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EFFECT OF NEUROHUMORS ON SPINAL VASOMOTOR NEURONES
EFFECT
OF
NEUROHUMORS
J.N.
SINHA,
ON
SPINAL
G.P. GUPTA
Department of Pharmacology
VASOMOTOR
NEURONES
AND K.N. DHAWAN
and Therapeutics,
King George's Medical College,
Lucknow University, Lucknow-3, India Received
for
publication
August
2,
1968
The role of central nervous system in the regulation of blood pressure is now well established. concerned in the regulation of blood pressure are situated all along the neuraxis.
The loci
Vasomotor center situated
in the medulla oblongata plays the key role in the regulation of the vascular tone. Existence of vasoactive neurones in the spinal cord, which can function independent of the supra spinal influences has also been re ported (1). We have earlier demonstrated that acetylcholine acts as an excitatory transmitter in the medul lary vasomotor loci (2). The purpose of the present investigation was to throw some light on the nature of the neurohumor in spinal vasomotor neurones by observing the effect of alleged neurohumors on the spinal compression vasomotor response (3). The present study was carried out on 18 adult mongrel dogs of either sex, anaesthetized with pentobar bitone sodium (35 mg/kg i.v.).
The animals were routinely vagotomized and maintained on artificial posi
TABLE I
tive pressure respiration.
The blood pressure was recorded from right common carotid artery through a
mercury manometer on smoked kymograph paper. injection.
Femoral vein of one side was cannulated for intravenous
The spinal cord was ligated within the meninges at C,.
A number one needle was inserted in
trathecally and was connected with a pressor bottle containing normal saline. pressure produced spinal vasomotor compression responses (SCVR). various agents was studied on this response.
Increase in the intrathecal
Effect of intrathecal administration of
The drugs used in the present study were adrenaline hydrochloride, histamine phosphate, 5-hydroxytryp tamine creatinine sulphate, hydrochloride
acetylcholine
chloride, choline tricitrate,
and hemicholinium compound
propranolol,
yohimbine,
procaine
(HC,).
Amongst the neurohumors studied only adrenaline produced significant potentiation of the SCVR, while histamine, 5-HT and acetylcholine failed to produce any significant effect (see Table I and Fig. 1). Adrena line (200 pg) produced no significant effect on the blood pressure (5 mm rise) but markedly potentiated (two and a half times of the control) the spinal compression vasomotor response.
The effect appeared within ten
minutes of administration and lasted for about 30 minutes. Tricholine citrate, a precursor of acetylcholine, and hemicholinium which is known to block the synthesis of acetylcholine were also studied for their effect on the SCVR.
Both the drugs did not produce any signi
ficant effect on the spinal vasomotor reponses (Table 1). In an attempt to investigate the nature of receptors concerned in the adrenaline induced potentiation of SCVR, effect of a and f3-adrenergic blocking agents was studied. blocked the spinal compression response.
Propranolol (1.0 mg i.t.) completely
Similar results were obtained with yohimbine (1.0 mg i.t.).
In
order to ascertain the part played by local anaesthetic activity of propranolol and yohimbine in abolishing the SCVR the effect of intrathecal
administration
of procaine (10.0 nig) was studied.
Similar to a and
13-adrenergic blocking agents it also blocked both SCVR and its potentiation. From the results of the present study it is clear that amongst various drugs only adrenaline significantly potentiates the spinal vasomotor compression response (SCVR).
The fact that
the adrenaline
induced
potentiation of spinal vasomotor responses as well as control SCVR is blocked by a-adrenergic blocking agents, ~-adrenergic blocking agents and procaine, makes it difficult to suggest the type of adrenergic receptors present in the spinal vasoactive neurones.
All these agents produced a blockade probably because
of their local anaesthetic activity. Acknowledgement: The authors are grateful for the financial
to the Indian Council of Medical Research, New Delhi
assistance and to Dr. J.P. Long for the generous supply of hemicholinium.
FiG. 1. Effect
of 5-hydroxytryptamine,
histamine,
acetylcholine
and
adre
naline on SCVR (pressure 150 mmHg for 10 seconds) observed in four different dogs. The panels in the first column show the control re sponses whereas the responses shown in the panels of the third columns were obtained 15 and 60 minutes respectively thecal administration of the drugs. the responses after adrenaline.
Note
the
marked
second and after intra
potentiation
of
REFERENCES
1)
ALEXANDER,R.S.: Am. J. Phvsiol. 143, 698 (1945) ; 2)
ANDGUPTA, G.P.: Can. J. Phvsiol. Pharmac. 45, 503 (1966); Archs int. Pharmacodvn. Ther. 120, 85 (1959)
SINHA,J.N., DHAWAN,K.N., CHANDRA,0. 3)
BHARGAVA, K.P. ANDKuLSRESHTHA,.J.K.:
OF
NEUROHUMORS
J.N.
SINHA,
ON
SPINAL
G.P. GUPTA
Department of Pharmacology
VASOMOTOR
NEURONES
AND K.N. DHAWAN
and Therapeutics,
King George's Medical College,
Lucknow University, Lucknow-3, India Received
for
publication
August
2,
1968
The role of central nervous system in the regulation of blood pressure is now well established. concerned in the regulation of blood pressure are situated all along the neuraxis.
The loci
Vasomotor center situated
in the medulla oblongata plays the key role in the regulation of the vascular tone. Existence of vasoactive neurones in the spinal cord, which can function independent of the supra spinal influences has also been re ported (1). We have earlier demonstrated that acetylcholine acts as an excitatory transmitter in the medul lary vasomotor loci (2). The purpose of the present investigation was to throw some light on the nature of the neurohumor in spinal vasomotor neurones by observing the effect of alleged neurohumors on the spinal compression vasomotor response (3). The present study was carried out on 18 adult mongrel dogs of either sex, anaesthetized with pentobar bitone sodium (35 mg/kg i.v.).
The animals were routinely vagotomized and maintained on artificial posi
TABLE I
tive pressure respiration.
The blood pressure was recorded from right common carotid artery through a
mercury manometer on smoked kymograph paper. injection.
Femoral vein of one side was cannulated for intravenous
The spinal cord was ligated within the meninges at C,.
A number one needle was inserted in
trathecally and was connected with a pressor bottle containing normal saline. pressure produced spinal vasomotor compression responses (SCVR). various agents was studied on this response.
Increase in the intrathecal
Effect of intrathecal administration of
The drugs used in the present study were adrenaline hydrochloride, histamine phosphate, 5-hydroxytryp tamine creatinine sulphate, hydrochloride
acetylcholine
chloride, choline tricitrate,
and hemicholinium compound
propranolol,
yohimbine,
procaine
(HC,).
Amongst the neurohumors studied only adrenaline produced significant potentiation of the SCVR, while histamine, 5-HT and acetylcholine failed to produce any significant effect (see Table I and Fig. 1). Adrena line (200 pg) produced no significant effect on the blood pressure (5 mm rise) but markedly potentiated (two and a half times of the control) the spinal compression vasomotor response.
The effect appeared within ten
minutes of administration and lasted for about 30 minutes. Tricholine citrate, a precursor of acetylcholine, and hemicholinium which is known to block the synthesis of acetylcholine were also studied for their effect on the SCVR.
Both the drugs did not produce any signi
ficant effect on the spinal vasomotor reponses (Table 1). In an attempt to investigate the nature of receptors concerned in the adrenaline induced potentiation of SCVR, effect of a and f3-adrenergic blocking agents was studied. blocked the spinal compression response.
Propranolol (1.0 mg i.t.) completely
Similar results were obtained with yohimbine (1.0 mg i.t.).
In
order to ascertain the part played by local anaesthetic activity of propranolol and yohimbine in abolishing the SCVR the effect of intrathecal
administration
of procaine (10.0 nig) was studied.
Similar to a and
13-adrenergic blocking agents it also blocked both SCVR and its potentiation. From the results of the present study it is clear that amongst various drugs only adrenaline significantly potentiates the spinal vasomotor compression response (SCVR).
The fact that
the adrenaline
induced
potentiation of spinal vasomotor responses as well as control SCVR is blocked by a-adrenergic blocking agents, ~-adrenergic blocking agents and procaine, makes it difficult to suggest the type of adrenergic receptors present in the spinal vasoactive neurones.
All these agents produced a blockade probably because
of their local anaesthetic activity. Acknowledgement: The authors are grateful for the financial
to the Indian Council of Medical Research, New Delhi
assistance and to Dr. J.P. Long for the generous supply of hemicholinium.
FiG. 1. Effect
of 5-hydroxytryptamine,
histamine,
acetylcholine
and
adre
naline on SCVR (pressure 150 mmHg for 10 seconds) observed in four different dogs. The panels in the first column show the control re sponses whereas the responses shown in the panels of the third columns were obtained 15 and 60 minutes respectively thecal administration of the drugs. the responses after adrenaline.
Note
the
marked
second and after intra
potentiation
of
REFERENCES
1)
ALEXANDER,R.S.: Am. J. Phvsiol. 143, 698 (1945) ; 2)
ANDGUPTA, G.P.: Can. J. Phvsiol. Pharmac. 45, 503 (1966); Archs int. Pharmacodvn. Ther. 120, 85 (1959)
SINHA,J.N., DHAWAN,K.N., CHANDRA,0. 3)
BHARGAVA, K.P. ANDKuLSRESHTHA,.J.K.: