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Biomedical subjects

V Kapoor

Publications and source records attributed to V Kapoor.

At least 91 records · Page 5Linked to original sources
PubMed1987

Do pressor neurons in the ventrolateral medulla release amines and neuropeptides?

Activation of neurons arising in the rostral ventrolateral medulla evokes a pressor response in the rat and the rabbit. This region of the medulla gives rise to bulbospinal neurons containing many different neurotransmitters, including amines such as adrenaline, noradrenaline and serotonin, and neuropeptides such as substance P and neuropeptide Y. Colocalization of amines and neuropeptides has been described in some neurons descending from the rostral ventrolateral medulla. In this paper we discuss the evidence that bulbospinal serotonin-containing neurons (B3) and adrenaline-containing neurons (C1) arising from this part of the medulla exert pressor effects by distinct central pathways and conclude that they do. We also consider the possibility that the pressor effects of activating these two groups of neurons are associated with release of neuropeptides and highlight evidence that substance P is released into the spinal cord by activation of descending serotonin-containing neurons, while neuropeptide Y may be released by activation of bulbospinal adrenaline-containing neurons.

Animals↗
PubMed1986

Spinal cord serotonin release and raised blood pressure after brainstem kainic acid injection.

The recently developed technique of in vivo dialysis has permitted us to make direct measurements of serotonin release in a specific region of the spinal cord and to relate this to changes in blood pressure elicited by chemical stimulation of the brainstem. In the present experiments we have shown that chemical stimulation of bulbospinal neurons in the region of the B3 cell group in the ventromedial medulla, causes an increase in the release of serotonin in the thoracic spinal cord and that this release is associated with an increase in blood pressure.

Animals↗
PubMed1986

Role of renal nerve activity, plasma catecholamines and plasma vasopressin in cardiovascular responses to intracisternal neurotoxins in the rabbit.

We have examined the acute (0-3 h) effect of intracisternally administered 5,7-dihydroxytryptamine (DHT) and 6-hydroxydopamine (6-OHDA) on blood pressure, heart rate, renal nerve activity, plasma adrenaline, plasma noradrenaline and plasma vasopressin in conscious rabbits. The increase in blood pressure seen following 5,7-DHT treatment was associated with increases in adrenaline and vasopressin levels and renal nerve activity throughout the response. The increase in blood pressure which followed 6-OHDA administration was associated with an increase in renal nerve activity alone. These findings indicate that the rise in blood pressure elicited by these drugs involves an increase in sympathetic nerve activity. The absence of a rise in vasopressin levels during the response to 6-OHDA suggests that the rise in blood pressure seen in these animals is due entirely to a bulbospinal sympathoexcitatory pathway.

5,6-Dihydroxytryptamine↗
PubMed1986

Increases in plasma neuropeptide Y concentrations during sympathetic activation in man.

Neuropeptide Y (NPY) coexists with noradrenaline in postganglionic sympathetic neurons. In order to test the hypothesis that NPY may be released along with catecholamines by activation of the sympathoadrenal system we measured plasma NPY-like immunoreactivity (NPY-LI) concentrations during cold pressor test, head up tilt and bicycle exercise in healthy volunteers. All 3 manoeuvres resulted in elevation of blood pressure, heart rate and plasma noradrenaline and adrenaline concentrations. These were accompanied by increases in plasma NPY-LI concentrations on cold pressor test and exercise, but not with head up tilt. The increases in both NPY-LI and catecholamines were greatest with exercise. These findings suggest that NPY is released at the same time as noradrenaline when sympathetic noradrenergic nerves are activated.

Adult↗
PubMed1986

Relative importance of sympathetic nerves and of circulating adrenaline and vasopressin in mediating hypertension after lesions of the caudal ventrolateral medulla in the rat.

Electrolytic lesions of the A1 noradrenaline cells in the caudal ventrolateral medulla cause transient hypertension and bradycardia in the conscious rat, as previously described in the rabbit. The lesions produced 100-fold increases in plasma arginine vasopressin, 40-fold increases in plasma adrenaline and fourfold increases in plasma noradrenaline levels. Absence of circulating vasopressin [homozygous diabetes insipidus rats (DI)] or circulating adrenaline (adrenalectomized rats) did not affect A1 hypertension, but sympathectomy with systemic 6-hydroxydopamine (6-OHDA) significantly attenuated A1 hypertension. A factorial experiment was performed to assess the relative contributions of these three peripheral effector mechanisms in a quantitative manner, with combined deficiencies of any two or of all three of these effector systems. Results suggest A1 hypertension in the rat to be primarily mediated through increased sympatho-adrenal activity. The largest component of hypertension (66%) results from increased sympathetic vasoconstrictor nerve activity, and a smaller part (34%) reflects the action of circulating adrenaline. Increases in vasopressin levels do not contribute to A1 hypertension, although vasopressin makes a major contribution to A1 lesion bradycardia.

Adrenalectomy↗
PubMed1986

Plasma neuropeptide y levels rise in patients undergoing exercise tests for the investigation of chest pain.

Neuropeptide Y (NPY) is colocalised with noradrenaline in post-ganglionic sympathetic neurons. In order to examine the possibility that activation of the sympathetic nervous system might cause release of NPY into the plasma NPY levels were measured in 16 patients undergoing exercise tests for investigation of chest pain. Plasma NPY concentrations rose in 14 out of the 16 patients, and the mean level of plasma NPY increased from 335 (s.e.m. = 37) to 455 (s.e.m. = 41) pg/ml. Plasma noradrenaline and adrenaline levels increased four- and two-fold respectively. The increase in NPY correlated with the increase in noradrenaline, suggesting that NPY may be released with noradrenaline when sympathetic noradrenergic nerves are activated.

Adult↗
PubMed1985

The mechanism of hypertension and bradycardia following lesions of the caudal ventrolateral medulla in the rabbit: the role of sympathetic nerves, circulating adrenaline, vasopressin and renin.

Lesions of the ventrolateral medulla of the rabbit, coinciding with the A1 noradrenaline cell bodies (A1 lesions) produced fortyfold increases in the plasma levels of vasopressin and adrenaline, a twofold increase in plasma noradrenaline and a substantial increase in plasma renin activity. These increases accompanied the hypertension and bradycardia that follow A1 lesions. The vasoconstriction and hypertension were completely abolished by phentolamine, an alpha-adrenoceptor antagonist, when it was administered before lesions and were markedly reduced when it was given after lesions. On the other hand, administration of an antagonist to the vasoconstrictor action of vasopressin (d(CH2)5Tyr(Me)AVP) or an angiotensin converting enzyme inhibitor had little effect. Prior removal of the adrenal glands prevented any rise in plasma adrenaline levels but had no effect on the pressure response to subsequent A1 lesions. These results indicate that the vasoconstriction and hypertension were predominantly mediated by alpha-adrenoceptor stimulation, acting mainly through sympathetic vasoconstrictor nerves. The fall in heart rate following A1 lesions was approximately halved by pretreatment either with d(CH2)5Tyr(Me)AVP alone, or by blockade of the vagus and sympathetic with scopolamine and propranolol; it was completely abolished by combined pretreatment with all three agents. The experiments show that vasopressin release makes a major contribution to the bradycardia acting at least in part through mechanisms that are independent of cardiac vagal or sympathetic nerves.

Adrenalectomy↗
PubMed1985

Methyldopa hypotension and ascending projections from midline serotonin (B3) cells in the medulla.

Micro-injection of methyldopa into the area of the midline B3 serotonin cell group in the ventral medulla of spontaneously hypertensive rats, stroke-prone strain (SHRSP), caused a fall in blood pressure of 30-40 mmHg, maximally 2-3 h after administration. This hypotension was abolished by the selective serotonin neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) injected intracerebroventricularly, but it was not affected by intraspinal injection of 5,7-DHT to produce a selective lesion of serotonin nerves descending into the spinal cord, or by injection of 5,7-DHT into the median forebrain bundle, one of the main ascending pathways from the B3 serotonin cells. It seems likely that the midline serotonin B3 cells in the medulla contribute to the hypotensive action of methyldopa through a projection restricted to the caudal brainstem.

5,7-Dihydroxytryptamine↗
PubMed1985

New approaches to the study of bulbospinal (B3) serotonergic neurons in the control of blood pressure.

The technique of in vivo brain dialysis, recently described by Ungerstedt et al. (1982) provides an opportunity for the direct collection, identification and measurement of neurotransmitters released by activation of a particular pathway. Whereas Ungerstedt et al. used the method for the study of dopamine release by nigrostriatal neurons, it is applied here for the first time to the study of serotonin released by descending spinal neurons regulating sympathetic activity and in turn blood pressure. The first set of experiments performed were designed to test the hypothesis, arising out of previous experiments in the authors' laboratory, that bulbospinal serotonin neurons can exert a pressor effect through release of serotonin in the intermedio-lateral cell column. Micro-injections of kainic acid were made into the area of the lateral B3 serotonin cell group in the medulla. This elicited an increase in the release of serotonin in the spinal cord, measured using in vivo dialysis, accompanied by an increase in blood pressure. Pretreatment with 5.7-dihydroxytryptamine (5.7DHT) 2 weeks earlier completely prevented the increase in serotonin release and in blood pressure evoked by micro-injection of kainic acid into the B3 serotonin cells. These experiments used the technique of brain dialysis to support the hypothesis that bulbospinal serotonin nerves can exert a pressor action. In a second set of experiments L-glutamate was injected into the region of the lateral B3 serotonin cells near to the ventral surface of the medulla, and also into the midline B3 serotonin cells in the raphe, in order to activate neuronal cell bodies without stimulating fibres of passage.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Observation of cultured peripheral non-neuronal cells implanted into the transected spinal cord.

We have previously reported that cultured peripheral non-neuronal cells could be used as an adjunct to spinal cord reconstruction with the delayed nerve graft technique. The cultured cells appeared to enhance axonal regeneration and with their use the time it took for axons from the spinal cord stumps to reach the nerve graft was reduced. To gain insight into the possible mechanisms through which peripheral non-neuronal cells can foster CNS regeneration, we have now investigated the behaviour of the peripheral non-neuronal cells after implantation into the spinal cord. Autologous mixed non-neuronal cell cultures were prepared from cat sciatic nerve biopsies and labeled in culture with tritiated thymidine. The labeled cells were implanted so as to completely fill the gap in the spinal cord produced by a narrow "slit transection". Light-and electron-microscopic autoradiography was used to identify the cells 3 and 7 days after implantation and to determine their proximity to, and possible interaction with, axons in the spinal cord stumps. The implanted peripheral cells were frequently found near spinal cord axons and axon terminals. Some of the labeled cells ensheathed axons in which case they displayed morphological characteristics of Schwann cells. Other labeled cells had characteristics of fibroblasts and were surrounded by an extracellular matrix rich in collagen fibrils. Many of the labeled cells contained phagocytosed myelin debris. These observations are consistent with the implanted cells acting to enhance regeneration in the spinal cord either by direct interaction with axons (ensheathment) or indirectly via the production of soluble neuronotrophic factors or a favorable extracellular matrix. The ability of the implanted cells to rapidly move into the spinal cord stumps and attain positions close to spinal cord axons would be an important factor for any of these mechanisms.

Animals↗
PubMed1984

Hypertension after brainstem (A1) lesions in normal rats and in rats with adrenalectomy, sympathectomy or diabetes insipidus.

Lesions of the ventrolateral medulla coinciding with the A1 noradrenaline cell group, in either the rabbit or the rat, cause hypertension and bradycardia accompanied by 50-fold increases in plasma vasopressin and adrenaline and a two-to-four-fold increase in plasma noradrenaline. Following adrenalectomy in normal rats, the A1 hypertension and bradycardia were unchanged. In Brattleboro rats with diabetes insipidus, A1 hypertension was not altered but the bradycardia was reduced by 40%. In Brattleboro rats subjected to adrenalectomy, the hypertension was reduced by 50%. In normal rats, chemical sympathectomy with intravenous 6-hydroxydopamine (6OHDA) reduced the hypertension by about 50%, and when combined with adrenalectomy it abolished the hypertension altogether. In Brattleboro rats, 6OHDA reduced the hypertension after A1 lesions by about 40%. We suggest that A1 hypertension is predominantly mediated through increased activity of sympathetic vasoconstrictor nerves, and that circulating adrenaline and vasopressin only make a minor contribution to the increase in pressure.

Adrenal Glands↗
PubMed1981

Regional changes in cerebral glucose utilization associated with amygdaloid kindling and electroshock in the rat.

A method using [3H]2-deoxyglucose was used to identify brain areas activated during partial and generalized amygdaloid kindled seizures and generalized seizures following electro-convulsive shock in rats. The amygdala, hippocampus. septal nuclei and hypothalamus were bilaterally activated in kindled convulsions. Electroshock caused a more widespread involvement including the thalamus, striatum, reticular formation and cerebellum. Changes in the amygdala and hippocampus but not hypothalamus, were found after partial kindling.

Amygdala↗
PubMed1981

A mutation affecting L-serine and energy metabolism in E. coli K12.

The effects of a pleiotropic mutation ssd are described. This mutation results in decreased efficiency in the use of glucose and fructose as carbon source, inability to use succinate or to grow anaerobically, an alteration in the activity of enzymes responsible for the synthesis and degradation of L-serine, increased resistance to certain antibiotics, and a deficiency in proline transport. This mutation resembles various previously described mutations thought to affect' energy coupling factor' and is located in the same region of the chromosome. While the gene product affected by this mutation is still unidentified, it is clear that L-serine metabolism cannot be understood merely in terms of providing L-serine and its derivatives.

Anaerobiosis↗
PubMed1980

In vitro studies on L-serine deaminase activity of Escherichia coli K12.

Extracts of Escherichia coli K12 contain an enzyme which deaminates L-serine. This serine deaminase appears to be a soluble enzyme and is inhibited by substrate analogues, metal ions, and chelators. The activity, which is very unstable in vitro, is protected, and in some cases, even activated by substrate, substrate analogues, and by ferrous ion. The enzyme has proved unstable in all attempts at purification. It resembles closely the L-serine deaminase activity in other microorganisms, but is very different from the mammalian enzyme. As judged by comparison with organisms in which this enzyme serves as part of the principal carbon-handling pathway, L-serine deaminase activity is present in E. coli extracts in physiologically significant amounts.

Escherichia coli↗
PubMed1978

A single mutation affects L-serine deaminase, L-leucyl-, L-phenylalanyl-tRNA protein transferase, and proline oxidase activity in Escherichia coli K-12.

A mutation at a single locus, wyb, results in several phenotypic changes in Escherichia coli K-12. The Wyb- phenotype includes: (i) an increase in L-serine deaminase activity, together with a loss of inducibility by L-leucine; (ii) an absence of L-leucyl-, L-phenylalanyl-tRNA protein transferase activity; (iii) inducibility of proline oxidase by proline; and (iv) a loss of ability to use maltose as a carbon and energy source.

Acyltransferases↗
PubMed1977

Role of threonine dehydrogenase in Escherichia coli threonine degradation.

Threonine was used as nitrogen source by Escherichia coli K-12 through a pathway beginning with the enzyme threonine dehydrogenase. The 2-amino-3-ketobutyrate formed was converted to glycine, and the glycine was converted to serine, which acted as the actual nitrogen donor. The enzyme formed under anaerobic conditions and known as threonine deaminase (biodegradative) is less widespread than threonine dehydrogenase and may be involved in energy metabolism rather than in threonine degradation per se.

Adenylyl Cyclases↗