UMLS:C0020538 - FACTA Search

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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monocrotaline (MONO), a pyrrolizidine alkaloid, causes pulmonary arterial hypertension and right ventricular hypertrophy due to hepatic metabolism to the alkylating pyrrole dehydromonocrotaline. Taurine a sulfonic amino acid, is hepato- and cardioprotective in a variety of conditions. We have examined the effects of taurine and its amidino analog, guanidinoethane sulfonate (GES), in rats injected i.p. with MONO (65 mg/kg). Taurine and GES were given as 1% solutions in drinking water beginning 14 days before administration of MONO and continuing for 14 days therafter, when the rats were killed. The MONO group had right ventricular hypertrophy and pulmonary hyperplasia. Compared with control, no significant changes in the right ventricle/left ventricle weight ratio, or the right ventricle/body weight ratio occurred in rats also given taurine of GES. Lung weights in these two groups were higher than in the control group, but below that of the MONO-alone group. The lethality of MONO over 14 days was decreased by taurine (LD50 for MONO alone 80 mg/kg; for MONO + taurine 121 mg/kg). Rats given only MONO had lower hepatic concentrations of GSH and cysteine (Cys), and higher activities of microsomal GSH transferase activity were no different from control. Gamma-Glutamylcysteine (Glu-Cys) synthetase and gamma-glutamyl transpeptidase activities were elevated. In MONO-injected rats given GES, hepatic GSH levels were higher and Cys levels were lower than in either the MONO alone or MONO + taurine groups. Gamma-Glu-Cys synthetase activity was depressed. Microsomal GSH transferase, GSH peroxidase and gamma-glutamyl transpeptidase activities were elevated. Livers of MONO-injected animals showed higher levels of serine (reversed by both taurine and GES) and glycine (Gly; reversed by GES) and lower levels of glutamine. Compared with control rats, the following changes occurred in serum amino acids: MONO alone: increased aspartate, taurine and lysine; taurine-supplemented: increased taurine, methionine (Met) and lysine, and decreased Gly; GES-supplemented: decreased asparagine, serine, Gly, arginine, taurine, and valine. Compared with the MONO-alone group, the taurine-supplemented group had higher glutamate (Glu), Met and alanine, and the GES-supplemented group higher alanine and lower serine, Gly, arginine and valine. We conclude that taurine protects against MONO-induced lethality and right ventricular hypertrophy. GES also protects against right ventricular hypertrophy. However, these agents act by different mechanisms, taurine preventing many of the biochemical changes induced by MONO, with GES inducing additional changes.
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PMID:Effects of taurine and guanidinoethane sulfonate on toxicity of the pyrrolizidine alkaloid monocrotaline. 857 99

Jugular venous oxygen saturation (SjvO2) measures the balance between cerebral oxygen delivery and cerebral oxygen consumption. Abnormalities that increase oxygen consumption (e.g., fever or seizures) or that decrease oxygen delivery (e.g., increased ICP, hypotension, hypoxia, hypocapnia, or anemia) can decrease SjvO2. Measuring SjvO2 continuously in the ICU in 177 patients with severe head injury, jugular venous desaturation (SjvO2 < 50%) was identified at least once in 39% of the patients. Approximately half of the episodes of desaturation were due to intracranial hypertension and half were due to systemic causes. The occurrence of one or more episodes of desaturation was strongly associated with a poor outcome, suggesting that the reduction in oxygen delivery identified with the SjvO2 monitoring contributed to the neurological injury. In the operating room, jugular venous desaturation was identified in 6 of 8 patients who were monitored during emergency evacuation of a traumatic intracranial hematoma. The lowest SjvO2 observed was 28%. In all 8 cases, the SjvO2 increased, from 47 +/- 10% to 63 +/- 5% after evacuation of the hematoma. Additional data supporting the hypothesis that these secondary insults identified with the SjvO2 monitoring contribute to the patient's neurological injury come from measurement of the extracellular concentrations of lactate and excitatory amino acids in the brain using microdialysis. Lactate concentration increased from 0.9 +/- 0.3 to 2.4 +/- 0.5 mumol/L and glutamate increased from 11.5 +/- 8.5 to 55.0 +/- 10.4 mumol/L during 8 episodes of jugular venous desaturation in 7 of 22 patients monitored with microdialysis. SjvO2 identifies global reductions in cerebral oxygenation due to a variety of causes, and is useful as a monitor for secondary insults in patients with severe head injury.
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PMID:SjvO2 monitoring in head-injured patients. 859 16

We previously reported that adenosine elicited site-dependent neuronal and cardiovascular responses in two subareas of the nucleus tractus solitarius (NTS) of normotensive rats. Pressor and tachycardic responses were obtained from the rostral NTS (adenosine pressor system), and depressor and bradycardic responses were obtained from the caudal NTS (adenosine depressor system). In both areas, adenosine inhibited the firing rate of barosensitive neurons. The present study investigated whether spontaneously hypertensive rats (SHR) exhibit abnormal neuronal and cardiovascular responses mediated by the adenosine pressor and depressor systems within the NTS. Male SHR and Wistar-Kyoto rats (WKY) were anesthesized with urethane and prepared for blood pressure and heart rate recording, stereotaxic microinjection of adenosine into the NTS, and extracellular recording of single-unit neuronal activity of NTS neurons. Chemical identification of the targeted neuronal pool was made by L-glutamate (5 nmol) and confirmed by histology. SHR exhibited significantly higher mean arterial pressure and firing rate of caudal NTS neurons (45.0 +/- 4.5 versus 27.3 +/- 4.7 spikes per 2.5 seconds, P <.05) but similar heart rate and neuronal firing rate of rostral NTS neurons compared with WKY. Adenosine (0.1, 1, and 10 nmol) elicited dose-related neuronal and cardiovascular responses in both strains. However, SHR exhibited differential alterations in both adenosine systems. Compared with WKY, SHR exhibited attenuated pressor, tachycardic, and neuronal responses mediated by the adenosine pressor system and exaggerated depressor, bradycardic, and neuronal responses mediated by the adenosine depressor system. In both strains, the responses elicited by adenosine were virtually abolished by theophylline (10 mg/kg IV), suggesting that these responses were mediated by adenosine receptors in the NTS. Furthermore, the theophylline-evoked increase in blood pressure was twofold higher in SHR (15.0 +/- 1.7 versus 6.9 +/- 1.5 mm Hg, P <.05); larger but nonsignificant increases in heart rate and neuronal firing rate also were evident in SHR compared with WKY. These findings suggest differential alterations in adenosine pressor and depressor systems in the NTS of SHR, which may be implicated in the pathophysiology of this model of hypertension.
Hypertension 1996 Apr
PMID:Differential alteration of neuronal and cardiovascular responses to adenosine microinjected into the nucleus tractus solitarius of spontaneously hypertensive rats. 861 72

The microinjection of L-glutamate (1-6 nmol/rat) and N-methyl-D-aspartate (NMDA 1-10 nmol/rat), ionotropic glutamate receptor (iGluR) agonists, into the nucleus raphe obscurus caused a concentration -dependent increase of arterial blood pressure. In contrast, (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (t-ACPD, 14-42 nmol/rat), a metabotropic glutamate receptor (mGluRs) agonist, caused a concentration-dependent decrease in blood pressure. Pretreatment with D,L-2-amino-phosphono valeric acid (2-APV, 5 nmol/rat) a selective NMDA iGluR antagonist, and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,b] cyclohepten-5,10-imine hydrogen maleate (MK801, 0.9 nmol/rat), a noncompetitive NMDA iGluR antagonist, blocked both the glutamate and NMDA pressor responses, while pretreatment with (+)-alpha-methyl-4-carboxyphenylglycine (MCPG, 0.05 nmol/rat), a mGluR1 antagonist, increased the glutamate-induced pressor effects and blocked the fall in blood pressure induced by t-ACPD. 6-Cyano-7-nitroquinoxaline-2,3-dione (CNQX, 0.4 nmol/rat) a non-NMDA iGluR antagonist, did not affected the glutamate-induced hypertension. These observations indicate opposing roles for ionotropic and metabotropic receptors in the glutamate-induced blood pressure changes elicited from the nucleus raphe obscurus. Moreover, we suggest that the glutamate-induced hypertension may be due to the activation of NMDA ionotropic receptor subtypes and the metabotropic receptors may influence this activation through a reduction of excitability at level of synapses.
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PMID:Opposing effects on blood pressure following the activation of metabotropic and ionotropic glutamate receptors in raphe obscurus in the anaesthetized rat. 869 85

Electrical stimulation of dorsal raphe (DR) nuclei, in addition to enhancing serotonin (5-HT) release in the hypothalamus, elicited proportional hypertension and tachycardia in anesthetized rats. This could be mimicked by microinjection of two excitatory amino acids, kainic acid and glutamate, into the DR of rat brain. Intrahypothalamic administration of DOI (a 5-HT2 agonist), but not 8-OH DPAT (a 5-HT1 agonist) or 2-methyl-serotonin (a 5-HT3 agonist), also produced both hypertension and tachycardia in rats. The DR stimulation-induced hypertension, tachycardia, or increased hypothalamic 5-HT release were attenuated by prior destruction of the ascending serotonergic system produced by ICV injection of 5,7-dihydroxytryptamine and by prior blockade of postsynaptic serotonergic receptors produced by intrahypothalamic injection of 5-HT2 antagonists, cyproheptadine and ketanserin. The DOI-induced hypertension and tachycardia were also reduced by prior blockade of 5-HT2 receptors with cyproheptadine or ketanserin. Thus, it appears that DR stimulation activates the 5-HT release in the hypothalamus, then activates the hypothalamic 5-HT2 receptors and results in both hypertension and tachycardia in rats.
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PMID:Hypothalamic serotonin release and raised blood pressure after raphe nuclei stimulation in rats. 870 18

The average total intake of sodium was 6.11 g in a Chinese urban diet and 6.49 g in the rural sample in China. Discretionary use of salt provided 53% of the total sodium intake in the urban and 63% in the rural diet. Sodium intakes derived from processed foods, soy sauce and monosodium glutamate were 17%, 16% and 6% respectively in the urban diet, and 4%, 16%, 2% respectively in the rural diet. The mean intake of potassium was 1.95 g in the urban and 1.83 g in the rural diet. Cereals and vegetables were the major sources of dietary potassium. The intakes of total sodium, salt and soy sauce decreased as educational level increased. Similar results were found in white-collar workers and blue-collar workers or farmers. Nevertheless, an inverse association between blood pressure and education was found. The results suggest that reduction in sodium intake, especially cooking salt, and increased potassium intake are needed for nutritional control of hypertension in population-based interventions aimed at all social classes.
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PMID:Dietary sodium and potassium, socioeconomic status and blood pressure in a Chinese population. 880 Apr 80

It has been proposed that central cholinergic neurons may actively participate in blood pressure control and other cardiovascular regulations. The present study was performed to investigate the role of the glutamate receptors in the regulation of acetylcholine release in rat central nervous system in vitro. In the Mg2+-free condition, L-glutamate, an endogenous ligand for glutamate receptors, elicited [3H]acetylcholine release from striatal slices of Sprague-Dawley rats in a dose-related fashion. Glycine, an allosteric agonist for the N-methyl-D-aspartate type of glutamate receptor, significantly potentiated the increase in [3H]acetylcholine release evoked by L-glutamate. A non-competitive N-methyl-D-aspartate receptor antagonist, MK-801, blocked the L-glutamate-induced increase in [3H]acetylcholine release, although MK-801 had no effects on its own. In spontaneously hypertensive rats, the facilitatory effect of L-glutamate on [3H]acetylcholine release was significantly smaller than that in Wistar-Kyoto rats. Moreover, L-glutamate in combination with glycine increased the release of [3H]acetylcholine to a lesser extent in SHR than in WKY rats. These results show that L-glutamate increased acetylcholine release from rat striatum, which was highly dependent on the N-methyl-D-aspartate type of glutamate receptor. Furthermore, the lesser facilitation of acetylcholine release by L-glutamate in spontaneously hypertensive rats suggests that the excitatory amino acid may be, at least in part, involved in the regulation of central cholinergic nerve activity in hypertension.
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PMID:Glutamatergic regulation of [3H]acetylcholine release in striatal slices of normotensive and spontaneously hypertensive rats. 888 81

L-DOPA is proposed to be a neurotransmitter and/or neuromodulator in CNS. It is released probably from neurons, which may contain L-DOPA as an end-product, and/or from some compartment other than catecholamine-containing vesicles. The L-DOPA itself produces presynaptic and postsynaptic responses. All are stereoselective and most are antagonized by competitive antagonist. In striatum, L-DOPA is neuromodulator, mother of catecholamines, not only a precursor for dopamine but also a potentiator of children for presynaptic beta-adrenoceptors to facilitate dopamine release and postsynaptic D2 receptors, and ACh release inhibitor. All may cooperate for Parkinson's disease. Meanwhile, supersensitization of increase in L-glutamate release to nanomolar levodopa was seen in Parkinson's model rats, which may relate to dyskinesia or "on-off" during chronic therapy. In lower brainstem, L-DOPA tonically activates postsynaptic depressor sites of NTS and CVLM and pressor sites of RVLM. L-DOPA is probably a neurotransmitter of primary baroreceptor afferents terminating in NTS. GABA, the inhibitory neuromodulator for baroreflex in NTS, tonically functions to inhibit, via GABAA receptors, L-DOPA release and depressor responses to levodopa. Levodopa inversely releases GABA. L-DOPAergic monosynaptic relay from NTS to CVLM and from PHN to RVLM is suggested. Tonic L-DOPAergic baroreceptor-aortic nerve-NTS-CVLM relay seems to carry baroreflex information. Disturbance of neuronal activity to release L-DOPA in NTS, loss of the activity in CVLM, enhancement of the activity with decreased decarboxylation and increase in sensitivity to levodopa in RVLM may be involved in maintenance of hypertension in SHR. This is a story of "L-DOPAergic receptors" with extremely high affinity and low density.
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PMID:Neurobiology of L-DOPAergic systems. 889 95

The rostral ventrolateral medulla (RVLM) is part of the vasomotor centre which controls the cardiovascular system and may therefore be critical to the genesis of postoperative hypertension. This area is probably a common site of termination of different inputs involved in the baroreflex. It contains at least two classes of neurons exhibiting spontaneous activities and projecting to sympathetic preganglionic neurons located in the intermediolateral cell-column (IML) of the spinal cord. The first class of neurons corresponds to cells with slow axonal conduction velocities (< 0.8 m s-1) and which contain immunoreactive phenylethanolamine-N-methyltransferase (CI cells); the second class, characterized by faster conduction velocities (2.5-8 m s-1), is considered as glutamatergic, although the C1 cells may also release glutamate alongside catecholamine. The purpose of the present study was to investigate the involvement of the "fast-conducting' RVLM barosensitive bulbospinal (RVLM-BB) neurons in the hypertension occurring upon emergence from halothane anaesthesia. Rats were anaesthetized with halothane, paralysed, and their lungs mechanically ventilated. Avoidable pain, distress or discomfort was consistently avoided as required by the fundamental principles of ethical animal research. Hence, all pressure points and surgical wounds, as well as tracheal tube were carefully covered or infiltrated with adequate local anaesthetic. Control experiments have been performed, allowing us to assert that hypertension accompanying halothane withdrawal was not due to suffering (see Discussion). Under halothane anaethesia, fast conducting (2.7 +/- 1.0 m s-1) RVLM-BB neurons (n = 10) exhibited a continuous discharge (8.4 +/- 7.5 Hz). Five minutes after discontinuing halothane, in increase in arterial blood pressure was recorded (AP 19 +/- 6 mmHg), which was accompanied by an increase in the unitary activities (n = 8.43 +/- 23%). Afterwards, both AP and unitary activity frequencies further increased to reach a maximum value at the end of the sequence (34 +/- 9 mmHg and 161 +/- 120% respectively, n = 10). After resumption of halothane administration, both AP and unitary activities fall down to the baseline level within 5 min (n = 10). This study shows that emergence from halothane anaesthesia reversibly induces RVLM-BB units activation, suggesting that a putative glutamatergic bulbospinal pathway may be involved in the genesis of hypertension occurring upon emergence from anaesthesia. These data may therefore contribute to better understanding of postoperative hypertension and to improve its pharmacological treatment in man.
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PMID:Increased activity of bulbospinal cardiovascular neurons in the rat rostral ventrolateral medulla upon emergence from anaesthesia. 891 58

We investigated the role of galanin (Gal) in the suppression of baroreceptor reflex (BRR) response by the paraventricular nucleus of the hypothalamus (PVN) in adult male Sprague-Dawley rats that were anesthetized with pentobarbital sodium. Electrical stimulation (10-s train of 1-ms rectangular pulses at 20-40 microA and 10-20 Hz) of, and microinjection of L-glutamate (1 nmol) into, the PVN significantly inhibited BRR response to transient hypertension induced by phenylephrine (5 micrograms/kg iv). Such a PVN-induced BRR suppression was appreciably antagonized by local administration of Gal antiserum (1:20), but not heat-inactivated Gal antiserum (1:20), to the nucleus tractus solitarius (NTS) bilaterally. Microinjection of Gal (100 pmol) into the NTS bilaterally also resulted in a Gal antiserum-reversible inhibition of the BRR response. Immunohistochemical results demonstrated that the distribution of Gal-containing neurons in the parvocellular subnucleus of the PVN overlapped substantially with the hypothalamic loci on which electrical or chemical activation elicited suppression of the BRR response that was significantly blunted by microinjection of Gal antiserum into the NTS. These results suggest that the PVN may participate in central cardiovascular regulation by suppressing the BRR response via galaninergic neurotransmission at the NTS.
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PMID:Participation of galanin in baroreflex inhibition of heart rate by hypothalamic PVN in rat. 894 97

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