UMLS:C0020538 - FACTA Search

Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Galanin, a 29-amino acid peptide, is widely distributed in both the central and peripheral nervous systems and is colocalized with catecholamines, although its physiological significance remains to be elucidated. In the present study we investigated the regulatory mechanisms of galanin on norepinephrine release in rat medulla oblongata. In slices of medulla oblongata of Sprague-Dawley rats, galanin inhibited the stimulation-evoked [3H]norepinephrine release in a concentration-dependent manner (fractional release ratio during electrical stimulation: control 0.937 +/- 0.043, mean +/- SEM, n = 6; galanin 1 x 10(-7) M 0.501 +/- 0.037, n = 6, p less than 0.05; and galanin 1 x 10(-6) M 0.299 +/- 0.018 n = 6, p less than 0.05). Galanin potentiated inhibition of [3H]norepinephrine release by the alpha 2-agonists (UK 14,304 and clonidine). The blockade of alpha 2-adrenergic receptors by RX 781094 diminished the inhibition of norepinephrine release by galanin. Pretreatment of pertussis toxin, which interferes with the coupling of inhibitory guanosine triphosphate-binding proteins to adenylate cyclase, significantly attenuated the suppressive effects of galanin on norepinephrine release. In slices of medulla oblongata obtained from spontaneously hypertensive rats (SHR), the inhibitory effect of galanin on norepinephrine release was significantly less than in those from age-matched Wistar-Kyoto rats. These results show that galanin might inhibit the stimulation-evoked norepinephrine release in rat medulla oblongata, at least partially mediated by alpha 2-adrenergic receptors and the pertussis toxin-sensitive guanosine triphosphate-binding proteins. Moreover, less suppression of norepinephrine release by galanin in SHR suggests that galanin might be involved in the regulation of central sympathetic nervous activity in hypertension.
Hypertension 1992 Sep
PMID:Modulation of norepinephrine release by galanin in rat medulla oblongata. 138 36

Effect of angiotensin converting enzyme inhibitor (ACEI) and calcium channel blockers (CaB) on renal blood flow (RBF), glomerular filtration rate (GFR), and autoregulation (AR) of RBF were studied on the uninephrectomized spontaneously hypertensive rat (SHR) under the conditions of high (H) and low (L) salt loading. SHR was given with 0.9% or 0.09% NaCl solution as drinking water (GH, GL). Each group was divided into three groups for treatment with enalapril (Enp) and nitredipine (Nit); i.e. Enp group (GHE, GLE), Nit group (GHN, GLN) and control group (GHC, GLC). After 6 weeks, inulin clearance (Cin) was determined and RBF was measured by means of an electromagnetic flow meter. The renal arterial pressure was lowered by clamping and changes in RBF and AR were examined. Cin showed higher values of 1.85 and 1.69 ml/min in GHN and GLN, as compared to be 1.33 and 1.28 ml/min in GHC and GLC (p less than 0.01). Filtration fraction (FF) showed lower values of 0.18 and 0.20 ml/min in GHE and GLE (p less than 0.01), whereas 0.29 and 0.30 in GHC and GLC respectively. RBF was markedly lower at 7.4 ml/min in GLC as compared to 9.9 ml/min in GHC (p less than 0.01). In GH, GHE showed a higher value of 11.6 ml/min, as compared to GHC (p less than 0.01). In GL, comparing with GLC the value was much higher of 12.1 ml/min in GLE (p less than 0.01). AR of RBF diminished in GLC at higher blood pressure as compared to GHC (p less than 0.01). It was maintained at lower blood pressure in GLE (p less than 0.01), but there were no significant differences between four groups; i.e. GLN, GHC, GHE and GHN. In summary, low salt loading reduced RBF and suppressed AR. Enp elevated RBF, lowered FF and caused AR to be maintained even at lower blood pressure. Nit elevated RBF and GFR without changing FF, and did not suppress AR. These results indicate that, in hypertension complicated with moderate dysfunction, both ACEI and CAB are expected to exhibit the beneficial effects on maintenance of renal circulation, despite though the different mechanism.
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PMID:[Effect of angiotensin converting enzyme inhibitor and calcium channel blocker on renal function of spontaneously hypertensive rat]. 180 67

Noradrenergic neurons in the locus ceruleus contain neuropeptide Y and galanin, which project to the hypothalamic region. We have investigated the regulatory mechanisms of these peptides on norepinephrine release in rat hypothalamic slices in vitro. Neuropeptide Y and galanin significantly inhibited the stimulation-evoked [3H]norepinephrine release in a dose-dependent manner (1 Hz: S2/S1 ratio (mean +/- SEM), control 0.947 +/- 0.040, n = 11, neuropeptide Y 1 x 10(-8) M 0.509 +/- 0.013, n = 8, p less than 0.01, neuropeptide Y 1 x 10(-7) M 0.283 +/- 0.021, n = 8, p less than 0.01; galanin 1 x 10(-7) M 0.448 +/- 0.026, n = 8, p less than 0.01, galanin 1 x 10(-6) M 0.261 +/- 0.023, n = 8, p less than 0.01). The inhibition of norepinephrine release by the alpha-2 agonist UK 14,304 was potentiated by neuropeptide Y and galanin. The blockade of the alpha 2-adrenergic receptors by RX 781094 diminished the inhibitory effects of neuropeptide Y and galanin on norepinephrine release. Pretreatment of hypothalamic slices with islet activating protein (a toxin that interferes with the coupling of inhibitory receptors to adenylate cyclase) attenuated the suppression of norepinephrine release by UK 14,304, neuropeptide Y, and galanin. These results support the idea that neuropeptide Y and galanin are involved in the regulation of central adrenergic transmission partially mediated by alpha 2-adrenergic receptors and islet-activating protein-sensitive guanosine triphosphate-binding proteins in rat hypothalamus.
Hypertension 1989 Jul
PMID:Neuropeptide Y and galanin in norepinephrine release in hypothalamic slices. 247 59

The occurrence and distribution of peptide-containing nerve fibers to the cerebral circulation are described. Immunocytochemical studies have revealed that cerebral blood vessels are invested with nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), peptide histidine isoleucine (PHI), substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP). In addition, there are studies reporting the occurrence of putative neurotransmitters such as cholecystokinin, dynorphin B, galanin, gastrin releasing peptide, vasopressin, neurotensin, and somatostatin. The nerves occur as a longitudinally oriented network around large cerebral arteries. There is often a richer supply of nerve fibers around arteries than veins. The origin of these nerve fibers has been studied by retrograde tracing and denervation experiments. These techniques, in combination with immunocytochemistry, have revealed a rather extensive innervation pattern. Several ganglia, such as the superior cervical ganglion, the sphenopalatine ganglion, the otic ganglion, and small local ganglia at the base of the skull, contribute to the innervation. Sensory fibers seem to derive from the trigeminal ganglion, the jugular-nodose ganglionic complex, and from dorsal root ganglia at level C2. The noradrenergic and most of the NPY fibers derive from the superior cervical ganglion. A minor population of the NPY-containing fibers contains VIP instead of NA and emanates from the sphenopalatine ganglion. The cholinergic and the VIP-containing fibers derive from the sphenopalatine ganglion, the otic ganglion, and from small local ganglia at the base of the skull. Most of the SP-, NKA-, and CGRP-containing fibers derive from the trigeminal ganglion. Minor contributions may emanate from the jugular-nodose ganglionic complex and from the spinal dorsal root ganglia. NPY is a potent vasoconstrictor in vitro and in situ. VIP, PHI, SP, NKA, and CGRP act via different mechanisms to induce cerebrovascular dilatation. The sympathetic, the parasympathetic, and the sensory systems appear to be involved in modulating cerebrovascular tone in hypertension and in conditions of threatening vasoconstriction, e.g., subarachnoid hemorrhage and migraine.
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PMID:Neuropeptides in the cerebral circulation. 270 77

A lot of over 60 atherosclerotics with clinical manifestations of senile depressive illness was studied comparatively with a lot of subjects of the same age with essential arterial hypertension (EAH). As concerns the behaviour of the catecholamine content in CSF and blood, the total catecholamines are approxiately equal in the two lots, but with a clear difference of the catecholamine fractions. The CSF catecholamines behaviour in old atherosclerotics is characterized by the presence of increased values of noradrenaline (NA) and of adrenaline (A), with increased statistical significance, but without modifications of the adrenaline percentage (A %) from the total catecholamines, comparatively to the values found in normal subjects. The serotonin (5-HT) content of the CSF in men with atherosclerotic senile depressive illness was lower even than in subjects with coronary atherosclerosis. In atherosclerosis protides modifications precede the histologic changes. In CSF, GLU, ALA, TYR increase in old subjects. In blood, GLU, ALA, TYR, HIS, LEU, SER increase in the same subjects. ARG decreases with age. THR is higher in men than in women. In the urine of all the men as well as of all the women of more than 60 years, GLN and ALA have increased values. LYS increases with age. GLN and ARG are higher in men than in women.
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PMID:Pattern of the cerebrospinal fluid (CSF) and blood biogenic amines and of the CSF, blood and urine amino acids as pathogenetic ground of the senile depressive illness. 677 91

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

It has been demonstrated previously that central administration of the N-terminal galanin fragment (1-15) elicits hypertension and tachycardia and antagonizes the hypotensive effect of the parent molecule galanin-(1-29). In order to further clarify the role of galanin in central cardiovascular control, the possible modulation of the baroreceptor reflex by both galanin molecules has been studied. Different groups of rats were injected in the lateral ventricle with subthreshold doses of galanin-(1-15) (0.1 nmol/rat, or 0.3 nmol/rat), with subthreshold doses of galanin-(1-29) (0.1 nmol/rat, and 0.3 nmol/rat) or with an effective dose of galanin-(1-29) (3.0 nmol/rat). The baroreceptor reflex was elicited by intravenous injections of different doses of L-phenylephrine before and after the intraventricular administration of galanin peptides. The changes of the bradycardic responses after galanin peptide injections as well as the modifications of the baroreceptor reflex sensitivity were evaluated. Intraventricular injections of galanin-(1-15) significantly inhibited the reflex bradycardia elicited by intravenous L-phenylephrine and thus decreased the baroreceptor sensitivity. However, neither subthreshold doses of galanin-(1-29) nor its effective dose were able to modulate these cardiovascular responses. From these data it may be suggested that the galanin fragment (1-15) plays a more important role in central cardiovascular regulation than galanin-(1-29), possibly acting on a specific receptor subtype which exclusively recognizes N-terminal fragments of galanin, and exists on cardiovascular areas of the central nervous system.
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PMID:Centrally infused galanin-(1-15) but not galanin-(1-29) reduces the baroreceptor reflex sensitivity in the rat. 900 1

Galanin is a 29-amino acid peptide and widely distributed in the brain, although its significance in the control of neural activities is undefined. In the present study, we describe the effects of galanin on the electrically evoked release of dopamine in the rat central nervous system. In addition, to elucidate a possible role of galanin in the regulation of dopaminergic transmission in hypertension, we examined whether the effect of galanin on dopamine release might be altered in the central nervous system of spontaneously hypertensive rats (SHR). Galanin (1 x 10(-8) to 1 x 10(-7) mol/L) inhibited the stimulation (1 Hz)-evoked [3H]dopamine release by a comparable amount in striatal slices of Sprague-Dawley rats, although the basal release of dopamine was not affected by the peptide. In the striatum of SHR, the electrical stimulation (1 Hz)-evoked [3H]dopamine release was significantly smaller than in the striatum of Wistar-Kyoto (WKY) rats. However, the inhibitory effect of galanin on the stimulation-evoked [3H]dopamine release was significantly more pronounced in SHR than in WKY rats. These results show that galanin significantly reduced the release of dopamine in rat striatum. Furthermore, the greater inhibitory effect of galanin on dopamine release in SHR suggests that galanin might actively participate in the regulation of dopaminergic nerve activity in hypertension.
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PMID:Effects of galanin on dopamine release in the central nervous system of normotensive and spontaneously hypertensive rats. 988 Jan 30

Calcitonin gene-related peptide (alpha CGRP) and galanin (GAL) are peptides known to participate in central mechanisms of blood pressure control. Nonetheless, variations in the synthesis of the peptides in response to a hypertensive challenge are not well described, specially using a model, which allows acute and chronic analyses. In this study, we have employed in situ hybridization to analyse changes in mRNA expression of alpha CGRP and GAL in the nucleus tractus solitarii (NTS), hypothalamic paraventricular nucleus (PVN) as well as petrosal and nodose ganglia after aortic coarctation-induced hypertension in rats. Acute (2h) and chronic (3 and 7 days) analyses were performed in order to evaluate the involvement of both peptides in different periods of hypertension. The analysis of relative mRNA levels showed significant differences between sham-operated and aortic coarcted hypertensive rats. alpha CGRP mRNA expression was decreased 2h (40%) and 3 days (42%) in nodose and petrosal ganglia, respectively, after coarctation. No changes in CGRP mRNA signal were seen in the NTS and PVN in the analysed periods. GAL mRNA expression was decreased in the NTS (19%) and PVN (55%), 3 and 7 days, respectively, after coarctation-induced hypertension. No changes in GAL mRNA expression were observed in petrosal and nodose ganglia following aortic coarctation. Data suggest that alpha CGRP and GAL may participate in the mechanisms involved in the establishment/maintenance of hypertension induced by aortic coarctation. Acute changes might be involved with the adaptation to the hypertensive state, while changes at the chronic phase might be related to counteraction of hypertension.
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PMID:Decreases in the expression of CGRP and galanin mRNA in central and peripheral neurons related to the control of blood pressure following experimental hypertension in rats. 1527 58

The aim of the present study is to provide a review of the expression and action of trophic factors in the carotid body. In glomic type I cells, the following factors have been identified: brain-derived neurotrophic factor, glial cell line-derived neurotrophic factor, artemin, ciliary neurotrophic factor, insulin-like growth factors-I and -II, basic fibroblast growth factor, epidermal growth factor, transforming growth factor-alpha and -beta1, interleukin-1beta and -6, tumour necrosis factor-alpha, vascular endothelial growth factor, and endothelin-1 (ET-1). Growth factor receptors in the above cells include p75LNGFR, TrkA, TrkB, RET, GDNF family receptors alpha1-3, gp130, IL-6Ralpha, EGFR, FGFR1, IL1-RI, TNF-RI, VEGFR-1 and -2, ETA and ETB receptors, and PDGFR-alpha. Differential local expression of growth factors and corresponding receptors plays a role in pre- and postnatal development of the carotid body. Their local actions contribute toward producing the morphologic and molecular changes associated with chronic hypoxia and/or hypertension, such as cellular hyperplasia, extracellular matrix expansion, changes in channel densities, and neurotransmitter patterns. Neurotrophic factor production is also considered to play a key role in the therapeutic effects of intracerebral carotid body grafts in Parkinson's disease. Future research should also focus on trophic actions on carotid body type I cells by peptide neuromodulators, which are known to be present in the carotid body and to show trophic effects on other cell populations, that is, angiotensin II, adrenomedullin, bombesin, calcitonin, calcitonin gene-related peptide, cholecystokinin, erythropoietin, galanin, opioids, pituitary adenylate cyclase-activating polypeptide, atrial natriuretic peptide, somatostatin, tachykinins, neuropeptide Y, neurotensin, and vasoactive intestinal peptide.
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PMID:Trophic factors in the carotid body. 1877 56

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