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

The effects of intraventricularly (third, fourth and lateral cerebral ventricles) applied GABA and picrotoxin on blood pressure and reflexogenic hypertension and nictitating membrane contractions after central sciatic nerve stimulation were studied in lightly anaesthetized cats. The interactions between both substances were also studied. It was shown that picrotoxin caused a strong elevation of blood pressure and a long lasting contraction of the nictitating membrane when infused into each part of the cerebral ventricular system. These effects of picrotoxin were antagonized by GABA. GABA inhibited the reflexogenic hypertension when given into the fourth ventricle and the reflexogenic nictitating membrane contractions given into the third and fourth ventricles. Picrotoxin antagonized the inhibitory effects of GABA on the reflexogenic nictitating membrane contractions. It is concluded that in the central regulation of some somato-vegetative reflexes the GABA-ergic transmitter system takes part.
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PMID:The effects of intraventricularly administered GABA and picrotoxin and their interactions on somato-vegetative reflexes in cats. 63 18

Stimulation of the sympathetic nerves to the brain is known to make the resistance vessels able to withstand a higher blood pressure, i.e. to prevent blood-brain barrier (BBB) dysfunction and overperfusion in acute hypertension. When hypertension occurs concomitantly with a metabolic vasodilatation e.g. during epileptic seizures and after amphetamine-administration, protein leakage in the brain is more pronounced than in hypertension per se. Unilateral stimulation of the cervical sympathetic chain during the administration of amphetamine or bicuculline--the latter a GABA-receptor blocking substance that induces epileptic activity--attenuated the leakage of Evans blue-albumin and 125IHSA into the brain. Our results thus indicate a prophylactic effect of sympathetic stimulation also when hypertension is combined with a metabolically induced vasodilatation. The sympathetic nerves may constrict both extracerebral arteries and intracerebral resistance vessels. Unexpectedly the effect on the BBB of unilateral stimulation was to a great extent bilateral under the present experimental conditions.
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PMID:Effect of sympathetic stimulation on the blood brain barrier dysfunction induced by amphetamine and by epileptic seizures. 71 82

The effects of microinjection of an excitatory amino acid (glutamate, 10 micrograms) or several inhibitory amino acids (taurine 10 micrograms, GABA 10 ug or glycine 10 ug) into the dorsal raphe region on cardiovascular function were assessed in rats under pentobarbital sodium. Intra-raphe administration of glutamate, but not saline, caused an increase in the mean arterial pressure. By contrast, intra-raphe administration of taurine, GABA or glycine, but not saline, caused a decrease in both the mean arterial pressure and the heart rate. The glutamate-induced hypertension or both the hypotension and the bradycardia induced by taurine, GABA or glycine was antagonized by pretreatment with intra-raphe injection of a serotonergic receptor antagonist (1 ug cyproheptadine). In addition, the vasopressor and bradycardia responses to an intravenous dose of epinephrine (2.5 ug/kg) were assessed in saline-treated rats and amino acid-treated rats. Intra-raphe injection of glutamate produced a significant decrease in reflex bradycardia compared to the controls. On the other hand, administration of taurine, GABA or glycine into the dorsal raphe region led to an enhancement of epinephrine-induced bradycardia. Again, the reduction or the facilitation of the epinephrine-induced bradycardia following administration of these amino acids was antagonized by pretreatment with cyproheptadine. The results suggest that the serotonergic receptor mechanisms in the dorsal raphe region play a role in the elaboration or modulation of the cardiovascular responses to amino acids (including glutamate, taurine, GABA and glycine).
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PMID:Effects of intra-raphe injection of amino acids on cardiovascular function in rats. 145 72

The influence of chronically administered propranolol on the functional state of the gamma-aminobutyric acid-ergic (GABAergic) system in spontaneously hypertensive rats was studied and compared with the effect of dihydralazine. GABA content, synthesis and turnover rate in selected brain areas were assessed. Hypotensive activity of propranolol and dihydralazine after injection of GABA antagonist pictrotoxin was examined in acute experiment. Prolonged administration of propranolol increased GABA content, synthesis and turnover rate in the hypothalamus and the pons-medulla. After chronic injections of dihydralazine there was no change in GABA indices. Antihypertensive activity of dihydralazine in picrotoxin-treated animals remained unchanged. On the contrary, picrotoxin suppressed the propranolol-induced decrease in blood pressure. Our results indicate that propranolol increases GABAergic system activity. Therefore, we conclude that down-regulation of the GABAergic system in hypertension may be compensated by the regulatory action of propranolol.
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PMID:Increased activity of the GABAergic system in selected brain areas after chronic propranolol treatment in spontaneously hypertensive rats. 151 Jun 97

Inactivation of GABA was inhibited by gamma-vinyl GABA (GVG) and the effects of the increased GABA level in the brain on blood pressure and body weight of spontaneously hypertensive rats (SHR) and normotensive rats (WKY) were investigated. When started at the age of 8 weeks or 5 weeks, treatment of SHR and WKY with GVG (150 mg/kg, s.c.) for several weeks did not influence systolic blood pressure. In 1-week old SHR, treatment with GVG (up to 150 mg/kg, s.c.) abolished the rise in blood pressure until animals were 8 weeks old. Thereafter, arterial blood pressure started to increase but it remained distinctly lower than that in untreated animals. When started at the age of 1 week, treatment with GVG for 7 weeks did not influence arterial blood pressure in WKY. GVG delayed increase in body weight in SHR and WKY, irrespective of their age. GVG greatly increased GABA levels in the hypothalamus, frontal cortex, brainstem and rest of the brain in both WKY and SHR. It is concluded that an increase in the GABA level in the brain leads to a delay in the development of hypertension in young SHR. Hence, development of genetic hypertension seems to be susceptible to activation of the GABAergic system in a very early critical phase only.
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PMID:Effects of gamma-vinyl GABA (vigabatrin) on blood pressure and body weight of hypertensive and normotensive rats. 157 22

Two women with typical stiff-man syndrome (SMS) developed increasingly frequent attacks of muscle spasms with severe paroxysmal autonomic dysfunctions such as transient hyperpyrexia, diaphoresis, tachypnea, tachycardia, pupillary dilation, and arterial hypertension. Autoantibodies to GABA-ergic neurons were identified in the serum of both patients and in the cerebrospinal fluid of one. Both died suddenly and unexpectedly. General autopsy did not reveal the cause of death. Neuropathological studies revealed perivascular gliosis in the spinal cord and brain stem of one patient and lymphocytic perivascular infiltration in the spinal cord, brain stem, and basal ganglia of the other. The occurrence of a chronic inflammatory reaction in one of the two patients supports the idea that an autoimmune disease against GABA-ergic neurons may be involved in SMS. A review of the literature indicates that functional impairment in SMS is severe and prognosis is unpredictable because of the potential for sudden and unexpected death. Both muscular abnormalities and autonomic dysfunctions may result from autoimmunity directed against GABA-ergic neurons.
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PMID:Sudden death and paroxysmal autonomic dysfunction in stiff-man syndrome. 164 13

If we consider the chemical messengers in the central nervous system, there are about ten classic transmitters--the catecholamines, biogenic amines and amino acids--as opposed to over 50 different neuropeptides. These include previously well-established circulating hormones such as angiotensin, atrial natriuretic peptide, vasopressin and oxytocin, calcitonin and calcitonin gene related peptide (CGRP), the opioid family of peptides, gastrointestinal peptides, pituitary peptides and their releasing factors, and miscellaneous peptides such as the kinins, bombesin, gallanin, and others; all occur as neuropeptides in the brain. There is evidence supporting a role in central cardiovascular control for angiotensin, opioid peptides, substance P, neuropeptide Y, vasopressin, atrial natriuretic peptide, kinins, corticotropin releasing factor, bombesin, somatostatin, and some other peptides. They have been localized in brain areas known to be important for blood pressure regulation, and specific high-affinity peptide receptors have also been discovered. Upon central administration, these peptides produce cardiovascular effects, partly by interacting with other blood pressure-controlling neuroregulators, e.g. catecholamines and GABA. Central inhibition of brain peptide synthesis or interaction with competitive antagonists at the receptor site results in marked cardiovascular effects. Altered peptide levels and activity of synthesizing enzymes, as well as supersensitivity to the pressor action of some brain peptides, have been described in experimental models of hypertension. We are using angiotensin as a model peptide to study the peptidergic control of cardiovascular function.
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PMID:Peptidergic control of cardiovascular function: the angiotensin paradigm. 219 11

This study sought to determine whether release of acetylcholine (ACh) within the C1 area of nucleus reticularis rostroventrolateralis (RVL) contributes to the tonic maintenance of arterial pressure (AP) in the rat. The activity of choline acetyltransferase (ChAT), the biosynthetic enzyme for ACh, varied 5.5-fold in micropunches of the 6 medullary regions examined. ChAT activity in the C1 area (179 +/- 35 nmol [14C]ACh formed/mg protein/60 min; n = 4) was intermediate between that of the hypoglossal nucleus (249 +/- 38; highest) and the pyramids (45 +/- 11; lowest) and equivalent to that found in the parietal cortex (147 +/- 15). Release of [3H]ACh from C1 area micropunches was increased by raising extracellular K+ concentrations (5-55 mM) and was entirely Ca2(+)-dependent. Muscarinic receptor binding density was assessed using [3H]quinuclidinyl benzylate ([3H]QNB) as ligand and a recently developed 'electronic micropunch' technique which allows measurement of quench-corrected [3H]QNB binding within corresponding cylinders of tissue obtained by the mechanical micropunch cannula. [3H]QNB binding density varied 2.6-fold: lateral reticular nucleus pars lateralis greater than C1 area greater than nucleus ambiguus = hypoglossal nucleus = pyramid = oral spinal trigeminal nucleus. In urethane-anesthetized rats, inhibition of ACh synthesis by hemicholinium-3 (HC-3, 3 nmol/50 nl), or blockade of muscarinic receptors by scopolamine (SCOP, 3 nmol/50 nl), reduced resting mean AP by 18-24 mm Hg following bilateral microinjection into the C1 area. These concentrations of HC-3 and SCOP were sufficient to attenuate by 70-80% the increase in local cholinergic neurotransmission elicited by the cholinesterase inhibitor physostigmine given systemically. High concentrations of SCOP (30-150 nmol/50 nl) lowered AP by 46-60 mm Hg. Similarly, bilateral microinjections of GABA (10 nmol/50 nl) into the C1 area markedly reduced mean AP by 51 +/- 6 mm Hg to levels normally found after transection of the spinal cord. Thus, a substantial portion of tonic sympathetic activity may be driven by activation of muscarinic receptors in the C1 area. In the spontaneously hypertensive rat (SHR), a genetic model of hypertension, neither spontaneous nor K(+)-evoked release of [3H]ACh from the C1 area differed from that of normotensive Wistar-Kyoto rats (WKY).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Synthesis, release and receptor binding of acetylcholine in the C1 area of the rostral ventrolateral medulla: contributions in regulating arterial pressure. 233 21

The GABA receptor agonists GABA (400 micrograms icv) and muscimol (1 microgram icv) induced hypotension in urethane-anesthetized rats, while the GABA receptor antagonist bicuculline (2 micrograms icv) elicited hypertension. An endogenous GABA receptor binding inhibitor (1 mg), prepared from bovine cerebellum, showed bicuculline-like hypertensive action in a dose-dependent manner. It was antagonized by icv muscimol, but not by the alpha 2-adrenoceptor agonist clonidine. These in vivo results agree quite well with our previous in vitro receptor binding assay experiments.
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PMID:[Effects of an endogenous GABA receptor binding inhibitor on rat blood pressure]. 255 70

The relevance of GABA-ergic system in hypertensive state has been studied. GABA content, GAD activity and GABA-A receptor binding in various brain areas in age-matched spontaneously hypertensive (SHR) and normotensive Wistar-Kyoto rats (WKY) was compared. Out of 9 brain areas studied the GABA content was significantly lower in the substantia nigra, hypothalamus, hypothalamus posterior and hippocampus of SHR rats. GAD activity was lowered in the hypothalamus and hippocampus of young SHR and adult SHR rats (4, 8, 14 weeks old). Scatchard analysis of the binding isotherms indicated a lower Bmax of the binding sites in the hypothalamus and hippocampus of 8 and 14 weeks old SHR rats. These results suggest that activity of GABA-ergic system differs substantially in SHR and WKY rats brain. Furthermore, these differences appear already in young prehypertensive SHR rats as well as in the early stages of hypertension.
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PMID:Down-regulation of the GABA-ergic system in selected brain areas of spontaneously hypertensive rats (SHR). 256 65


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