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I S de la Lande

Publications and source records attributed to I S de la Lande.

At least 19 recordsLinked to original sources
PubMed2000

Nitroglycerin tolerance in human vessels: evidence for impaired nitroglycerin bioconversion.

BACKGROUND: The basis for progressive attenuation of the effects of organic nitrates during long-term therapy (nitrate tolerance) remains controversial; proposed mechanisms include impaired nitrate bioconversion resulting in decreased release of nitric oxide (NO) from nitrates and/or increased NO clearance through a reaction with incrementally generated superoxide (O(2)(-)). METHODS AND RESULTS: Patients undergoing elective coronary artery bypass were randomized to receive 24 hours of intravenously infused nitroglycerin (NTG; nitrate group) or no nitrate therapy (control group). Discarded segments of the internal mammary artery and saphenous vein were used to examine (1) vascular responsiveness to NTG, sodium nitroprusside, and the calcium ionophore A23187; (2) bioconversion of NTG to 1,2- and 1,3-glyceryl dinitrate; and (3) the generation of O(2)(-). Responses to NTG were reduced 3- to 5-fold in vessels from the nitrate group compared with control vessels (P:<0. 01 for both types of segments), whereas responses to sodium nitroprusside and A23187 were unchanged. Tissue content of 1, 2-glyceryl dinitrate was lower (P:=0.012) in the saphenous veins from the nitrate group than in those from the control group. O(2)(-) generation was greater (P:<0.01) in internal mammary artery samples from the nitrate group than in those from the control group. However, incremental O(2)(-) generation induced by an inhibitor of superoxide dismutase did not affect NTG responses. CONCLUSIONS: NTG tolerance in patients with coronary artery disease is nitrate-specific and is associated with evidence of impaired NTG bioconversion. Tolerance was associated with incremental O(2)(-) generation, but short-term elevation of O(2)(-) did not affect NTG responsiveness, suggesting increased NO clearance by O(2)(-) has a minimal contribution to tolerance.

Blood Vessels↗
PubMed2000

Failure of presynaptic purinoceptors to modulate noradrenaline release from sympathetic nerves in human dental pulp.

The effects of putative presynaptic P1- and/or P2-purinoceptors on the release of noradrenaline from sympathetic nerves in human dental pulp were examined by testing the effects of agonists and an antagonist of these receptors on the stimulation-induced overflow of [(3)H]noradrenaline from tissue treated with desipramine (0.3 micromol/l) and preincubated with [(3)H]noradrenaline (0.6 micromol/l). The P1-purinoceptor agonists adenosine (1.0 mmol/l) and 2-chloroadenosine (0.01-1.0 mmol/l) and the antagonist 8-cyclopentyl-1,3-dipropyl xanthine (1.0 micromol/l), and the P2-purinoceptor agonists ATP (0.1 mmol/l) and beta, gamma-methylene-ATP (0.01 mmol/l), did not modulate the release of noradrenaline. Adenosine was also without effect in dental pulp treated with the alpha(2)-adrenoceptor antagonist rauwolscine. It is concluded that presynaptic P1-purinoceptors and those P2-purinoceptors activated by adenine nucleotides are either not present on sympathetic nerves in human dental pulp or that they exert little or no effect on the release of noradrenaline.

2-Chloroadenosine↗
PubMed1999

Inhibitory effects of adrenaline on the release of noradrenaline from sympathetic nerves in human dental pulp.

The effects of adrenaline on the release of noradrenaline from sympathetic nerves in human dental pulp in vitro were examined. Sympathetic nerves were stimulated at 5 Hz for 100 sec following incubation of pulp with [3H]noradrenaline (0.6 micromol/l). In the presence of desipramine (DMI, 0.3 micromol/l), adrenaline (0.1 and 1.0 micromol/l) inhibited the release of [3H]noradrenaline, an effect which was inhibited by the alpha2-adrenoceptor antagonist rauwolscine (0.1 micromol/l) and by the alpha2-adrenoceptor agonist UK 14,304 (0.1 micromol/l). The release of [3H]noradrenaline was unaffected by adrenaline (0.001 and 0.01 micromol/l) in the presence of DMI and DMI plus rauwolscine. Although presynaptic inhibitory alpha2- and facilitatory beta-adrenoceptors are present on sympathetic nerves in human dental pulp, these results imply that adrenaline activates only the inhibitory alpha2-receptors.

Adolescent↗
PubMed1998

Evidence for presynaptic cholinergic receptors in sympathetic nerves in human dental pulp.

The purpose of this study was to determine whether presynaptic cholinergic receptors are present in sympathetic nerves in human dental pulp. Pulp was incubated with [3H]noradrenaline (0.6 mumol/l) for 30 min and then superfused with Krebs' solution at 1.0 ml/min. Electrical stimulation (100 sec, 5 Hz) increased the overflow of [3H]noradrenaline into the superfusate. Carbachol (10 and 100 mumol/l), an agonist of muscarinic receptors, decreased the stimulation-induced (SI) overflow of 3H, an effect blocked by atropine but not hexamethonium. Carbachol, atropine and hexamethonium had no effect on the resting overflow. Nicotine (10 mumol/l) increased the resting overflow and inhibited the SI overflow, although the inhibition was variable. Cytisine, another agonist of nicotinic receptors, also increased the resting overflow, but did not affect the SI overflow. To ascertain whether the actions of nicotine and electrical stimulation were influenced by the release of nitric oxide (NO), the effects of an NO donor and two NO-synthase inhibitors were examined. With the exception of one of the NO-synthase inhibitors (L-NAME), the agents were without effect on the overflow of 3H in the absence or presence of nicotine. It was concluded that sympathetic nerves in human dental pulp possess (a) presynaptic muscarinic receptors that inhibit the SI release of noradrenaline, and (b) nicotinic receptors that evoke the release of noradrenaline and that inhibit the SI release of the transmitter. The results do not point to a significant role for NO in the effects of stimulation or nicotine on the overflow of 3H.

Adolescent↗
PubMed1998

Modulation by presynaptic beta-adrenoceptors of noradrenaline release from sympathetic nerves in human dental pulp.

This study was undertaken to test for the presence of presynaptic beta-adrenoceptors on sympathetic nerves in human dental pulp and, if present, to investigate the subtype. Pulp was excised from freshly extracted teeth, incubated with [3H]-noradrenaline (0.6 micromol/l) and subsequently superfused with Krebs solution. Sympathetic nerves were stimulated at 5 Hz for 100 sec. The non-specific beta-adrenoceptor agonist isoprenaline (1.0 micromol/l), and the selective beta2-agonist salbutamol (10 micromol/l) facilitated the release of [3H]-noradrenaline; isoprenaline, but not salbutamol, also facilitated this release in the presence of desipramine (DMI, 0.3 micromol/l), corticosterone (10 micromol/l) and rauwolscine (0.1 micromol/l). BRL 37344 (1.0 micromol/l), a beta3-agonist, had no effect on [3H]-noradrenaline release. The facilitatory effects of isoprenaline and salbutamol were inhibited by the non-specific beta-antagonist propranolol (1.0 micromol/l), while that of salbutamol was inhibited in the presence of ICI-188,551 (1.0 micromol/l), a selective beta2-antagonist, as well. The beta1-antagonist atenolol (1.0 micromol/l) potentiated the facilitatory effects of isoprenaline in the presence of DMI and corticosterone. Neither propranolol nor ICI-188,551 alone affected the release of [3H]-noradrenaline. These results establish the presence of presynaptic beta-adrenoceptors on sympathetic nerves in human dental pulp. It is suggested that they are of the beta2-subtype, although a greater range of agonists and antagonists needs to be used to clarify the nature of the the beta-adrenoceptors.

Adolescent↗
PubMed1998

Heterogeneous cholinergic reactions of ringed seal coronary arteries.

Coronary blood flow of some seal species is unusual in that it is highly variable in both non-diving and diving conditions and shows intermittent fluctuations, especially during dives when it frequently ceases for brief periods. We sought regulatory mechanisms governing these reactions by studying isometric tension recordings of isolated left circumflex (LC) and left anterior descending (LAD) coronary arteries of ringed seals, Phoca hispida, during reactions to a variety of agents for stimulating or blocking autonomic responses of the vascular smooth muscle. Micromolar acetylcholine (ACh) produced constriction of the small diameter segments of the LAD, but relaxation of the LC and larger segments of LAD. Both constrictions and dilations were prevented by atropine. Small vessel constriction by ACh was prevented by micromolar indomethacin and by a thromboxane receptor antagonist. Large vessel ACh dilations were prevented or reduced by rubbing off the endothelium and by the L-arginine analog, L-NG-nitro-arginine, an inhibitor of nitric oxide synthesis. We conclude that cholinergic, muscarinic, dilation of ringed seal large coronary arteries is mediated by endothelial-derived relaxing factor (EDRF), whereas ACh constriction of small arteries is mediated by a prostaglandin.

Acetylcholine↗
PubMed1995

Effects of glyceryl trinitrate tolerance on vascular responsiveness to constrictor agents in bovine isolated coronary artery.

1. Recent clinical studies have raised the possibility that intermittent nitrate dose regimens, while limiting the extent of nitrate tolerance development, may trigger rebound aggravation of ischaemia after abrupt withdrawal of nitrate. To date, only limited studies have been performed to examine the mechanism of this phenomenon. 2. In a bovine isolated coronary artery model, we tested the hypothesis that induction of glyceryl trinitrate (GTN) tolerance might affect large coronary artery responsiveness to a variety of non-catecholamine constrictor agents. Glyceryl trinitrate tolerance was induced by pre-exposure to GTN (10 mumol/L) for 60 min followed by 15 min washout. In some experiments, the effect of prior endothelial removal on putative interactions was also examined. 3. Our results showed that GTN tolerance did not affect responses to KCl, the thromboxane A2 mimetic U46619, endothelin-1 and 5-HT, irrespective of presence or absence of endothelium. None of the constrictor agents tested induced endothelium-dependent constriction. 4. We conclude that in this model of GTN tolerance induction, there is no evidence of 'rebound' vasoconstriction to this group of non-catecholamine vasoconstrictors with GTN withdrawal.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1994

Effects of 6-hydroxydopamine on noradrenaline metabolism linked to neuronal uptake1 and extraneuronal uptake1 in dental pulp in vitro.

The study was undertaken to determine the relative roles of neuronal and extraneuronal uptake1 in the metabolism of 3H-noradrenaline in human dental pulp. Rabbit dental pulp was used as a reference since it was already known that normetanephrine (NMN) formation in this tissue utilised extraneuronal uptake1. Slices of pulp were preincubated in the absence and presence of 6-hydroxydopamine (1.6 mmol/l, for 10 or 20 min at pH 4.5) and subsequently incubated with 3H-noradrenaline (0.18 mumol/l for 30 min at pH 7.4). The principal metabolites formed were normetanephrine in rabbit pulp and deaminated catechols (dihydroxymandelic acid and dihydroxyphenylglycol) in human pulp. In both tissues 6-hydroxydopamine strongly inhibited formation of the deaminated catechols, but was without effect on normetanephrine formation. It is concluded that: i) in vitro 6-hydroxydopamine does not influence the metabolic process which is dependent on extraneuronal uptake1, namely normetanephrine formation in rabbit dental pulp, and ii) the deaminated catechols are largely neuronal in origin in human pulp. Attention is drawn to an unusual feature of the neuronal metabolism in human pulp, namely the appearance of dihydroxymandelic acid as the principal metabolite.

Adult↗
PubMed1994

Presynaptic control of noradrenaline release from sympathetic nerves in human dental pulp.

This study was undertaken to determine whether release of noradrenaline from sympathetic nerves in human dental pulp in vitro was modulated by presynaptic adrenoceptors and by dopamine receptors. Pulp was incubated for 30 min with 3H-noradrenaline (0.6 mumol/l) and then perfused continuously with Krebs solution. Field stimulation of the sympathetic nerves at 5 Hz increased the overflow of 3H into the perfusate three-to fourfold. The stimulation-induced overflow of 3H was abolished by tetrodotoxin (0.1 mumol/l) and under Ca(2+)-free conditions, indicating that the increased 3H was derived from nerves. The stimulation-induced overflow was inhibited by noradrenaline (0.1 and 1.0 mumol/l), the alpha 2-adrenoceptor agonist UK14,304 (0.1 mumol/l), dopamine (1.0 mumol/l) and the dopamine receptor agonist, apomorphine (1.0 mumol/l). When the receptor agonists were noradrenaline or dopamine, desipramine (0.3 or 3.0 mumol/l) was present to prevent their uptake by the sympathetic nerves. Clonidine (1.0 mumol/l; tested at 2 Hz as well as 5 Hz) and the alpha 1-receptor agonist methoxamine (1.0 mumol/l) were without effect. The alpha 2-receptor antagonist/rauwolscine (0.1 mumol/l) prevented the inhibitory effects of noradrenaline and UK14,304, but had little effect on the inhibition produced by dopamine. Inhibition of the stimulation-induced overflow by apomorphine was prevented by the dopamine receptor antagonist haloperidol (0.1 mumol/l). The resting overflow of 3H was unaffected by any of the above agents except dopamine, which caused a small increase. It is concluded that the sympathetic nerves in human dental pulp possess inhibitory presynaptic alpha 2-adrenoceptors and dopamine receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

Metabolism of [3H]-noradrenaline in human dental pulp in vitro.

Slices of pulp from human maxillary and mandibular molar and promolar teeth were incubated with [3H]-noradrenaline (0.2 mumol/l) for 30 min after which the [3H]-noradrenaline and [3H]-metabolites in the tissue and medium were assayed by column chromatography. The deaminated metabolites 3,4-dihydroxy phenyl glycol (DOPEG) and 3,4-dihydroxy mandelic acid (DOMA) constituted 81% of the metabolites formed. Cocaine, an inhibitor of uptake1, decreased the formation of DOPEG and DOMA as well as the accumulation of [3H]-noradrenaline. In contrast to findings in rabbit pulp, when the disposition of exogenous noradrenaline in human pulp was examined by monoamine fluorescence histochemistry there was no evidence of extraneuronal accumulation of noradrenaline by connective tissue cells. In further experiments, pulp that had been incubated in [3H]-noradrenaline (0.6 mumol/l) for 30 min and superfused for 200 min contained [3H]-noradrenaline (183 pmol/g) and [3H]-DOMA (89 pmol/g). The 3H that overflowed into the perfusate between 85 and 90 min consisted mainly of metabolites. Stimulation of the sympathetic nerves through field electrodes increased the overflow of [3H]-noradrenaline into the perfusate threefold without affecting the overflow of metabolites. The increase was much greater (eightfold) in the presence of an alpha-adrenoceptor antagonist (rauwolscine; 0.1 mumol/l), plus inhibitors of uptake1 (desipramine; 0.3 mumol/l) and uptake 2 (corticosterone; 10 mumol/l). The results are interpreted as evidence that in human dental pulp the disposition of exogenous noradrenaline is determined largely by uptake by sympathetic nerves. After uptake, noradrenaline is deaminated by intraneuronal monoamine oxidase to DOPEG and DOMA.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Interactions between 5-hydroxytryptamine, noradrenaline and the thromboxane-A2 mimetic U44069 in the marmoset isolated aorta.

1. The effects of 5-hydroxytryptamine (5-HT) in the absence and presence of noradrenaline (NA) or the thromboxane-A2 mimetic, U44069, were investigated in ring preparations of marmoset aorta. 2. 5-HT (0.001-10 mumol/L) produced little or no contractile response in preparations at basal tone. When the tone was elevated to 50% of maximum with NA the predominant response to 5-HT was relaxation. The 5-HT2 receptor antagonist LY53857 (0.1 mumol/L) unmasked a contractile response to low concentrations of 5-HT (0.01-1.0 mumol/L) and reduced relaxation to high concentrations of 5-HT (1.0-10 mumol/L) in vessels precontracted with NA. 3. In U44069-contracted vessels, 5-HT was contractile in the range 0.01-1 mumol/L and relaxant in concentrations of 6.0-10.0 mumol/L. Ketanserin (1.0 mumol/L) had no effect on the contraction or relaxation to 5-HT. 4. The relaxant response to 5-HT was not significantly diminished in endothelium-impaired arteries. 5. In conclusion, 5-HT exerts complex inhibitory and excitatory actions on the marmoset aorta. The inhibitory actions are not endothelium-dependent and the excitatory actions do not appear to involve the 5-HT2 receptor.

Animals↗
PubMed1993

Evidence for uptake2-mediated O-methylation of noradrenaline in the human amnion FL cell-line.

The uptake and metabolism of 3H-noradrenaline has been examined in the FL cell-line derived originally from human amnion. Cell cultures metabolised 3H-noradrenaline (1.0 mumol/l) to 3H-normetanephrine and, to a lesser extent, to metabolites (not distinguished) of the O-methylated deaminated fraction; primary deaminated metabolites were not detected. 3H-normetanephrine formation a) was not saturable in the noradrenaline concentration range 0.2-150 mumol/l, b) was decreased to 20%-30% of control levels by uptake2 inhibitors (O-methylisoprenaline, 20 and 100 mumol/l; cimetidine, 10 mumol/l; hydrocortisone, 200 mumol/l) and c), was almost insensitive to uptake1 inhibitors (cocaine, 30 mumol/l; desipramine, 3 mumol/l). Uptake of noradrenaline was manifested after 30 minutes as a 6-fold increase in the cell content of the amine following inhibition of catechol-O-methyl transferase, either alone or in conjunction with inhibition of monoamine oxidase. Uptake was decreased maximally to 40% of control levels by O-methylisoprenaline. IC50 values for inhibition of the O-methylisoprenaline-sensitive component of uptake were (in mumol/l): corticosterone (0.3), papaverine (1.1), O-methylisoprenaline (3.0), cimetidine (6.0), (-)noradrenaline (460), and tetraethylammonium (2230). Except for the last agent, for which a comparative value is not available, the IC50's are in good agreement with those for inhibition of uptake2 in the Caki-1 cell-line reported by other investigators. The component of uptake resistant to O-methylisoprenaline was depressed by papaverine (a 50% decrease at 50 mumol/l), but was not affected by the other uptake2 inhibitors or by cocaine (30 mumol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Amnion↗
PubMed1992

Extraneuronal uptake of noradrenaline in rabbit dental pulp: evidence of identity with uptake1.

The extraneuronal removal and disposition of noradrenaline in rabbit dental pulp was examined in view of earlier evidence that the tissue possessed an extraneuronal uptake process resembling neuronal uptake1. Pulp, which had been depleted of sympathetic nerves by homolateral superior cervical ganglionectomy, was incubated in vitro with 3H-noradrenaline in low concentrations (0.025 or 0.18 mumol/l). When the metabolising enzymes (monoamine oxidase, catechol-O-methyl transferase) were active, 3H retention by the denervated pulp, as indicated by the 3H content after the tissue had been washed for 30 min following incubation with 3H-noradrenaline, was less than 3% of that of the innervated pulp. When the enzymes were inhibited, retention rose to approximately 30% of that of the innervated pulp. Analysis of the time course of the 3H efflux indicated that the 3H-noradrenaline in the denervated pulp had accumulated in a single compartment characterised by a t1/2 for efflux of several hours. Accumulation did not occur under Na(+)-free conditions, and was inhibited by desipramine (IC50 less than 0.03 mumol/l) and by substrates of neuronal uptake1. Mean IC50 values of the latter were very similar to those for inhibition of neuronal uptake1 and comprised (in mumol/l): (+)amphetamine (0.29), dopamine (0.31), tyramine (0.39), (-)noradrenaline (0.70), (-)adrenaline (1.50), 5-hydroxytryptamine (20) and bretylium (35). Uptake2 inhibitors were less active (O-methyl isoprenaline, IC50 = 60 mumol/l) than uptake1 inhibitors, or were without inhibitory effects at the concentrations tested (hydrocortisone, 210 mumol/l; 2-methoxy oestrone, 10 mumol/l).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Evidence for a 5-HT1-like receptor mediating the amplifying action of 5-HT in the rabbit ear artery.

1. The nature of the 5-hydroxytryptamine (5-HT) receptors which amplify the vasoconstrictor effect of methoxamine was examined in the rabbit isolated perfused ear artery with intact endothelium. Indices of amplification were leftward shifts of methoxamine dose-response (DR) curves produced by 5-HT (0.3 microM) (Method I), and the appearance of vasoconstrictor responses to 5-HT receptor agonists when methoxamine was present in a near-threshold concentration (Method II). 2. The amplifying effect of 5-HT (Method I) was unaffected by prazosin (0.08 microM), was partly depressed by 5-HT2-receptor antagonists in high concentrations (ketanserin 0.5 microM, LY53857, 1.0 microM), and was abolished by a non-selective antagonist of 5-HT1 and 5-HT2 receptors (methiothepin, 0.01 microM). 3. Amplifying potencies of agonists assessed by both Methods I and II were in the order 5-carbox-amidotryptamine (5-CT) greater than 5-HT greater than alpha-methyl 5-HT. The potency of sumatriptan (assessed by Method II only) was intermediate between those of 5-HT and alpha-methyl 5-HT. 4. Ketanserin and LY53857 inhibited the amplifying action of 5-CT to about the same extent as that of 5-HT. 5. The amplifying potencies of the agonists are in marked contrast to the reported contractile potencies in the rabbit aorta where the receptor is 5-HT2, but are almost identical with reported contractile potencies in the dog saphenous vein where the receptor is 5-HT1-like. 6. It is concluded that a 5-HT,-like receptor mediates the amplifying interaction between 5-HT and methoxamine in the rabbit ear artery which can be weakly blocked by ketanserin and LY53857.7. Since 5-CT was equipotent when applied separately to the intimal and adventitial surfaces of the artery, it is suggested that the 5-HT,-like receptors are distributed uniformly across the artery wall.

Acetylcholine↗
PubMed1991

Distribution of extraneuronal uptake1 in reproductive tissues: studies on cells in culture.

Cultures of stromal cells from pregnant mouse uterus, and an FL cell line derived from human amnion, displayed significant capacities to O-methylate noradrenaline. O-methylation was inhibited in the stromal cells by uptake1-inhibitors, and in the FL cell line by uptake2 inhibitors. These findings are discussed in terms of the distribution and possible functional importance of catecholamine metabolising systems in the female reproductive system.

Amnion↗
PubMed1991

Postsynaptic alpha-adrenoceptors in the perfused canine saphenous vein in vitro.

To study the relative localization of alpha 1 and alpha 2-adrenoceptors in relation to the intima and the adventitia of canine saphenous vein, a comparison was made of the potency of alpha 1- and alpha 2-adrenoceptor agonists applied by intraluminal and extraluminal route of perfused segments of that vessel. Noradrenaline was the most potent of the agonists used and was approximately as potent by intraluminal as by extraluminal route. Cocaine (12 mumol/l) caused supersensitivity to noradrenaline which was of about the same magnitude (threefold) irrespective of the route of administration of noradrenaline. The selective alpha 1-agonist phenylephrine was about 10 times less potent than noradrenaline and was also equieffective by both routes. The selective alpha 2-agonist UK-14,304, at concentrations lower than 0.3 mumol/l, caused very small responses and only in 3 out of 14 experiments. In all cases it caused responses at concentrations higher than 0.3 mumol/l. Cocaine did not change the sensitivity to either phenylephrine or UK-14,304. Thus, it is concluded that the results obtained with cocaine agreed with expectations for a homogeneously innervated tissue. Furthermore, alpha 1-adrenoceptors seem to predominate and to be evenly distributed throughout the media. The lack of responses to the low concentrations of UK-14,304--those selectively acting on alpha 2-adrenoceptors--was ascribed to the very low efficacy of this agonist on the distal part of the canine saphenous vein and to the tone created by the perfusion pressure which might be high enough to mask this small response.

Adrenergic alpha-Agonists↗
PubMed1990

Failure of propranolol to inhibit the epinephrine-induced enhancement of responses to sympathetic nerve stimulation in the rat mesenteric vascular bed.

Experiments were designed to characterize the nature of the epinephrine-induced potentiation of responses to sympathetic nerve stimulation in the Hooded Wistar rat. The responses to sympathetic nerve stimulation were determined in the isolated perfused mesenteric vascular bed preparation before and after infusion of epinephrine (at 0.27 or 2.7 microM); at the conclusion of the experiment the content of epinephrine in the mesenteric artery was determined. The intraluminal infusion of epinephrine at both high and low concentrations potentiated the responses of the preparation to sympathetic nerve stimulation. Mesenteric artery concentrations of this catecholamine were unchanged at the lower concentration (0.27 microM), but were increased after perfusion of epinephrine at the higher concentration (2.7 microM). The beta adrenoceptor antagonist propranolol (0.5 microM) did not prevent the epinephrine-associated potentiation of responses to sympathetic nerve stimulation, nor did it influence the pressor effects of exogenous norepinephrine. The results suggest that beta adrenoceptors do not play a role in the epinephrine-induced potentiation of responses to sympathetic nerve stimulation in the rat mesenteric vascular bed preparation. This potentiation may, however, be related to a desensitization of presynaptic inhibitory alpha adrenoceptors.

Animals↗