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P R Howe

Publications and source records attributed to P R Howe.

90 records · Page 5Linked to original sources
PubMed1977

Immunochemical comparison of synaptic plasma membrane and synaptic vesicle membrane antigens.

A synaptic vesicle fraction and a synaptic plasma membrane fraction obtained after subfractionation of synaptosomes from chick forebrain have been used to produce antisera in rabbits. Immunofluorescence histology with the two antisera revealed that they reacted strongly with synaptic terminal regions present in the chick forebrain, cerebellum and spinal cord. In addition, the synaptic plasma membrane antiserum (but not the synaptic vesicle antiserum) reacted with preterminal axons in the cerebellum and spinal cord. Comparison of the two antisera by two-dimensional immunoelectrophoresis, revealed the presence of common antigens in the synaptosomal vesicle and plasma membrane fractions. Incubation of synaptosomes in vitro with the synaptosomal vesicle antiserum and complement produced a dose-dependent inhibition of synaptosome swelling up to a maximum of 55% of that obtained with the synaptosomal plasma membrane antiserum. The results of this test are consistent with the hypothesis that some synaptosomal vesicle antigens may be present also in the synaptosomal plasma membrane and imply that they face the external surface of the synaptosomes. The fate of vesicle membrane components in synaptosomal plasma membranes is not known. The possibility is discussed that they may be recycled locally by a mechanism similar to that proposed by Heuser and Reese (1973) for re-use of synaptic vesicle membranes at the neuromuscular junction.

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Blood pressure control by neurotransmitters in the medulla oblongata and spinal cord.

The roles of putative central neurotransmitters in the control of blood pressure have been reviewed with respect to the cardiovascular functions of individual nerve pathways in the medulla oblongata and spinal cord. Vasomotor activity of sympathetic preganglionic neurones originates from spinally-projecting neurones in the ventrolateral medulla which may include adrenaline neurones of the C1 group and serotonin neurones in the lateral B1 and B3 groups. Other bulbospinal monoamine nerves may modulate vasomotor activity at the spinal level, but the mechanism of this modulation is controversial. Evidence for two descending sympatho-inhibitory pathways has emerged: a noradrenergic projection from the A5 cell group and a serotonergic projection from the medullary raphe (medial B1 and B2 groups). The vasomotor influence of other bulbospinal pathways is unclear. Baroreflex control of blood pressure is mediated through the solitary tract nucleus (NTS). L-Glutamate and substance P are considered as candidates for transmitters in baroreceptor afferents to the NTS. Transmitters in efferent nerves relaying baroreflex activity from the NTS to cardiovagal motoneurones, medullary vasomotor neurones or sympathetic preganglionic neurones have not been identified but the monoamine transmitters present in the NTS appear to modulate baroreflexes. Noradrenaline and serotonin nerve endings may facilitate the vasodepressor component of the baroreflex while adrenaline nerves possibly inhibit the cardiovagal mechanism. Enkephalins and vasopressin act in the NTS to raise blood pressure and nerves containing these neuropeptides may constitute important links in reciprocal cardiovascular pathways between the lower brainstem and hypothalamus.

Amines↗
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Changes in cardiac norepinephrine in spontaneously hypertensive and stroke-prone rats.

The norepinephrine (NE) concentration of cardiac ventricles was determined by radioenzymatic assay in normotensive Wistar Kyoto rats (WKY), spontaneously hypertensive rats (SHR), and stroke-prone rats (SPR) at 3-6, 14-19, and over 31 weeks of age. There was no difference between strains prior to hypertension, but a progressive decrease in cardiac NE concentration occurred in SHR and particularly in SPR relative to WKY after hypertension was established. This decrease was not due to cardiac hypertrophy. The cardiac neuronal NE storage capacity in rats over 31 weeks of age was analyzed by determining the maximum concentration of NE obtained in a cardiac microsomal fraction, after saturation in vivo with exogenous NE. The results indicated that, after a long period of hypertension, there was a reduction in cardiac NE storage capacity resulting from a loss either of sympathetic nerve endings or of storage vesicles. Moreover, in addition to this reduction in the total size of the cardiac NE store, there was an independent reduction in the degree of filling of this store in both SHR and SPR. This could reflect an increased turnover of cardiac NE in chronically hypertensive SHR and SPR.

Aging↗
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Plasma catecholamines and neuropeptide-Y as indices of sympathetic nerve activity in normotensive and stroke-prone spontaneously hypertensive rats.

The suitability of plasma catecholamines (CAs) and neuropeptide-Y (NPY) as biochemical indices of sympathetic nerve activity (SNA) has been investigated, and these parameters have been compared between adult normotensive (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP). Plasma norepinephrine (NE), epinephrine (E) and NPY were measured in venous and arterial blood samples taken from conscious, unrestrained rats. Under resting conditions, both CAs were significantly higher in SHRSP than in WKY; plasma E in particular was raised threefold. SHRSP had higher plasma levels of NPY in arterial blood but not in venous blood. Acute hydralazine-induced hypotension caused a slight rise in NPY and striking increases of CAs, which were accentuated in SHRSP. Ganglion blockade with pentolinium reversed these increases but the differences in basal plasma CA levels between strains still persisted. Barbiturate anaesthesia had little effect on plasma levels of NPY or NE, but plasma E levels were depressed, particularly in SHRSP, so that the strain difference in plasma E taken from venous blood was no longer apparent. The results indicate that plasma levels of CAs but not NPY are useful indices of SNA in conscious rats. Comparisons between WKY and SHRSP after drug treatment demonstrate a major contribution by the adrenal medulla to plasma CA levels in SHRSP which, under resting conditions, may not be sympathetically evoked.

Anesthesia↗
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Adrenaline synthesizing nerve cells in the medulla of normotensive and hypertensive rats.

1. We have studied the number and distribution of adrenaline synthesizing nerve cells in the medulla oblongata of the rat, using a combination of immunofluorescence to visualize the enzyme phenylethanolamine-N-methyltransferase (PNMT) and catecholamine fluorescence to detect central catecholamines. 2. The distribution of adrenaline synthesizing nerve cells was similar in normotensive (Wistar Kyoto) rats, spontaneous hypertensive rats, and stroke-prone rats. Few of the cells visualized by PNMT immunofluorescence were detected by the Faglu fluorescence method for catecholamines. The C1 (ventrolateral) and C2 (dorsomedial) groups of PNMT cells were anatomically distinct from the A1 and A2 groups of catecholamine fluorescent cells and lay rostral to these cells within the medulla. There was a third group of adrenaline synthesizing cells close to the midline in the rostral medulla, and we have called this the C3 group. 3. There was a 32% increase in the number of PNMT cells in the medulla of 4-week-old stroke-prone rats. 4. PNMT enzyme activity in a cross-segment of the medulla containing the adrenaline synthesizing cells was also increased by 30% in both spontaneous hypertensive rats and stroke-prone rats.

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Elevation of blood pressure in hypertensive rats after lesioning serotonin nerves in the dorsomedial medulla oblongata.

The possibility that serotonin (5HT) nerve endings in the dorsomedial medulla oblongata participate in the control of blood pressure was investigated in stroke-prone hypertensive rats and in normotensive rats. 5HT nerves were destroyed by injecting 5,7-dihydroxytryptamine bilaterally into the solitary tract nucleus. Immunohistochemical and biochemical examination revealed a selective loss of 5HT nerves throughout the dorsomedial medulla with little damage in adjacent regions. Arterial blood pressure and heart rate, measured at daily intervals, were similar in lesioned and sham-operated normotensive rats. However, in the hypertensive rats, blood pressure was substantially elevated at 6-9 days after the lesions compared with sham operations. There were no accompanying changes in heart rate.

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Retarded development of hypertension in stroke-prone spontaneously hypertensive rats following chronic alcohol consumption.

The influence of chronic alcohol consumption on blood pressure was examined in normotensive Wistar/Kyoto rats (WKY) and in stroke-prone spontaneously hypertensive rats (SHR-SP). Ethanol, administered in drinking water from 5 weeks of age to produce moderate blood alcohol levels, substantially retarded the development of hypertension in SHR-SP and caused a mild reduction of blood pressure in WKY. Alcohol withdrawal caused an acute rise in blood pressure in both strains, followed by a reduction to the subnormal levels previously induced by alcohol treatment. This sustained antihypertensive effect of alcohol was not attributable to reductions of body weight or fluid intake.

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PubMedDate not supplied

Dietary fish oil prevents the development of renal damage in salt-loaded stroke-prone spontaneously hypertensive rats.

1. Stroke-prone spontaneously hypertensive rats (SHRSP) fed a high salt diet rapidly develop proteinuria, a marker of renal damage. We have recently shown that supplementing the diet of these rats with pure omega-3 fatty acids can inhibit the development of proteinuria. The aim of the present study was to examine the underlying renal pathology and to see whether a similar benefit could be obtained with fish oil or canola oil. 2. Diets containing sodium (2% by weight) and 5% fish oil, canola oil, olive oil or safflower oil (the latter two serving as controls) were fed to groups of eight young SHRSP and the development of hypertension and proteinuria was monitored. After 9 weeks, rats were killed and their kidneys were taken for histological examination and fatty acid analysis. Urinary protein was characterized electrophoretically. 3. Patterns of protein excretion were consistent with the appearance of pathological changes in both glomeruli and tubules. Fish oil inhibited the elevation of blood pressure, prevented the development of proteinuria and minimized histological lesions. However, in rats fed canola oil, hypertension and renal damage were equally severe as in rats fed olive or safflower oil. 4. The prevention of hypertensive renal damage by dietary fish oil may be attributable to the increased incorporation of long-chain omega-3 fatty acids in the kidney.

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