Brainstem and bulbospinal neurotransmitter systems in the control of blood pressure.
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Animals↗
Biomedical subjects
P Pilowsky
Publications and source records attributed to P Pilowsky.
GABA-immunoreactive boutons make synapses with inspiratory neurons of the dorsal respiratory group.
Intracellular labelling with horseradish peroxidase (HRP) combined with gamma-aminobutyric (GABA) immunocytochemistry was used to assess the GABAergic input to inspiratory bulbospinal neurons of the dorsal respiratory group in the cat. The relationship between GABA-immunoreactive (GABA-IR) boutons and intracellularly labelled neurons was examined at the light microscopic and ultrastructural levels. At the light microscopic level, GABA-IR boutons were frequently found in close apposition to dendrites and cell bodies of labelled neurons. The presence of synapses was confirmed with electron microscopy. In addition, synaptic specializations were observed between immunoreactive boutons and unlabelled terminals which in turn formed synaptic contacts with HRP-labelled dendrites, a finding consistent with presynaptic inhibition. These results demonstrate a direct GABAergic input to a functionally defined population of medullary respiratory neurons, and suggest involvement of this neurotransmitter in the control of these neurons.
Animals↗
Central serotonergic mechanisms in cardiovascular regulation.
This paper reviews the role of central serotonin-containing neurons in the control of blood pressure. Central serotonin nerves have their cell bodies in the brainstem in a number of discrete collections, from where they ascend to ramify throughout the brain, descend to terminate in the spinal cord, or send shorter projections terminating in medulla, pons, and midbrain. Activation of one important ascending serotonin pathway innervating the preoptic region of the hypothalamus causes an increase in blood pressure. Activation of a bulbospinal serotonin projection descending from the ventrolateral medulla (the B3 cell group) to terminate in the intermediolateral cell column (IML) also evokes a pressor response. This pressor response is independent of that elicited by stimulation of the ventrolateral medulla in the adjacent but separate area containing the C1 adrenaline cell group. The pressor action appears to depend on increased release of serotonin, as detected by microdialysis in the area of the IML, and to be mediated by serotonin receptors of the 5HT1 subclass, probably located on sympathetic preganglionic neurons. It is possible that neuroactive excitatory amino acids, such as glutamate or aspartate, and neuropeptides such as substance P, also play a part in the pressor response evoked by stimulation of the ventrolateral medulla in the area of the lateral B3 serotonin cells. This descending serotonin pathway also appears important in mediating the hypotensive action of the antihypertensive drugs methyldopa and clonidine.
Animals↗
Neuropeptide Y in the sympathetic control of blood pressure in hypertensive subjects.
Neuropeptide Y (NPY) coexists with noradrenaline in postganglionic sympathetic neurons and with noradrenaline and adrenaline in the central nervous system. The possibility that NPY is released into the circulation during activation of the sympathoadrenal system was investigated in ten moderately hypertensive volunteers using three different stimuli. In healthy moderately hypertensive volunteers cold pressor test, head up tilt and graded bicycle exercise resulted in increased blood pressure, heart rate and plasma catecholamine concentrations. While there was a trend for plasma NPY-like immunoreactivity (NPY-LI) to increase during cold pressor test and head up tilt, NPY-LI concentration only increased significantly during bicycle exercise, the stimulus of greatest duration. These results suggest that plasma NPY-LI can be released into the circulation on sympathoadrenal activation in moderately hypertensive subjects and demonstrate that the pattern of release is similar to that previously observed in normotensive subjects.
Adrenal Glands↗
Limitations of the technique of pressure microinjection of excitatory amino acids for evoking responses from localized regions of the CNS.
The aim of this study, performed on anaesthetized cats and rabbits, was to test the assumption that pressure microinjections of excitatory amino acids cause long-lasting excitation of neurones located close to the injection site. Unitary action potentials or antidromic field potentials were recorded from respiratory or 'reticular' neurones in the medulla oblongata and from phrenic motoneurones at different distances from the injection site. Injection of 10-150 nl (5-150 nmol) of L-glutamate or DL-homocysteic acid into these areas resulted in complex and widespread neuronal events. Generally, more distant neurones (500-1300 microns) were excited for variable periods of time (3-15 min), while neurones in the vicinity of the injection site (0-500 microns) showed, after a brief period of excitation time, a long-lasting (up to 30 min) decrease in excitability or silencing of discharge, probably due to a depolarizing block and disturbances in the ionic composition of the extracellular space. These findings show that interpretation of physiological responses following such injections should not be based on an assumption of local neuronal excitation. Some recommendations regarding the use of this technique are made.
Action Potentials↗
The use of microinjected colloidal gold and immunocytochemistry to localise pressor sites in the rostral medulla oblongata of the rat.
A new technique for localising the centre of sites of microinjection of drugs in the brain using the silver intensification of colloidal gold is described. The technique is compatible with immunocytochemistry and in this study was used in Wistar-Kyoto rats to investigate the relationship between the location of phenylethanolamine-N-methyltransferase-like immunoreactive (PNMT-LI) cell bodies in the medulla and the precise sites where microinjection of L-glutamate elicited pressor responses. Colloidal gold provided a simple technique for localising the centre of sites of microinjection with a high degree of spatial resolution and allowed pressor sites to be precisely localised in the region of ventrolateral medulla with the highest density of PNMT-LI cells.
Animals↗
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↗
Does substance P coexist with adrenaline in neurones of the rostral ventrolateral medulla in the rat?
Spinally projecting substance P- (SP) and adrenaline-containing neurones of the rostral ventrolateral medulla are believed to be important in the tonic and reflex control of blood pressure. In this paper we used dual immunofluorescence staining to investigate the degree of co-localisation of these two putative neurotransmitters in this region. In contrast to a recent report that SP and phenylethanolamine-N-methyltransferase (PNMT) are extensively co-localised, we report here that only a small number of neurones were found to be immunoreactive for both SP and PNMT.
Animals↗
Renal sympathetic nerve responses to stimulation, inhibition and destruction of the ventrolateral medulla in the rabbit.
The role of the sympathetic nervous system in the cardiovascular responses to lesions of the caudal ventrolateral medulla of the rabbit was investigated by measurement of renal sympathetic nerve activity. In addition, the effect of chemical stimulation and inhibition on renal sympathetic nerve activity was assessed. The results show that lesions or chemical inhibition of the caudal ventrolateral medulla result in an increase in sympathetic nerve activity and blood pressure, whilst excitation results in a decrease in blood pressure and nerve activity. These findings contrast with chemical stimulation or inhibition of the rostral ventrolateral medulla in the region of the C1 cells where stimulation results in a rise in blood pressure and renal nerve activity, and inhibition, a fall in blood pressure and nerve activity.
Animals↗
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)
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