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

Four experiments examined the role of the nucleus tractus solitarius (NTS) and subjacent nucleus reticularis ventralis (NRV) in the production of antinociception. Experiment 1 showed that microinjection of glutamate (50 nmol) into the caudal NTS resulted in inhibition of the tail-flick reflex, hypotension, and mild bradycardia, whereas microinjection of glutamate into the rostral NTS resulted only in hypotension and mild bradycardia. Microinjections of glutamate into the NRV resulted in inhibition of the tail-flick reflex, hypertension, and mild bradycardia. Experiment 2 demonstrated that the magnitude of the antinociceptive and cardiovascular responses resulting from glutamate microinjections into both the depressor and pressor regions were dose dependent. Experiment 3 showed that the antinociceptive effects resulting from microinjections of glutamate into either the depressor or pressor regions could not be antagonized by phentolamine (30 micrograms), methysergide (30 micrograms), or naloxone (30 micrograms) alone, but the combined intrathecal administration of phentolamine and methysergide (7.5, 15, or 30 micrograms of each) attenuated the antinociception resulting from microinjection of glutamate into either depressor or pressor regions in a dose-dependent fashion. Experiment 4 showed that systemic administration of hexamethonium blocked the pressor response produced by microinjection of glutamate into the NRV but did not reduce the antinociceptive effect of the microinjection. These findings are consistent with a role for the NTS and NRV in the production of antinociception.
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PMID:Characterization of antinociception produced by glutamate microinjection in the nucleus tractus solitarius and the nucleus reticularis ventralis. 290 91

Adenosine acts at many sites to modulate neuronal activity. The purpose of this study was to investigate a possible role for adenosine as a neuromodulator of brainstem cardiovascular control. Microinjections of adenosine (0-2.3 nmol) were made stereotaxically into various brainstem sites. Injection of adenosine into the nucleus tractus solitarii (NTS) produced dose-related decreases in heart rate and systolic and diastolic blood pressures. Maximal changes occurred 90 seconds after injection. Injection into the area postrema also produced decreased heart rate and systolic and diastolic blood pressures. No significant effect occurred following injection into the C1 area. Adenosine 5'-triphosphate and its analogue, beta, gamma-methylene adenosine 5'-triphosphate also produced dose-related and potent vasodepressor and bradycardia effects in the NTS. Injection of 1,3-dipropyl-8-p-sulfophenylxanthine (0.92 nmol), a potent adenosine receptor antagonist, produced no effect itself, but abolished for 45 minutes the actions of further injections of adenosine and adenosine 5'-triphosphate (but not L-glutamate) in both the NTS and area postrema. Thus, NTS and area postrema injections of adenosine decrease blood pressure and heart rate in anesthetized normotensive rats through adenosine receptors located in these areas. These findings support a role for endogenous adenosine as a central modulator in cardiovascular control.
Hypertension 1988 Feb
PMID:Purinergic receptors in the brainstem mediate hypotension and bradycardia. 327 13

The Restaurant syndromes can be caused by five major factors: food allergens, sulfites, monosodium glutamate (MSG), tartrazine, and scombroidosis (and other seafood poisoning). A history of atopy and ingestion of known food allergens such as peanuts, egg, fish, and walnuts, together with positive results of skin tests or RAST to these foods, will favor a diagnosis of food allergy. Allergic reactions to peanuts have produced fatalities in minutes through an IgE mediated reaction. An extremely rapid onset (minutes) of symptoms consisting of flushing, bronchospasm and hypotension is consistent with a sulfite reaction. Burning, pressure, and tightness or numbness in the face, neck, and upper chest following ingestion of Chinese food favors a diagnosis of adverse reaction to MSG. Also, development of late onset bronchospasm (up to 14 hours) may be related to MSG reactions. Bronchospasm and urticaria in a patient with a history of aspirin intolerance suggests tartrazine sensitivity. If everyone ingesting a fish meal develops flushing, urticaria, pruritus, gastrointestinal complaints, or bronchospasm, this implies scombroidosis, ciguatera, or other seafood poisoning. Finally, severe headache or hypertension can result from ingestion of naturally occurring amines, such as tyramine (cheese, red wine) and phenylethylamine (chocolate). A double-blind oral challenge test may be the only way of confirming the diagnosis for most of the etiological factors of the Restaurant syndromes. The treatment of choice for acute reaction is epinephrine followed by antihistamine. Proper labeling and avoidance of these ingredients in sensitive individuals are the best preventive measures.
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PMID:The restaurant syndromes. 330 66

Neonatal administration of monosodium glutamate (MSG) failed to alter blood pressure (BP) development in either SHR or WKY rats. Hypothalamic disturbance relevant to hypertension in the SHR is not contributed to by neonatal MSG treatment. All normotensive WKY animals show a transient rise in BP corresponding to the time at which BP peaks in SHR.
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PMID:Blood pressure development in SHR and WKY rats: effects of neonatal monosodium glutamate treatment and evidence for transient hypertension in WKY rats. 344 Dec 96

Vagal baroreflexes were studied by measuring the atropine-sensitive cardioinhibition produced by raising arterial pressure with phenylephrine in anesthetized rats pretreated with the beta-adrenergic receptor antagonist nadolol. Sympathetic baroreflexes were determined in halothane-anesthetized rats by measuring the inhibition of lumbar sympathetic discharge produced by elevating arterial pressure with gradual aortic constriction. Both reflexes were drastically reduced by bilateral injections of 2.2 nmol of the glutamate receptor antagonist kynurenic acid (KYN) into either the nucleus of the solitary tract (NTS) or the ventrolateral medulla between 0 and 1 mm posterior to the level of the obex. Injections of KYN elsewhere in the medulla were generally ineffective and injections of 8-OH kynurenate (an inactive analog) into the ventrolateral medulla or NTS were also without effect. KYN injections (2.2 nmol) into the intermediate portion of the NTS produced small increases in mean arterial pressure (0-15 mm Hg) and no change in heart rate while injections of similar amounts into the ventrolateral medulla at obex level were followed by large (35-116 mm Hg) increases in pressure and bradycardia. Both types of injections produced a similar degree of blockade of vagal and sympathetic baroreflexes. These results support previous evidence that baroreceptor primary afferents may release a glutamate-like transmitter in the NTS and indicate that a similar type of excitatory transmitter is involved at the level of the ventrolateral medulla in mediating or modulating both vagal and sympathetic baroreflexes. Finally the bradycardia and hypertension produced by blocking amino acid receptors in the ventrolateral medulla appear largely unrelated to the disruption of peripheral baroreceptor inputs.
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PMID:Role of excitatory amino acids in rat vagal and sympathetic baroreflexes. 356 46

Kainic acid, an analogue of L-glutamate, was microinjected into the nucleus tractus solitarii of cordotomized rats. Kainic acid (30 ng) injected bilaterally into the nucleus elicited hypertension. The pressor response to kainic acid was restricted to sites in the intermediate one-third of the nucleus tractus solitarii. Plasma vasopressin levels were markedly increased during the kainic acid-induced pressor response. Intravenous injection of atropine sulphate or mecamylamine, or intraventricular injection of captopril did not affect the pressor response. It is concluded that in cordotomized rats the pressor response to kainic acid injected into the nucleus tractus solitarii is mainly mediated via increased release of vasopressin. It seems unlikely that the central cholinergic and angiotensin mechanisms are mainly responsible for the response to kainic acid.
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PMID:Further studies on vasopressin-induced pressor responses to kainic acid injected into the nucleus tractus solitarii of the rat. 390 49

In urethane-anesthetized rats, vasodepressor neuron pools were located bilaterally in and adjacent to the A1 area of the ventrolateral medulla by injecting the neuroexcitatory amino acid, L-glutamate. Ventrolateral vasodepressor areas included the caudalateral part of the nucleus reticularis gigantocellularis, the rostrolateral part of the nucleus reticularis ventralis, and the dorsal nucleus reticularis lateralis. In the ventrolateral vasodepressor areas L-glutamate elicited a transient fall in blood pressure (BP) and heart rate (HR). The opiate agonist (D-ala2-met5)-enkephalinamide (DAME) was used to stimulate opiate receptors in vasodepressor sites, identified with L-glutamate. In these sites, bilateral injections (0.1 microliter/site) of DAME caused a dose-related (2.5-500.0 ng) increase in blood pressure and heart rate, as well as exaggeration of the response to occlusion of the carotid. The effects of DAME on blood pressure were completely abolished by alpha-adrenergic blockade (phentolamine, 2 mg/kg, i.v.) and all effects of DAME were reversed by the administration of naloxone HCl (1 mg/kg, i.v.). Naloxone reversal was accompanied by an unexpected "rebound" hypertension. Saline had no significant effects when injected, or administered intravenously, in the absence or presence of DAME. It was concluded that stimulation of opiate receptors in the ventrolateral vasodepressor areas activated sympathetic outflow. An enkephalinergic system in this area of the brain stem may serve to modulate blood pressure, heart rate and cardiovascular reflexes.
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PMID:Hypertensive response following stimulation of opiate receptors in the caudal ventrolateral medulla. 614 14

gamma-Aminobutyric acid (GABA) has been implicated in the development of hypertension and in the regulation of blood pressure. The spontaneously hypertensive rat (SHR) offers an opportunity to explore the role of central GABA and other neurotransmitters in the genesis of high blood pressure. The receptor binding of [3H]GABA, [3H]flunitrazepam, and [3H]glutamate to synaptic membranes from the cerebral cortex and cerebellum of SHR rats were measured in animals of various ages. No significant differences between the SHR and a normotensive control strain of rats were found for any of the assays. The results indicate that in this model of hypertension, neither GABA nor glutamate function are involved, at least not in the cerebral cortex or cerebellum.
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PMID:The GABA/benzodiazepine receptor complex in the nervous system of a hypertensive strain of rat. 614 79

Neurons of the lower brain stem maintain resting levels of arterial pressure (AP), mediate reflex responses from cardiopulmonary receptors, and are an important site of the hypotensive actions of alpha 2-adrenergic agonists. Details of the pathways and transmitters that mediate tonic and reflex control of AP are emerging. Afferent fibers of cardiopulmonary receptors in the ninth and tenth nerves terminate bilaterally in the nucleus of the tractus solitarius (NTS). Although some neurons contain substance P, the primary neurotransmitter appears to be the excitatory amino acid L-glutamate (L-glu). Neurons in rostral ventrolateral medulla, which most probably comprise the C1 group of epinephrine neurons, are also critical in AP control. C1 neurons project to innervate cholinergic preganglionic sympathetic neurons in the spinal cord. Stimulation of the C1 area electrically or with L-glu increases AP, while lesions or local injection of the inhibitory amino acid gamma-aminobutyric acid (GABA) lowers AP to levels comparable to spinal cord transection. Lesions of C1 neurons or their pathways abolish vasodepressor reflexes from baroreceptors and vagal afferents. In contrast, noradrenergic neurons of the caudal ventrolateral medulla, the A1 group, project rostrally to innervate, in part, vasopressin neurons of the hypothalamus. Stimulation of A1 neurons lowers AP, while lesions or GABA elevates it. We propose that C1 neurons comprise the so-called tonic vasomotor center of the brain stem and also mediate, via a projection from the NTS, the vasodepressor limb of baroreflexes. The NTS-C1 projection may be GABAergic.
Hypertension
PMID:Brain stem catecholamine mechanisms in tonic and reflex control of blood pressure. 615 1

This symposium reviewed the fundamental principles, pharmacology, and clinical pharmacology of central alpha-adrenergic blood pressure regulating mechanisms. Fundamental principles Arterial baro- and chemoreceptor signals reach the nucleus of the tractus solitarius (NTS) via vagal and glossopharyngeal afferents. The NTS communicates with sympathetic preganglionic neurons in the spinal cord via centers and tracts in the medulla, pons, and hypothalamus that include an alpha-adrenergic inhibitory network. Descending tracts emphasized in this symposium originate in the C-1 epinephrine cells of the medulla, B-1 and B-3 serotonin cells of the medulla, and A-5 norepinephrine cells of the pons. Transmitters involved are norepinephrine, epinephrine, serotonin, glutamate, and gamma-aminobutyric acid (GABA). Catecholamine enzymes share protein domains in their primary structures and may be coded by linked or single genes. New methods of purifying and locating alpha- and beta-receptors have been developed. Pharmacology Methyldopa, clonidine, and clonidine-like drugs lower blood pressure by stimulating postsynaptic alpha 2-receptors in a brain stem inhibitory network, which down-regulates these receptors. Alpha 1-receptors were found to be higher in normotensive than in hypertensive rats and were increased in the latter by methyldopa administration. Alpha 2-receptors were found to differ in various tissues, which permits the development of highly selective agonists and antagonists. Although alpha-methylnorepinephrine is probably the principal metabolite of methyldopa, alpha-methylepinephrine and alpha-methyldopamine may also contribute. The site of action usually is identified as the NTS. Possible roles for the descending tracts were suggested. Clinical pharmacology Methyldopa, clonidine, guanfacine, and related drugs lower blood pressure principally by CNS mechanisms but peripheral actions may also contribute.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension
PMID:In summary: satellite symposium on central alpha-adrenergic blood pressure regulating mechanisms. 615 4


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