This thesis describes the development of an in vivo model allowing the study of presynaptic modulation of endogenous NA overflow in the vasculature of freely moving unanesthetized rats. ...

Zie: Summary

Remie, René,

Remie, René

University of Groningen

   University of GroningenPresynaptic receptors in the vasculature of the freely moving ratRemie, RenéIMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.Document VersionPublisher's PDF, also known as Version of recordPublication date:1989Link to publication in University of Groningen/UMCG research databaseCitation for published version (APA):Remie, R. (1989). Presynaptic receptors in the vasculature of the freely moving rat. s.n.CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.Download date: 12-11-2019- 1 3 4 -7. SUMMARYUntil now modulation of neurotransmitter release by presynaptic receptors w.u;almost exclusively studied in isolated tissues and organs using radiolabelled catechol-amine as a marker for the release of endogenous noradrenaline (NA), other studieswere done in anesthetized animals.This thesis describes the development of an ln vlvo model allowing the study ofpresynaptic modulation of endogenous NA overflow in the vasculature of freelymoving unanesthetized rats. In supplement 6.1 the technique is described in which asilicon cannula was used for the permanent cannulation of the poÉal vein, togetherwith a bipolar platinum stimulation electrode around this vein. The method had ahigh success ratio of over 7Ol during a period of more than 2 months. The deter-mination of the endogenous catecholamines was performed using l00pl plasma withhigh performance liquid chromatography with electrochemical detection. The finalprocedure showed a detection limit of 450 fglml NA and I pglml adrenaline (ADru.Enhancement of all electrical stimulation parameters proportionally increased theevoked NA release. The first experiments using I mglkg yohimbine showed thatblockade of the presynaptic cb-adrenoceptors resulted in a 4.4-fold rise of the basalpoÉal NA level and an additional 4.7 -fold facilitation of the electrically evoked release.Once developed, the technique was further refined by inseÉion of a second cannuladistal from the stimulation electrodes, which allowed the injection and infusion ofspecific receptor agonists and antagonists fnr the pharmacological study of severaltypes of vascular presynaptic receptors.A facllitation of endogenous NA overflow was seen after stimulation of thepresynaptic pa-adrenoceptors in the rat poÉal vein (suppl. ó.2). This facilitation,hrrwever, was much more pronounced than one would expect on the basis of previouslyrepttrtecl ln vltro studies (160X). A maximal enhancement of about 30Of of the basalNA level was seen after a single dose of the Ê2-selective agonist fenoterol. In the- 1 3 5 -presence of the cr:-adrenoceptor antagonist yohimbine, a low - in its absence uneffective -dose of fenoterol, was able to enhance the NA level to l2OOf of the basal level,showing the pronounced counterregulatory role of the presynaptic qz-adrenoceptor.During electrical stimulation of the portal vein nervous plexus a comparable pro-nounced facilitation of evoked NA overflow was seen. both in the absence and inthe presence of yohimbine.In supplement 6.3 the nature of the vascular presynaptic p-adrenoceptors andthe possible heterogeneity of the receptor population was investigated, using thedifferential blockade technique. The $z-selective antagonist ICI ll8,55l was able toreverse the fenoterol-induced enhancement, both of basal and electrically evoked NAoverflow, to control values. The pr-selective antagonist, CGP 20712 A, even at a highdose, was inactive. Neither antagonist influenced the effect of high synaptic concen-trations of endogenous NA induced by administration of yohimbine. Since NA is a fullpr-adrenoceptor agonist these results showed that no pr-adrenoceptor subpopulationwas present in the portal vein of the unrestrained conscious rat. It could also be con-cluded that even at high concentrations, NA is unable to facilitate its own release viathe homogenous presynaptic pr-adrenoceptor population.In chapter 3, a number of experiments is described on the role of ADR as apossible cotransmitter in noradrenergic neurotransmission. It could be shown thatinfused ADR is taken up rapidly via cocaine-sensitive uptake carriers into portal veinsympathetic varicosities. Surprisingly, even low concentrations of ADR were capableof displacing endogenous NA from the vesicle. Followtng stimulation. both in absenceand in presence of yohimbine, this ADR-pool was rapldly released without a con'-comitant facilitation of remaining endogenous NA overflow. In the presence of thepa-selective adrenoceptor antagonist ICI ll8,55l a significant attenuation of the evokedADR overflow was seen. indicating presynaptic pz-adrenoceptors also facilitatlngneuronal ADR release.In supplement 6.4 we demonstrated that the spontaneously hypertensive rat- 1 3 6 -(SHR) respond to much lower dosages of fenoterol when compared to those of theWistar rat (WR). This strongly pronounced facilitation could, however not beattributed to a dysfunction of the pa-adrenoceptor but rather to a dysfunctionalcz-adrenoceptor, thus unmasking the pz-adrenoceptor-mediated facilitation of NAoverflow.Supplements 6.5 and 6.ó describe the invesigations on the presence and thecharacter of the presynaptic muscarinic receptors in the rat portal vein. Infusion ofmethacholine (MCH had no effect on the basal NA level. During electrical stimulation,however. MCh strongly inhibited (952) the evoked NA overflow, while atropine wasable to reverse this inhibition. ln the presence of the cr2-adrenoceptor antagonistyohimbine, MCh again was able to reduce the yohimbine-induced enhanced NAoverflow. Using selective antagonlsts like pirenzepine (M'), AF-DX 116 (Ma) and4-DAMP (M:), the receptor subtype was determined. From the order of the plC-values it could be concluded that the presynaptic muscarinic receptor was of thecardiac Mz-subclass.Finally, some preliminary experiments using morphine showed the presence andfunctioning of inhibitory presynaptic opioid receptors in the vascular sympatheticvaricosities of the unrestrained conscious rat. The precise nature of these presynapticopioid receptor(s) remains to be elucidated.i

Presynaptic receptors in the vasculature of the freely moving rat

NARCIS 

ARTS repository - University of Groningen

   University of GroningenPresynaptic receptors in the vasculature of the freely moving ratRemie, RenéIMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.Document VersionPublisher's PDF, also known as Version of recordPublication date:1989Link to publication in University of Groningen/UMCG research databaseCitation for published version (APA):Remie, R. (1989). Presynaptic receptors in the vasculature of the freely moving rat. s.n.CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license.More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne-amendment.Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.Download date: 13-02-2023- 1 3 4 -7. SUMMARYUntil now modulation of neurotransmitter release by presynaptic receptors w.u;almost exclusively studied in isolated tissues and organs using radiolabelled catechol-amine as a marker for the release of endogenous noradrenaline (NA), other studieswere done in anesthetized animals.This thesis describes the development of an ln vlvo model allowing the study ofpresynaptic modulation of endogenous NA overflow in the vasculature of freelymoving unanesthetized rats. In supplement 6.1 the technique is described in which asilicon cannula was used for the permanent cannulation of the poÉal vein, togetherwith a bipolar platinum stimulation electrode around this vein. The method had ahigh success ratio of over 7Ol during a period of more than 2 months. The deter-mination of the endogenous catecholamines was performed using l00pl plasma withhigh performance liquid chromatography with electrochemical detection. The finalprocedure showed a detection limit of 450 fglml NA and I pglml adrenaline (ADru.Enhancement of all electrical stimulation parameters proportionally increased theevoked NA release. The first experiments using I mglkg yohimbine showed thatblockade of the presynaptic cb-adrenoceptors resulted in a 4.4-fold rise of the basalpoÉal NA level and an additional 4.7 -fold facilitation of the electrically evoked release.Once developed, the technique was further refined by inseÉion of a second cannuladistal from the stimulation electrodes, which allowed the injection and infusion ofspecific receptor agonists and antagonists fnr the pharmacological study of severaltypes of vascular presynaptic receptors.A facllitation of endogenous NA overflow was seen after stimulation of thepresynaptic pa-adrenoceptors in the rat poÉal vein (suppl. ó.2). This facilitation,hrrwever, was much more pronounced than one would expect on the basis of previouslyrepttrtecl ln vltro studies (160X). A maximal enhancement of about 30Of of the basalNA level was seen after a single dose of the Ê2-selective agonist fenoterol. In the- 1 3 5 -presence of the cr:-adrenoceptor antagonist yohimbine, a low - in its absence uneffective -dose of fenoterol, was able to enhance the NA level to l2OOf of the basal level,showing the pronounced counterregulatory role of the presynaptic qz-adrenoceptor.During electrical stimulation of the portal vein nervous plexus a comparable pro-nounced facilitation of evoked NA overflow was seen. both in the absence and inthe presence of yohimbine.In supplement 6.3 the nature of the vascular presynaptic p-adrenoceptors andthe possible heterogeneity of the receptor population was investigated, using thedifferential blockade technique. The $z-selective antagonist ICI ll8,55l was able toreverse the fenoterol-induced enhancement, both of basal and electrically evoked NAoverflow, to control values. The pr-selective antagonist, CGP 20712 A, even at a highdose, was inactive. Neither antagonist influenced the effect of high synaptic concen-trations of endogenous NA induced by administration of yohimbine. Since NA is a fullpr-adrenoceptor agonist these results showed that no pr-adrenoceptor subpopulationwas present in the portal vein of the unrestrained conscious rat. It could also be con-cluded that even at high concentrations, NA is unable to facilitate its own release viathe homogenous presynaptic pr-adrenoceptor population.In chapter 3, a number of experiments is described on the role of ADR as apossible cotransmitter in noradrenergic neurotransmission. It could be shown thatinfused ADR is taken up rapidly via cocaine-sensitive uptake carriers into portal veinsympathetic varicosities. Surprisingly, even low concentrations of ADR were capableof displacing endogenous NA from the vesicle. Followtng stimulation. both in absenceand in presence of yohimbine, this ADR-pool was rapldly released without a con'-comitant facilitation of remaining endogenous NA overflow. In the presence of thepa-selective adrenoceptor antagonist ICI ll8,55l a significant attenuation of the evokedADR overflow was seen. indicating presynaptic pz-adrenoceptors also facilitatlngneuronal ADR release.In supplement 6.4 we demonstrated that the spontaneously hypertensive rat- 1 3 6 -(SHR) respond to much lower dosages of fenoterol when compared to those of theWistar rat (WR). This strongly pronounced facilitation could, however not beattributed to a dysfunction of the pa-adrenoceptor but rather to a dysfunctionalcz-adrenoceptor, thus unmasking the pz-adrenoceptor-mediated facilitation of NAoverflow.Supplements 6.5 and 6.ó describe the invesigations on the presence and thecharacter of the presynaptic muscarinic receptors in the rat portal vein. Infusion ofmethacholine (MCH had no effect on the basal NA level. During electrical stimulation,however. MCh strongly inhibited (952) the evoked NA overflow, while atropine wasable to reverse this inhibition. ln the presence of the cr2-adrenoceptor antagonistyohimbine, MCh again was able to reduce the yohimbine-induced enhanced NAoverflow. Using selective antagonlsts like pirenzepine (M'), AF-DX 116 (Ma) and4-DAMP (M:), the receptor subtype was determined. From the order of the plC-values it could be concluded that the presynaptic muscarinic receptor was of thecardiac Mz-subclass.Finally, some preliminary experiments using morphine showed the presence andfunctioning of inhibitory presynaptic opioid receptors in the vascular sympatheticvaricosities of the unrestrained conscious rat. The precise nature of these presynapticopioid receptor(s) remains to be elucidated.i

English

University of Groningen Research Database

  
 University of Groningen
Presynaptic receptors in the vasculature of the freely moving rat
Remie, René
IMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite from
it. Please check the document version below.
Document Version
Publisher's PDF, also known as Version of record
Publication date:
1989
Link to publication in University of Groningen/UMCG research database
Citation for published version (APA):
Remie, R. (1989). Presynaptic receptors in the vasculature of the freely moving rat s.n.
Copyright
Other than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of the
author(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).
Take-down policy
If you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediately
and investigate your claim.
Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons the
number of authors shown on this cover page is limited to 10 maximum.
Download date: 11-02-2018
- 1 3 4 -
7. SUMMARY
Until now modulation of neurotransmitter release by presynaptic receptors w.u;
almost exclusively studied in isolated tissues and organs using radiolabelled catechol-
amine as a marker for the release of endogenous noradrenaline (NA), other studies
were done in anesthetized animals.
This thesis describes the development of an ln vlvo model allowing the study of
presynaptic modulation of endogenous NA overflow in the vasculature of freely
moving unanesthetized rats. In supplement 6.1 the technique is described in which a
silicon cannula was used for the permanent cannulation of the poÉal vein, together
with a bipolar platinum stimulation electrode around this vein. The method had a
high success ratio of over 7Ol during a period of more than 2 months. The deter-
mination of the endogenous catecholamines was performed using l00pl plasma with
high performance liquid chromatography with electrochemical detection. The final
procedure showed a detection limit of 450 fglml NA and I pglml adrenaline (ADru.
Enhancement of all electrical stimulation parameters proportionally increased the
evoked NA release. The first experiments using I mglkg yohimbine showed that
blockade of the presynaptic cb-adrenoceptors resulted in a 4.4-fold rise of the basal
poÉal NA level and an additional 4.7 -fold facilitation of the electrically evoked release.
Once developed, the technique was further refined by inseÉion of a second cannula
distal from the stimulation electrodes, which allowed the injection and infusion of
specific receptor agonists and antagonists fnr the pharmacological study of several
types of vascular presynaptic receptors.
A facllitation of endogenous NA overflow was seen after stimulation of the
presynaptic pa-adrenoceptors in the rat poÉal vein (suppl. ó.2). This facilitation,
hrrwever, was much more pronounced than one would expect on the basis of previously
repttrtecl ln vltro studies (160X). A maximal enhancement of about 30Of of the basal
NA level was seen after a single dose of the Ê2-selective agonist fenoterol. In the
- 1 3 5 -
presence of the cr:-adrenoceptor antagonist yohimbine, a low - in its absence uneffective -
dose of fenoterol, was able to enhance the NA level to l2OOf of the basal level,
showing the pronounced counterregulatory role of the presynaptic qz-adrenoceptor.
During electrical stimulation of the portal vein nervous plexus a comparable pro-
nounced facilitation of evoked NA overflow was seen. both in the absence and in
the presence of yohimbine.
In supplement 6.3 the nature of the vascular presynaptic p-adrenoceptors and
the possible heterogeneity of the receptor population was investigated, using the
differential blockade technique. The $z-selective antagonist ICI ll8,55l was able to
reverse the fenoterol-induced enhancement, both of basal and electrically evoked NA
overflow, to control values. The pr-selective antagonist, CGP 20712 A, even at a high
dose, was inactive. Neither antagonist influenced the effect of high synaptic concen-
trations of endogenous NA induced by administration of yohimbine. Since NA is a full
pr-adrenoceptor agonist these results showed that no pr-adrenoceptor subpopulation
was present in the portal vein of the unrestrained conscious rat. It could also be con-
cluded that even at high concentrations, NA is unable to facilitate its own release via
the homogenous presynaptic pr-adrenoceptor population.
In chapter 3, a number of experiments is described on the role of ADR as a
possible cotransmitter in noradrenergic neurotransmission. It could be shown that
infused ADR is taken up rapidly via cocaine-sensitive uptake carriers into portal vein
sympathetic varicosities. Surprisingly, even low concentrations of ADR were capable
of displacing endogenous NA from the vesicle. Followtng stimulation. both in absence
and in presence of yohimbine, this ADR-pool was rapldly released without a con'-
comitant facilitation of remaining endogenous NA overflow. In the presence of the
pa-selective adrenoceptor antagonist ICI ll8,55l a significant attenuation of the evoked
ADR overflow was seen. indicating presynaptic pz-adrenoceptors also facilitatlng
neuronal ADR release.
In supplement 6.4 we demonstrated that the spontaneously hypertensive rat
- 1 3 6 -
(SHR) respond to much lower dosages of fenoterol when compared to those of the
Wistar rat (WR). This strongly pronounced facilitation could, however not be
attributed to a dysfunction of the pa-adrenoceptor but rather to a dysfunctional
cz-adrenoceptor, thus unmasking the pz-adrenoceptor-mediated facilitation of NA
overflow.
Supplements 6.5 and 6.ó describe the invesigations on the presence and the
character of the presynaptic muscarinic receptors in the rat portal vein. Infusion of
methacholine (MCH had no effect on the basal NA level. During electrical stimulation,
however. MCh strongly inhibited (952) the evoked NA overflow, while atropine was
able to reverse this inhibition. ln the presence of the cr2-adrenoceptor antagonist
yohimbine, MCh again was able to reduce the yohimbine-induced enhanced NA
overflow. Using selective antagonlsts like pirenzepine (M'), AF-DX 116 (Ma) and
4-DAMP (M:), the receptor subtype was determined. From the order of the plC-
values it could be concluded that the presynaptic muscarinic receptor was of the
cardiac Mz-subclass.
Finally, some preliminary experiments using morphine showed the presence and
functioning of inhibitory presynaptic opioid receptors in the vascular sympathetic
varicosities of the unrestrained conscious rat. The precise nature of these presynaptic
opioid receptor(s) remains to be elucidated.
i


University of Groningen Digital Archive

Presynaptic receptors in the vasculature of the freely moving rat.

   University of GroningenPresynaptic receptors in the vasculature of the freely moving ratRemie, RenéIMPORTANT NOTE: You are advised to consult the publisher's version (publisher's PDF) if you wish to cite fromit. Please check the document version below.Document VersionPublisher's PDF, also known as Version of recordPublication date:1989Link to publication in University of Groningen/UMCG research databaseCitation for published version (APA):Remie, R. (1989). Presynaptic receptors in the vasculature of the freely moving rat. s.n.CopyrightOther than for strictly personal use, it is not permitted to download or to forward/distribute the text or part of it without the consent of theauthor(s) and/or copyright holder(s), unless the work is under an open content license (like Creative Commons).The publication may also be distributed here under the terms of Article 25fa of the Dutch Copyright Act, indicated by the “Taverne” license.More information can be found on the University of Groningen website: https://www.rug.nl/library/open-access/self-archiving-pure/taverne-amendment.Take-down policyIf you believe that this document breaches copyright please contact us providing details, and we will remove access to the work immediatelyand investigate your claim.Downloaded from the University of Groningen/UMCG research database (Pure): http://www.rug.nl/research/portal. For technical reasons thenumber of authors shown on this cover page is limited to 10 maximum.Download date: 09-09-2023- 1 3 4 -7. SUMMARYUntil now modulation of neurotransmitter release by presynaptic receptors w.u;almost exclusively studied in isolated tissues and organs using radiolabelled catechol-amine as a marker for the release of endogenous noradrenaline (NA), other studieswere done in anesthetized animals.This thesis describes the development of an ln vlvo model allowing the study ofpresynaptic modulation of endogenous NA overflow in the vasculature of freelymoving unanesthetized rats. In supplement 6.1 the technique is described in which asilicon cannula was used for the permanent cannulation of the poÉal vein, togetherwith a bipolar platinum stimulation electrode around this vein. The method had ahigh success ratio of over 7Ol during a period of more than 2 months. The deter-mination of the endogenous catecholamines was performed using l00pl plasma withhigh performance liquid chromatography with electrochemical detection. The finalprocedure showed a detection limit of 450 fglml NA and I pglml adrenaline (ADru.Enhancement of all electrical stimulation parameters proportionally increased theevoked NA release. The first experiments using I mglkg yohimbine showed thatblockade of the presynaptic cb-adrenoceptors resulted in a 4.4-fold rise of the basalpoÉal NA level and an additional 4.7 -fold facilitation of the electrically evoked release.Once developed, the technique was further refined by inseÉion of a second cannuladistal from the stimulation electrodes, which allowed the injection and infusion ofspecific receptor agonists and antagonists fnr the pharmacological study of severaltypes of vascular presynaptic receptors.A facllitation of endogenous NA overflow was seen after stimulation of thepresynaptic pa-adrenoceptors in the rat poÉal vein (suppl. ó.2). This facilitation,hrrwever, was much more pronounced than one would expect on the basis of previouslyrepttrtecl ln vltro studies (160X). A maximal enhancement of about 30Of of the basalNA level was seen after a single dose of the Ê2-selective agonist fenoterol. In the- 1 3 5 -presence of the cr:-adrenoceptor antagonist yohimbine, a low - in its absence uneffective -dose of fenoterol, was able to enhance the NA level to l2OOf of the basal level,showing the pronounced counterregulatory role of the presynaptic qz-adrenoceptor.During electrical stimulation of the portal vein nervous plexus a comparable pro-nounced facilitation of evoked NA overflow was seen. both in the absence and inthe presence of yohimbine.In supplement 6.3 the nature of the vascular presynaptic p-adrenoceptors andthe possible heterogeneity of the receptor population was investigated, using thedifferential blockade technique. The $z-selective antagonist ICI ll8,55l was able toreverse the fenoterol-induced enhancement, both of basal and electrically evoked NAoverflow, to control values. The pr-selective antagonist, CGP 20712 A, even at a highdose, was inactive. Neither antagonist influenced the effect of high synaptic concen-trations of endogenous NA induced by administration of yohimbine. Since NA is a fullpr-adrenoceptor agonist these results showed that no pr-adrenoceptor subpopulationwas present in the portal vein of the unrestrained conscious rat. It could also be con-cluded that even at high concentrations, NA is unable to facilitate its own release viathe homogenous presynaptic pr-adrenoceptor population.In chapter 3, a number of experiments is described on the role of ADR as apossible cotransmitter in noradrenergic neurotransmission. It could be shown thatinfused ADR is taken up rapidly via cocaine-sensitive uptake carriers into portal veinsympathetic varicosities. Surprisingly, even low concentrations of ADR were capableof displacing endogenous NA from the vesicle. Followtng stimulation. both in absenceand in presence of yohimbine, this ADR-pool was rapldly released without a con'-comitant facilitation of remaining endogenous NA overflow. In the presence of thepa-selective adrenoceptor antagonist ICI ll8,55l a significant attenuation of the evokedADR overflow was seen. indicating presynaptic pz-adrenoceptors also facilitatlngneuronal ADR release.In supplement 6.4 we demonstrated that the spontaneously hypertensive rat- 1 3 6 -(SHR) respond to much lower dosages of fenoterol when compared to those of theWistar rat (WR). This strongly pronounced facilitation could, however not beattributed to a dysfunction of the pa-adrenoceptor but rather to a dysfunctionalcz-adrenoceptor, thus unmasking the pz-adrenoceptor-mediated facilitation of NAoverflow.Supplements 6.5 and 6.ó describe the invesigations on the presence and thecharacter of the presynaptic muscarinic receptors in the rat portal vein. Infusion ofmethacholine (MCH had no effect on the basal NA level. During electrical stimulation,however. MCh strongly inhibited (952) the evoked NA overflow, while atropine wasable to reverse this inhibition. ln the presence of the cr2-adrenoceptor antagonistyohimbine, MCh again was able to reduce the yohimbine-induced enhanced NAoverflow. Using selective antagonlsts like pirenzepine (M'), AF-DX 116 (Ma) and4-DAMP (M:), the receptor subtype was determined. From the order of the plC-values it could be concluded that the presynaptic muscarinic receptor was of thecardiac Mz-subclass.Finally, some preliminary experiments using morphine showed the presence andfunctioning of inhibitory presynaptic opioid receptors in the vascular sympatheticvaricosities of the unrestrained conscious rat. The precise nature of these presynapticopioid receptor(s) remains to be elucidated.i

Presynaptic receptors in the vasculature of the freely moving rat.

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