOO compared with controls. MATERIALS AND METHODS: Detrusor biopsies were obtained from 7 men with BOO undergoing prostatectomy and 7 undergoing cystectomy for bladder cancer (controls). Patients were characterized by symptom score and urodynamics. Isometric tension was measured in detrusor biopsies with an especially built mini myograph. RESULTS: Mean International Prostate Symptom Score +/- SEM in patients with BOO and controls were 22.3 +/- 2.3 and 4.0 +/- 0.8, respectively. Phenylephrine (10(-6) to 10(-3) M) induced a significant contractile response increase in detrusor biopsies from patients with BOO compared with controls at all concentrations. Tamsulosin (0.1 to 3.0 nM) inhibited phenylephrine induced contraction in a dose dependent manner. CONCLUSIONS: To our knowledge this functional study shows for the first time a highly significant increase in contractile force to phenylephrine in patients with BOO compared with controls. These results suggest up-regulation of alpha1-AR function in BOO since contractile responses were potently inhibited by the alpha1A/D-AR antagonist tamsulosin.

Adrenergic alpha-1 Receptor Antagonists↗

PubMed1993

Effects of age and indomethacin on response and sensitivity of pulmonary artery to phenylephrine and to histamine in pigs.

The vasoconstrictor effects of phenylephrine and histamine were investigated in isolated strips of pulmonary arteries in pigs during ageing. Interactions between phenylephrine-induced responses and arachidonic acid derivatives were also studied by incubating the blood-vessels with indomethacin. Potency (pD2 values) and maximal effects (EmaxX) recorded in 5-week-old piglets (group I, n = 5) with phenylephrine [5.71 +/- 0.17 and 0.76 +/- 0.22 g/mg of dry tissue respectively (mean +/- SEM)] were similar to values found in 12-week-old animals (group 2, n = 5) (5.49 +/- 0.30 and 1.06 +/- 0.27 g/mg of dry tissue respectively). The sensitivity and responsiveness of tissues to this agonist were significantly reduced in 26-week-old mature pigs (group 3, n = 6) as indicated by the decrease in pD2 (3.91 +/- 0.23; P < 0.01) and Emax (0.27 +/- 0.13 g/mg of dry tissue; P < 0.05) values observed in this group. Histamine (10(-3) M)-induced maximal responses (Emax) were significantly higher in group 2 (2.23 +/- 0.49 g/mg) than in group 1 (0.85 +/- 0.11 g/mg; P < 0.05) and in group 3 (0.48 +/- 0.10 g/mg; P < 0.01). In 5-week-old animals, indomethacin (3 x 10(-5) M) significantly (P < 0.05) shifted the concentration-response curve to phenylephrine to the right (0.28 log. units) and depressed contractions to this drug as shown by the significant decrease of 39.5% (P < 0.05) in Emax. This cyclo-oxygenase inhibitor had no effect in other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗

PubMed1995

Phenylephrine in treating maternal hypotension due to spinal anaesthesia for caesarean delivery: effects on neonatal catecholamine concentrations, acid base status and Apgar scores.

Maternal and neonatal catecholamine concentrations, following the use of either phenylephrine or ephedrine to treat a drop in maternal blood pressure after spinal anaesthesia for caesarean delivery, were compared. Patients were randomly assigned to one of two groups: Group 1 patients (n = 20) were treated with ephedrine given as 5 mg intravenous bolus injections; Group 2 patients (n = 20) were treated with phenylephrine given as 40 micrograms intravenous bolus injections, for decreases in maternal systolic blood pressure to maintain maternal systolic blood pressure above 100 mmHg. Maternal vein (MV), umbilical vein (UV), and umbilical artery (UA) blood samples were taken at the time of delivery. Samples were analyzed for catecholamine concentrations and blood gas values. Noradrenaline concentrations in UA, UV and MV (at delivery) samples were significantly higher in group 1 compared to group 2; they were 6858 +/- 3689 vs 1674 +/- 944 pg.ml-1 (P < 0.0001), 1265 +/- 758 vs 395 +/- 470 pg.ml-1 (P < 0.001) and 239 +/- 165 vs 103 +/- 93 pg.ml-1 (P < 0.01), respectively. Comparing blood gas values between groups 1 and 2, statistically significant differences were observed in UA pH (7.28 +/- 0.01 and 7.32 +/- 0.01 pH units, P = 0.01), UA pCO2 (7.32 +/- 0.24 and 6.68 +/- 0.21 kPa, P = 0.03), UA base excess (2.2 +/- 0.4 and 0.9 +/- 0.4 mmol.1-1, P = 0.04) and UV base excess (2.0 +/- 0.3 and 0.7 +/- 0.3 mmol.1-1, P = 0.004). No significant differences in maternal characteristics, acid base values, incidence of nausea and vomiting, and Apgar scores were observed between groups. Phenylephrine appears to be as safe and effective as ephedrine in treatment of drop in blood pressure in healthy non-labouring parturients undergoing caesarean delivery. The use of phenylephrine was also associated with significantly lower noradrenaline concentrations in both mother and neonate.

Acid-Base Equilibrium↗

PubMedDate not supplied

Cardiovascular effects of topical ophthalmic 10% phenylephrine in dogs.

OBJECTIVE: To evaluate the effect of topical ophthalmic 10% phenylephrine on systolic arterial pressure (SAP), diastolic arterial pressure (DAP), mean arterial pressure (MAP), pulse rate (PR) and electrocardiogram (ECG) in dogs. ANIMALS STUDIED: Nine clinically normal dogs. PROCEDURE: Arterial catheters were placed in the dorsal pedal artery of awake dogs and ECG leads were attached. After a 15-min acclimatization period, baseline PR, SAP, DAP and MAP were recorded every 5 min for 20 min. Two treatment groups (eight dogs each) were studied. Group I: one drop of phenylephrine was placed in each eye once. Group II: one drop of phenylephrine was placed in each eye three times at 5-min intervals. Following treatment, PR, SAP, DAP and MAP were recorded every 5 min for 90 min. The mixed procedure of the SAS system was used to perform a repeated measures analysis of variance to test for linear and quadratic trends across time. RESULTS: Group I: There was a significant quadratic decrease in PR across time (P = 0.0051). Systolic arterial pressure increased linearly with time (P = 0.0002), MAP increased linearly with time (P = 0.0131), and DAP increased linearly with time (P = 0.0001). Group II: There was a significant quadratic decrease in PR across time (P = 0.0023). There was a significant quadratic increase in SAP (P = 0.0324), MAP (P = 0.0103) and DAP (P = 0.0131) across time. CONCLUSIONS: Topical ophthalmic application of 10% phenylephrine in normal dogs results in elevation of arterial blood pressure and reflex bradycardia.

Administration, Topical↗

PubMed1986

Direct cardiac actions of phenylephrine when used in assessment of baroreflex function in the rat.

In pentobarbitone-anaesthetised wistar rats, the baroreflex bradycardia in response to the vasopressor agent phenylephrine was converted to a tachycardia by propranolol. In pithed wistar rats, phenylephrine produced a marked tachycardia which was mediated largely by beta-adrenoreceptors since propranolol markedly antagonised the response. A component of the tachycardia was mediated by alpha 1-adrenoreceptors since the tachycardia to phenylephrine in the presence of propranolol was antagonised by prazosin and mimicked by the alpha 1-adrenoreceptor agonist amidephrine. It is concluded that phenylephrine is not a useful agent for assessment of baroreflex function in the rat due to its marked cardiac stimulant actions.

Animals↗

PubMed1989

Influence of thymoxamine eye-drops on the mydriatic effect of tropicamide and phenylephrine alone and in combination.

In a preliminary experiment in 12 healthy volunteers, one drop of thymoxamine 0.5% instilled into the conjunctival sac completely reversed the mydriasis produced by phenylephrine 2.5%, 5% and 10% after 20 minutes. In a second study in eight volunteers, thymoxamine 0.5% completely prevented the mydriasis produced by phenylephrine 2.5% and produced a miosis. It also completely reversed the mydriasis produced by tropicamide 0.5%. The mydriatic effect of tropicamide 0.5% plus phenylephrine 2.5%, however, was not completely reversed by thymoxamine 0.5% over a period of 180 minutes. Phenylephrine, tropicamide and thymoxamine are freely available for use by registered optometrists.

Adolescent↗

PubMed1972

The effects of isoprenaline and phenylephrine on oxygen consumption in isolated smooth muscle.

1. Simultaneous measurements of oxygen consumption and mechanical activity have been made in isolated preparations of guinea-pig taenia coli, rabbit abdominal aorta and the longitudinal muscle of rabbit duodenum.2. Mean resting oxygen consumption was greater in mechanically-active preparations (taenia coli and duodenum) than in the aorta which showed no spontaneous activity.3. The relaxation produced by isoprenaline in guinea-pig taenia coli and rabbit duodenum was accompanied by a dose-dependent fall in oxygen consumption.4. The relaxation produced by phenylephrine in guinea-pig taenia coli was accompanied by a dose-dependent fall in oxygen consumption whereas, in the rabbit duodenum, the transient fall in tension was not accompanied by any significant change in oxygen consumption.5. The increase in tension produced by phenylephrine in rabbit abdominal aorta was accompanied by an increase in oxygen consumption.6. Changes in mechanical activity and oxygen consumption produced by isoprenaline and phenylephrine were antagonized by propranolol and phentolamine respectively.7. It is concluded that the variations in oxygen consumption associated with spontaneous or drug-induced mechanical changes are simple reflections of altered mechanical activity. The possibility of additional direct metabolic actions of isoprenaline and phenylephrine is discussed.

Animals↗

PubMed1984

Differences between the prejunctional effects of phenylephrine and clonidine in guinea-pig isolated atria.

The prejunctional effects of clonidine and phenylephrine were studied in guinea-pig isolated atria by means of field stimulation of the sympathetic nerve terminals during the cardiac refractory period, in the presence of 1 microM atropine. Clonidine (10-100 nM) produced a dose-dependent decrease in the stimulus-inotropic response curve; the IC50 for clonidine was increased about 70 times by the pretreatment of the preparations with 1 microM yohimbine. The effect of clonidine was not modified by 0.5 microM prazosin. Unlike clonidine, phenylephrine (1-10 microM) induced a statistically insignificant increase in the contractile force of preparations stimulated at 4 Hz. The inhibitory effect of phenylephrine (1-10 microM) was partially prevented by either 1 microM yohimbine or 0.5 microM prazosin. However, it was antagonized, to about the same degree as that observed with clonidine, by the pretreatment of the preparations with both 1 microM yohimbine and 0.5 microM prazosin. The results seem to indicate that one component of the prejunctional effects of phenylephrine may be mediated by presynaptic alpha-adrenoceptors belonging to the alpha 1-subtype.

Animals↗

PubMed1993

Vasoconstrictor effects of various neuropeptide Y analogues on the rat tail artery in the presence of phenylephrine.

1. The increase in perfusion pressure induced by neuropeptide Y (NPY), peptide YY (PYY) and related peptides were compared in the perfused rat tail artery precontracted by a submaximal concentration (1 microM) of the vasoconstrictor, phenylephrine. 2. NPY, PYY, [Leu31,Pro34]NPY, [Glu16,Ser18,Ala22,Leu28,31]NPY (ESALL-NPY) and the centrally truncated and stabilized analogues [D-Cys5,8-aminooctanoic acid7-20, Cys24]-NPY (D-Cys5-NPY) and [D-Cys7, 8-aminooctanoic acid8-17,Cys20]-NPY (D-Cys7-NPY) produced a concentration-dependent enhancement of the vasoconstrictor response induced by 1 microM phenylephrine. PYY was two times more potent than NPY and [Leu31,Pro34]NPY while ESALL-NPY, D-Cys7-NPY and D-Cys5-NPY were approximately 3, 5 and 16 times less potent than NPY respectively. NPY, D-Cys5-NPY and D-Cys7-NPY gave similar maximal responses whereas those observed for PYY, [Leu31,Pro34]NPY and ESALL-NPY were much greater than that of NPY. 3. NPY 13-36 and [des-Ser3,Lys4,Cys2,8-aminooctanoic acid3-24, D-Cys27]-NPY ([es-Ser3,Lys4]Cys2-NPY) were practically inactive at concentrations up to 3 microM, whereas [des-Ser3,Lys4,D-Cys2,8-aminooctanoic acid3-24,Cys27]-NPY ([des-Ser3,Lys4]D-Cys2-NPY), which differs from [des-Ser3,Lys4]Cys2-NPY in the disulphide bridge (a D-Cys in position 2 for [des-Ser3,Lys4]D-Cys2-NPY instead of an L-CYs for [des-Ser3,Lys4]Cys2-NPY) was a weak agonist the maximal effect of which could not be ascertained. 4. The contractile effects of [des-Ser3,Lys4]D-Cys2-NPY were additive with those of NPY and [Leu31,Pro34]NPY demonstrating that it is not a partial agonist but may simply not interact competitively with the receptor binding site for NPY. NPY and PYY interacted in a manner expected of agonists competing for the same binding site.5. PYY, NPY and [Leu31,Pro34]NPY were equipotent in displacing the I125-labelled PYY from binding sites on membranes from Y1-receptor expressing SK-N-MC cells, while the centrally truncated analogues were much less potent. The rank order of potencies for displacement of the I125-PYY binding by these peptides in SK-N-MC cells correlated with their activity in enhancing the vasoconstrictor response of phenylephrine in the tail artery. For the [des-Ser3,Lys4]D-Cys2-NPY analogue, the displacement pattern was more complex in that the displacement analysis revealed the presence of two binding sites.6. In conclusion, these data provide no evidence for other than postjunctional Y1-receptors mediating the enhancement of the contractile response elicited by phenylephrine in the perfused rat tail artery. The effects of [des-Ser3,Lys4]D-Cys2-NPY indicate that the Y1-receptor may possess an allosteric binding site.

Amino Acid Sequence↗

PubMed1994

Effects of cyclopiazonic acid on phenylephrine-induced contractions in the rabbit ear artery.

1. Upon stimulation with phenylephrine, the rabbit ear artery displays endothelium-regulated rhythmic contractions, which may be attributed to the periodical activation of the dihydropyridine-sensitive Ca2+ channel, presumably regulated by the Ca(2+)-activated K+ channel. The effect of cyclopiazonic acid (CPA), an inhibitor of the Ca(2+)-ATPase of the sarcoplasmic reticulum (SR), on phenylephrine-induced contractions was examined in endothelium-denuded rabbit ear arteries suspended in an organ chamber for isometric tension recordings. 2. Phenylephrine-induced tonic contractions were converted to rhythmic ones by the addition of CPA. 3. The CPA-induced rhythmic contractions were abolished by the blockade of the dihydropyridine-sensitive Ca2+ channel and the Ca(2+)-activated K+ channel by nifedipine and charybdotoxin, respectively. In contrast, glibenclamide, an ATP-sensitive K+ channel antagonist, had no effect on the CPA-induced rhythmic responses. 4. CPA attenuated both Ca2+ repletion by the SR and Ca2+ influx across the plasmalemma without having a significant effect on Ca2+ release from the SR, as evaluated by phenylephrine-induced contractions. In contrast, these three parameters were not altered by the presence of the endothelium. 5. These findings indicate that the CPA-induced rhythmic contractions in the endothelium-denuded rabbit ear artery may be induced by the same ionic mechanism as endothelium-regulated rhythmic responses, by which the K+ channel could regulate the probability of the Ca2+ channel being opened. The CPA-induced rhythmic contractions may correlate with the inhibitory effects of CPA on the SR function, although this is not true for the endothelium-regulated rhythmic contractions.

Animals↗

PubMed1996

The effect of ovariectomy on depressed contractions to phenylephrine and KCl and increased relaxation to acetylcholine in isolated aortic rings of female compared to male rabbits.

1. Differences in vascular responses to phenylephrine, acetylcholine (ACh) and potassium chloride (KCl) were studied in rabbit aorta from female and male rabbits, in the absence and presence of an inhibitor of nitric oxide (NO) production, NG-nitro-L-arginine methyl ester (L-NAME, 100 microM). 2. Phenylephrine and KCl-induced contractions, were significantly reduced in amplitude (P < 0.01) in the rings from female rabbits compared to those from male rabbits. 3. ACh-induced relaxation was greater (P < 0.01) in aortic rings from females than from males. 4. Incubation of the rings with L-NAME abolished the phenylephrine-induced contraction differences between rings from male and female rabbits. 5. Ovariectomy eliminated the differences in vascular responses to phenylephrine, KCl and ACh of aortic rings from the female rabbits. 6. Both basal and ACh-stimulated release of nitrites from aortic rings was greater (P < 0.01) in vascular tissue from female than male rabbits. 7. These results indicate that differences in vascular reactivity in aortic rings from male and female rabbits may be associated with a higher release of NO, resulting in an increased vasodilator response in the female rabbits.

Acetylcholine↗

PubMed1983

Factors contributing to blood pressure elevation during norepinephrine and phenylephrine infusions in dogs.

To examine the factors contributing to the rise in systemic blood pressure during alpha- and beta-adrenergic stimulation, phenylephrine, an alpha-adrenergic agonist, and norepinephrine, an alpha- and beta-adrenergic agonist, were infused intravenously to anesthetized dogs until mean aortic blood pressure was raised equally by 40-60 mmHg. Changes in preload were estimated by changes in left ventricular end-diastolic pressure or segment length recorded by an ultrasonic technique. By obstructing the inferior vena cava (IVC), the increase in preload could be reduced to control level during phenylephrine and norepinephrine infusions without altering peripheral resistance (mean aortic blood pressure/cardiac output). Normalization of preload reduced the pressure response by 2/3 during phenylephrine infusion and by 1/4 during norepinephrine infusion. However, after beta-adrenergic blockade by propranolol, normalization of preload reduced the pressure response by 2/3 during both phenylephrine and norepinephrine infusions. Thus, during alpha-adrenergic stimulation, the increase in preload is a more important factor than the increase in peripheral resistance. Norepinephrine raised stroke volume by 24 +/- 5%. When the increase in stroke volume was prevented by IVC obstruction, the pressure response to norepinephrine was halved. Thus, during norepinephrine infusion the rise in stroke volume caused by beta-adrenergic stimulation is as important as alpha-adrenergic stimulation for the pressure response.

Adrenergic alpha-Agonists↗

PubMed1994

Discrepant effects of angiotensin II and phenylephrine on plasma volume in conscious goats.

Pressor doses of angiotensin II induced haemodilution in goats despite renal fluid losses. This study was undertaken to determine if this response is dose-dependent and correlated to the vasoconstrictor action of angiotensin II. Angiotensin II at the doses 0.025, 0.05 and 0.1 micrograms min-1 was given intravenously to five goats. Mean arterial blood pressure increased by 3, 10 and 20 mmHg, respectively, and the renal Na excretion rose. The haematocrit decreased by 7, 10, and 9% (percentage of control values) and the plasma protein concentration by 1% (n.s.), 4.5, and 3.5%, respectively. Infusions of phenylephrine (40 micrograms min-1; n = 6) caused an equivalent increase of blood pressure and renal Na excretion as angiotensin II (0.1 micrograms min-1), but the haematocrit increased by 16% and the plasma protein concentration by 6.5%. Infusions of atrial natriuretic peptide (1 microgram min-1) alone or together with angiotensin II (0.1 microgram min-1), or phenylephrine were also given (n = 6). Infusions of atrial natriuretic peptide alone did not change blood pressure, but renal Na excretion increased. The haematocrit rose by 10.5% and the plasma protein concentration by 7.6%. Adding atrial natriuretic peptide to the angiotensin II solution attenuated the rise of MAP and counteracted the haemodilution, but did not decrease the natriuresis. Infusions of phenylephrine plus atrial natriuretic peptide caused similar elevations of blood pressure and renal Na excretion as phenylephrine alone. The haematocrit rose by 24% and the plasma protein concentration by 13%. These results show that in the intact conscious goat rapid and marked changes in haematocrit and plasma protein concentration can be provoked by intravenous infusions of vasoactive agents and that these effects are not correlated to changes in arterial blood pressure or renal Na excretion.

Angiotensin II↗

PubMed1996

Circadian variation of alpha 1-adrenoceptor-mediated pressor response to phenylephrine in man.

The variability in the pressor effects of the alpha 1-adrenoceptor agonist phenylephrine was observed under placebo conditions in ten healthy subjects in a double blind randomized study. Phenylephrine infusions were administered before administration of placebo (baseline) and 2, 4, 8, 12, 24 and 48 h later. The doses of phenylephrine required to increase systolic blood pressure by 20 mmHg after 8 and 12 h (5.30 and 9.30 pm, 81.4 +/- 15.3 and 71.1 +/- 16.0 micrograms min-1, respectively) were significantly (P < 0.01) less than the baseline values (8.30 am, 108.0 +/- 27.6 g min-1). These results might indicate a circadian variation in the phenylephrine-induced alpha-adrenoceptor-mediated vascular response in healthy subjects. These observations lend further insight into circadian variations of vascular tone that might contribute to circadian rhythms in cardiovascular disease.

Adrenergic alpha-Agonists↗

PubMed1993

Mechanism of pregnancy-induced attenuation of contraction to phenylephrine in rat aorta.

The role of endothelium in the decreased contraction to phenylephrine in aorta of pregnant Wistar rats has been studied. Contractions in response to phenylephrine were significantly decreased in aortic rings from pregnant rats compared to those from non-pregnant rats. Pretreatment of the rings with indomethacin did not significantly alter the pattern of responses. When endothelium was removed from the rings, contractions of rings from non-pregnant rats were similar to those from pregnant rats. Acetylcholine-induced relaxations of rings from pregnant and non-pregnant rats precontracted with phenylephrine were not significantly different. The results suggest that in the rat aorta and under in vitro conditions, pregnancy-induced attenuation of contraction to phenylephrine is, at least partly, endothelium dependent and that the release of the endothelium factor responsible for this alteration in response may be indomethacin insensitive.

Acetylcholine↗

PubMed1992

Contraction of single vascular smooth muscle cells by phenylephrine at constant [Ca2+]i.

The mechanism of alpha-adrenergic agonist-mediated force generation was investigated in single hyperpermeable vascular smooth muscle cells. By use of a previously described method, force was recorded from individual ferret aortic cells made hyperpermeable by exposure to saponin. When the cells were clamped at pCa 7, addition of protein kinase M (PKM), the constitutively active form of protein kinase C (PKC), caused a sustained increase in force, which was reversible upon addition of the PKC pseudosubstrate inhibitor peptide (PSSI) corresponding to residues 19-31 of PKC. Phenylephrine at pCa 7 caused a dose-dependent increase in contractile force of the hyperpermeable cells, which was reversible on addition of phentolamine. The phenylephrine contraction could also be inhibited by the same concentration of PSSI that was effective toward the PKM-induced contraction. The response of the cells to a constant [phenylephrine] in different Ca buffers showed a lack of Ca dependence between pCa 8.6 and 7.0. The addition of PSSI to unstimulated cells caused a small but significant drop in basal tone. Taken together, these results suggest that a fraction of the basal tone, as well as the phenylephrine contraction that occurs in the skinned cells at constant intracellular free Ca2+ concentration, is the result of activation of a Ca-independent isozyme of PKC.

Animals↗

PubMed1999

Human sympathetic and vagal baroreflex responses to sequential nitroprusside and phenylephrine.

We evaluated a method of baroreflex testing involving sequential intravenous bolus injections of nitroprusside followed by phenylephrine and phenylephrine followed by nitroprusside in 18 healthy men and women, and we drew inferences regarding human sympathetic and vagal baroreflex mechanisms. We recorded the electrocardiogram, photoplethysmographic finger arterial pressure, and peroneal nerve muscle sympathetic activity. We then contrasted least squares linear regression slopes derived from the depressor (nitroprusside) and pressor (phenylephrine) phases with 1) slopes derived from spontaneous fluctuations of systolic arterial pressures and R-R intervals, and 2) baroreflex gain derived from cross-spectral analyses of systolic pressures and R-R intervals. We calculated sympathetic baroreflex gain from integrated muscle sympathetic nerve activity and diastolic pressures. We found that vagal baroreflex slopes are less when arterial pressures are falling than when they are rising and that this hysteresis exists over pressure ranges both below and above baseline levels. Although pharmacological and spontaneous vagal baroreflex responses correlate closely, pharmacological baroreflex slopes tend to be lower than those derived from spontaneous fluctuations. Sympathetic baroreflex slopes are similar when arterial pressure is falling and rising; however, small pressure elevations above baseline silence sympathetic motoneurons. Vagal, but not sympathetic baroreflex gains vary inversely with subjects' ages and their baseline arterial pressures. There is no correlation between sympathetic and vagal baroreflex gains. We recommend repeated sequential nitroprusside followed by phenylephrine doses as a simple, efficientmeans to provoke and characterize human vagal and sympathetic baroreflex responses.

Adolescent↗