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Query: UNIPROT:P06889 (Mol)
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1. Plasma catecholamines, plasma renin activity, plasma aldosterone and haematocrit were measured in four subjects with physiologically complete cervical spinal cord transections, before, during and after head-up tilt to 45 degrees for 30 min. Plasma catecholamines were measured in five normal male volunteers in the supine position and after head-up tilt to 45 degrees for 10 min. 2. After 10 min of head-up tilt, the plasma noradrenaline rose 14% in the tetraplegic patients and 115% in the control subjects. These findings indicate a failure of sympathetic activity in response to head-up tilt in the tetraplegic patients, probably caused by interruption of pathways by which the brain normally controls sympathetic outflow. 3. In the tetraplegic patients the resting plasma renin activities were above normal, and rose more quickly and greater on head-up tilt than in published studies of normal subjects. It is likely that the renal baroreceptors are important in the control of renin release. 4. In the tetraplegic patients, there was a late rise in plasma aldosterone which was probably due to the elevation in plasma renin activity.
Clin Sci Mol Med 1975 Oct
PMID:Plasma catecholamines, plasma renin activity and plasma aldosterone in tetraplegic man, horizontal and tilted. 119 88

1. Sympathetic nervous system activity, measured by urinary noradrenaline excretion, was determined in a group of untreated hypertensive subjects (n = 35), a reference group (n = 80) and a normotensive group (n = 51), all derived from a random population sample of 50-year-old men. It was compared with casual and resting blood pressure, urinary sodium excretion, urinary cretinine concentration and glomerular filtration rate. Hypertension was defined as systolic pressure greater than 175 or diastolic greater than 115 mmHg on two separate occasions. Normotension was defined as systolic pressure less than 160 and diastolic pressure less than 95 mmHg. 2. There was no difference in the average excretion of noradrenaline during the day or night between the reference, normotensive and hypertensive groups. None of the hypertensive patients had values for urinary noradrenaline excretion during the day above the range found in normotensive subjects, indicating that hypertension with increased sympathetic nervous system activity is uncommon when hypertension in defined as above. 3. No correlation between urinary noradrenaline excretion during the day and blood pressure was found in the reference group or in the normotensive group. In the hypertensive group, there was a negative correlation between urinary noradrenaline excretion and blood pressure after rest. This finding might indicate that factors other than sympathetic nervous system activity determine the level of blood pressure in hypertensive subjects. 4. In the hypertensive group, urinary noradrenaline excretion during the day was positively correlated with both urinary sidium excretion during the day and glomerular filtration rate. Urinary noradrenaline excretion per 24 h was positively correlated with urinary sodium excretion during the same time. High resting blood pressure, low urinary sodium excretion, low glomerular filtration rate and a reversed diurnal rhythm of urinary excretion characterized hypertensive patients with low urinary noradrenaline excretion, indicating more severe hypertension in these hypertensive patients with reduced sympathetic nervous system activity.
Clin Sci Mol Med 1975 Nov
PMID:Urinary noradrenaline excretion and renal function in normal and hypertensive 50-year-old men. 119 7

1. The effect of physical exercise on blood pressure, plasma catecholamines and plasma renin activity was studied in fourteen patients with essential hypertension and in eight healthy subjects. 2. Resting plasma noradrenaline and adrenaline and plasma renin activity of the hypertensive patients did not differ from those of the control subjects. 3. In response to graded exercise producing successive heart rates of 120, 140 and 160 beats/min, significantly greater increases of blood pressure were found in the patients than in the control subjects. 4. Plasma noradrenaline increased significantly in both groups at all levels of exercise, the responses being significantly greater in the hypertensive patients. 5. The mean arterial blood pressure was significantly correlated with plasma noradrenaline concentration in the control subjects but not in the hypertensive patients. 6. In the hypertensive group plasma adrenaline increased significantly after exercise at all work loads whereas, in the control group, significant increase occurred only at the highest work load. The differences in the response of the two groups were significant at each work load. 7. Plasma renin activity increased significantly after exercise at the heart rate of 120 beats/min, both in the hypertensive patients and in the control subjects. The magnitude of the response was similar in the two groups.
Clin Sci Mol Med 1975 Nov
PMID:Plasma catecholamines and renin activity in response to exercise in patients with essential hypertension. 119 10

1. The effect of adrenaline and noradrenaline on renin secretion in the isolated perfuseed rat kidney was examined. The doses of catecholamines used were such that renal vasoconstriction and therefore increases in renal perfusion pressure were avoided. Under these conditions adrenaline and noradrenaline significantly increased renin secretion rates, compared with control experiments in which no catecholamine was infused. 2. Mean renal perfusion pressure during both adrenaline and noradrenaline infusion paralleled the control study by showing a progressive fall. 3. Administration of phenoxybenzamine did not impair the stimulation of renin secretion by adrenaline whereas this was prevented by racemic propranolol. 4. These observations suggest that catecholamines stimulate renin secretion by an intrarenal effect which is largely independent of changes in renal perfusion pressure. It is postulated that the beta-adrenoceptors mediating renin secretion are an integral component of the renin-producing cell.
Clin Sci Mol Med 1975 Dec
PMID:The stimulation of renin secretion by non-vasocontrictor infusions of adrenaline and noradrenaline in the isolated rat kidney. 120 91

1. The inactivation of noradrenaline and prostaglandin E2 was studied in the pulmonary circulation of anaesthetized dogs. 2. Under chloralose anaesthesia and ventilation with air, the inactivation of noradrenaline was 20% and that of prostaglandin E2 was 91%. These values are in agreement with results from previous work. 3. When the dogs were ventilated with halothane-air mixtures, the inactivation of prostaglandin E2 was unaffected but that of noradrenaline was significantly reduced. 4. This effect of halothane is probably due to an interaction with the transport system for noradrenaline associated with cell membranes. 5. Analogous changes in pulmonary noradrenaline inactivation could occur in patients anaesthetized with halothane.
Clin Sci Mol Med 1976 Jan
PMID:Effects of halothane on pulmonary inactivation of noradrenaline and prostaglandin E2 in anaesthetized dogs. 124 7

alpha-Adrenergic receptors are present on the plasma membrane of normal anterior pituitary cells and alpha-adrenergic agonists may play a role in the secretion of corticotropin (ACTH) and thyrotropin (TSH). However, alpha-adrenergic involvement in prolactin (PRL) secretion is uncertain. We have therefore examined this question in the PRL-secreting clonal rat pituitary tumor-derived GH4C1 cells. Norepinephrine (NE), an alpha-adrenergic agonist, had no effect on basal PRL secretion but abolished thyrotropin-releasing hormone (TRH)-induced PRL secretion in a dose-dependent manner (EC50 100 nM). NE also significantly suppressed the TRH-stimulated rise in [Ca2+]i. Phentolamine (PA), a non-selective alpha-adrenergic antagonist, reversed the inhibitory effect of NE on both the TRH-stimulated PRL secretion and [Ca2+]i rise. NE did not inhibit the rise in PRL secretion or [Ca2+]i induced by depolarizing 30 mM K+, 30% hyposmolarity or BAY K-8644, a specific L-type Ca2+ channel agonist. The inhibitory effect of NE on TRH-induced PRL and [Ca2+]i changes was also present when Ca2+ influx was prevented by removing medium Ca2+ or by blocking L-type Ca2+ channels with 2 microM nifedipine. The TRH-stimulated first-phase rise in [Ca2+]i in GH4C1 cells is believed to result primarily from release of sequestered Ca2+ from an intracellular pool through the activation of inositol 1,4,5-trisphosphate (IP3) and this [Ca2+]i spike stimulates PRL secretion. Our data thus suggest that GH4C1 cells have alpha-adrenergic receptors and that alpha-adrenergic agonists either suppress IP3 generation or block IP3 release of sequestered intracellular Ca2+.
Mol Cell Endocrinol 1992 Sep
PMID:Alpha-adrenergic inhibition of thyrotropin-releasing hormone-induced prolactin secretion in GH4C1 cells is associated with a depressed rise in intracellular Ca2+. 128 Feb 33

1. Concentrations of the neurotransmitter amines noradrenaline (NA), dopamine (DA), and 5-hydroxytryptamine (5-HT) and the acid metabolites homovanillic acid (HVA) and 5-hydroxyindoleacetic acid (5-HIAA) were determined in four regions of postmortem brains of demented patients with or without Alzheimer's disease (AD). 2. NA was deficient in the temporal cortex (BA 21) of AD, but not of non-AD, patients. 3. Caudate, in particular, had an impaired dopaminergic system in AD patients, with low HVA levels. 4. In all regions investigated [amygdala, caudate, putamen, temporal cortex (BA 21)] 5-HT was significantly depleted in AD patients, and 5-HIAA was also depleted in amygdala and caudate. 5. These results indicate that neurotransmitter systems other than cholinergic systems are also widely affected in AD and suggest that these deficits may also play an important role in determining the symptomatology of AD.
Cell Mol Neurobiol 1992 Dec
PMID:Monoamine neurotransmitters and their metabolites in brain regions in Alzheimer's disease: a postmortem study. 128 63

The aim of this study was to clarify whether or not arachidonic acid metabolic disorders are caused by a substrate inavailability and whether such disorders might contribute to circulatory disturbances in the diabetic myocardium. Norepinephrine induced a decrease in the conductivity of both coronary arterial bed and myocardial microcirculation in alloxan-diabetic dogs. It was markedly (p less than 0.05) attenuated both by indomethacin and acetylsalicylic acid pretreatments indicating an imbalance among the vasoactive prostanoids in diabetes. TXA2 release from the diabetic coronary rings was found to be elevated and could be normalized after the blockade of vascular adrenoceptors by phentolamine (p less than 0.05). PGI2 synthesis was also enhanced by adrenergic blockade in the diabetic arterial rings. After pretreatment with 14C arachidonic acid, in order to measure substrate availability, the arachidonic acid metabolic rate was less in the diabetic coronary arteries than in healty vessels (p less than 0.05). Ten mumol/l norepinephrine decreased arachidonic acid metabolism in the presence of prelabelled substrate in the diabetic animals, compared to an increase observed in metabolically healthy dogs. Therefore diabetes appears to diminish arachidonic acid metabolism and uptake independent of adrenoceptors and to induce an imbalance between vasoconstrictor and vasodilator cyclooxygenase products, resulting in elevated TXA2 release controlled by adrenergic mechanisms which may contribute to an impairment in myocardial microcirculation.
Mol Cell Biochem 1992 Feb 12
PMID:Disturbed lipid metabolism in diabetic coronary vessels. 132 Jul 34

The presence of a functional Na+/Ca2+ exchange system was explored in the ligated cat hypogastric nerve, a preparation that has been proposed as a model of giant noradrenergic nerve terminal free of effector cells. The rationale for this study was to monitor noradrenaline secretion from the ligated cat hypogastric nerve promoted by the increase in intracellular Ca2+ levels after ouabain blockade of Na+,K(+)-ATPase molecules present in the plasma membrane of the ligated cat hypogastric nerve. Such an increase in intracellular Ca2+ levels is achieved by activation, in "reverse mode," of the Na+/Ca2+ exchange system. In the present study, [3H]ouabain binding sites were identified on crude preparations of hypogastric nerve membranes. A single, high affinity (Kd around 10 nM), binding site was observed in both ligated and nonligated nerves. The number of binding sites increased with the time of ligation, reaching a peak of about 1 pmol/mg of protein 48 hr after ligation. Blockade of these binding sites by ouabain induced a dose-dependent, Ca(2+)-dependent release of noradrenaline, with an ED50 around 50 microM. The maximum release amounted to 9% of the total noradrenaline content in the cells. As would be expected for ouabain-induced noradrenaline secretion mediated by a Na+/Ca2+ exchange system working in reverse mode, the effect of ouabain was dependent upon the presence of Na+ in the incubation medium, reaching a plateau at an extracellular Na+ concentration of 100 mM. Calcium uptake after Ca2+ reintroduction in ouabain-treated nerves increased with time of ligation, suggesting the incorporation of Na+/Ca2+ exchange carrier molecules into the axolemma of hypogastric nerves. The similarity between ouabain-induced noradrenaline secretion from the ligated cat hypogastric nerve and from other adrenergic systems strongly supports the idea that the ligated cat hypogastric nerve is equipped with a functional Na+/Ca2+ exchange system that would contribute to the regulation of intracellular Ca2+ levels. Furthermore, these data, together with previously published reports, fully characterize, from a biochemical point of view, the ligated hypogastric nerve as a model of giant noradrenergic nerve terminal free of effector cells.
Mol Pharmacol 1992 Jul
PMID:Axoplasmic transport of [3H]ouabain binding sites and catecholamine secretion from an adrenergic nerve trunk. 132 54

Mouse brain cortex slices preincubated with 3H-noradrenaline were superfused with physiological salt solution containing desipramine plus a drug with alpha 2-adrenoceptor antagonist properties, and the effects of histamine receptor ligands on the electrically (0.3 Hz) evoked tritium overflow were studied. The evoked overflow (from slices superfused with phentolamine) was inhibited by histamine (pIC35 6.53), the H3 receptor agonist R-(-)-alpha-methylhistamine (7.47) and its S-(+)-enantiomer (5.82) but not influenced by the H1 receptor agonist 2-(2-thiazolyl)-ethylamine 3.2 mumol/l and the H2 receptor agonist dimaprit 10 mumol/l. The inhibitory effect of histamine was not affected by the H1 receptor antagonist dimetindene 1 mumol/l and the H2 receptor antagonist ranitidine 10 mumol/l. The concentration-response curve of histamine (determined in the presence of rauwolscine) was shifted to the right by the H3 receptor antagonists thioperamide (apparent pA2 8.67), impromidine (7.30) and burimamide (6.82) as well as by dimaprit (6.16). The pA2 values of the four drugs were compared with their affinities for H3A and H3B binding sites in rat brain membranes (West et al. 1990 Mol Pharmacol 38:610); a significant correlation was obtained for the H3A, but not for the H3B sites. The results suggest that noradrenaline release in the mouse brain cortex is inhibited by histamine via H3A receptors and that dimaprit is an H3 receptor antagonist of moderate potency.
 ...
PMID:Histamine H3A receptor-mediated inhibition of noradrenaline release in the mouse brain cortex. 135 85


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