Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have examined the distribution pattern and the density of various neuropeptide, neurotransmitter and enzyme containing neurons in the rat medial septum and the nucleus of the diagonal band of Broca to assess their possible involvement in the septohippocampal, septocortical and septobulbar pathways. Immunohistochemical methods were combined with the retrograde transport of a protein-gold complex injected in the hippocampus, the cingulate cortex or the olfactory bulb. Cholinergic neurons were the most numerous. Galanin-positive neurons were about two or three times less numerous than cholinergic cells. Both these cell types had a similar location though the choline acetyl transferase-like immunoreactive cells extended more caudally in the horizontal limb of the nucleus of the diagonal band of Broca. Immunoreactive cells for other neuroactive substances were few (calcitonin gene-related peptide, luteinizing hormone releasing hormone. [Met]enkephalin-arg-gly-leu) or occasional (dynorphin B, vasoactive intestinal polypeptide, somatostatin, neurotensin, cholecystokinin, neuropeptide Y and substance P). No immunoreactive cells for bombesin, alpha atrial natriuretic factor, corticotropin releasing factor, 5-hydroxytryptamine, melanocyte stimulating hormone, oxytocin, prolactin, tyrosine hydroxylase or arg-vasopressin were present. Choline acetyltransferase- and galanin-like immunoreactive cells densely participate to septal efferents. Cholinergic neurons constituted the bulk of septal efferent neurons. Galanin-positive cells were 22% of septohippocampal, 8% of septocortical, and 9% of septobulbar neurons. Galanin containing septohippocampal neurons were found in the medial septum and the nucleus of the diagonal band of Broca; galanin-positive septobulbar and septocortical cells were limited to the nucleus of the diagonal band of Broca. Occasional double-labellings were noticed with some peptides other than galanin. Luteinizing hormone-releasing hormone, calcitonin gene-related peptide and enkephalin were the most often observed; some other projecting cells stained for vasoactive intestinal polypeptide or dynorphin B. Luteinizing hormone-releasing hormone, calcitonin gene-related peptide and enkephalin were observed in septohippocampal neurons; luteinizing hormone-releasing hormone and vasoactive intestinal peptide were observed in septocortical neurons and calcitonin gene-related peptide, luteinizing hormone-releasing hormone and dynorphin B were observed in septo-bulbar cells. These results show that, in addition to acetylcholine, galanin is a major cellular neuroactive substance in septal projections to the hippocampus, the cingulate cortex and the olfactory bulb. The presence of septal projecting neurons immunoreactive for other peptides shows that a variety of distinct peptides may also participate, but in a smaller number, to septal efferent pathways.
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PMID:Cholinergic and peptidergic projections from the medial septum and the nucleus of the diagonal band of Broca to dorsal hippocampus, cingulate cortex and olfactory bulb: a combined wheatgerm agglutinin-apohorseradish peroxidase-gold immunohistochemical study. 247 18

A10 cultured smooth muscle cells from rat embryonic thoracic aorta bound 125I-labelled epidermal growth factor (125I-EGF), and responded to EGF by an increase in DNA synthesis. Scatchard analysis of binding data obtained at 4 degrees C showed curvilinearity consistent with there being two affinity classes of binding site. The amount of 125I-EGF that bound was decreased by treatment of the A10 cells at 37 degrees C with [Arg8]vasopressin or with 5-hydroxytryptamine (5-HT). Scatchard analysis of binding (at 4 degrees C after pretreatment at 37 degrees C) revealed this effect to be due to a loss of the high-affinity component of 125I-EGF binding, with no change in total receptor number. The presence of vasopressin or 5-HT raised the concentration of EGF required for the stimulation of DNA synthesis. Cultured A10 aortic smooth muscle cells therefore have receptors for EGF that mediate an increase in cell proliferation. EGF receptor function is modified by vasopressin and 5-HT, probably as a consequence of their effects on EGF receptor affinity.
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PMID:Heterologous regulation of EGF receptor function in cultured aortic smooth muscle cells. 271 68

1. Reversible contraction of canine basilar artery, produced by hypoxia, persisted after mechanical and chemical removal of the endothelium. The removal of endothelium was confirmed by scanning electron microscopy as well as by the abolition or reversal of the relaxant response to acetylcholine or arginine8-vasopressin. 2. Hydroquinone, believed to block selectively endothelium-mediated relaxation, also preferentially attenuated hypoxic contractions even in the absence of endothelium but did not reduce responses to 5-hydroxytryptamine (5-HT) or high external potassium. 3. Contractions induced by red blood cell haemolysate, which occur independently of the endothelium, were also selectively attenuated by hydroquinone. 4. Contractions caused by hypoxia were inhibited by pretreatment with adenosine or by its application after contraction had developed. 5. Hypoxic contraction in canine basilar artery may result partly from a direct effect on smooth muscle as well as through the endothelium. 6. Hydroquinone may have an additional locus of action in smooth muscle cells besides its well known effect on the endothelium.
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PMID:Role of endothelium in hypoxic contraction of canine basilar artery. 274 85

The contractile responses to various endogenous vasoactive agents were investigated in isolated human uteroplacental arteries from normotensive (NT) patients and patients with pre-eclampsia (PE) undergoing caesarian section. Tissue samples were obtained from the uterine incision and from macroscopically normal cotyledons. Vascular ring preparations of intramyometrial and stem villous arteries (length 1.0-1.3 mm, outer diameter 400-600 microns) were dissected and mounted in organ baths and isometric tension was recorded. Concentration-response relationships for vasopressin (VP), oxytocin (OX), angiotensin II (Ang II), noradrenaline (NA), 5-hydroxytryptamine (5-HT), prostaglandin F2 alpha (PGF2 alpha) and prostaglandin E2 (PGE2) were assessed. For each compound, the mean maximum contractile effect (Emax) and the drug concentration producing half-maximal response (EC50) were determined. In intramyometrial arteries from NT and PE patients, VP, Ang II, NA, 5-HT and PGF2 alpha induced contraction while OX and PGE2 produced weak or no responses. Preparations from PE patients showed higher Emax values, while no differences in EC50 were found between the two groups. In fetal stem villous arteries, Ang II, 5-HT, PGF2 alpha and PGE2 induced contractions, while VP, NA and OX produced weak responses. No differences in Emax or EC50 values were found between the fetal vessels of PE and NT patients. No qualitative differences were demonstrated in response to the agents tested between the vessels (fetal and maternal) from NT women at term and PE patients. However, the results may reflect quantitative differences, suggesting increased contractility of maternal uteroplacental arteries from women with PE.
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PMID:Effect of endogenous vasoconstrictors on maternal intramyometrial and fetal stem villous arteries in pre-eclampsia. 276 Apr 57

Depolarization of isolated [3H]inositol-labelled rat superior cervical sympathetic ganglia in a high-K+ medium stimulates an accumulation of labelled inositol phosphates. This accumulation occurs only when ganglia are incubated in a Ca2+-containing medium, suggesting that it represents a receptor-stimulated hydrolysis of inositol lipid(s) activated by an endogenously released neurotransmitter. A minor fraction of this accumulation appears to be activated by intraganglionically released acetylcholine, since it is slightly reduced by atropine. The accumulation of inositol phosphates is unaffected by blockade of appropriate catecholamine, histamine and 5-hydroxytryptamine receptors and also by aspirin and indomethacin. This response to depolarization is potentiated by incubation with proteinase inhibitors, suggesting that it might be caused by an endogenously released peptide neutrotransmitter. However, it is not prevented by a V1-vasopressin receptor antagonist, and none of the peptides tested so far fully reproduces the response: these include a stable substance P analogue, physalaemin, neurokinin alpha, bradykinin, angiotensin, pancreozymin, bombesin and luteinizing-hormone-releasing hormone. Stimulated inositol lipid breakdown in depolarized sympathetic ganglia seems likely to be activated by an as-yet-unidentified peptide neurotransmitter: this might serve as an intraganglionic mediator of postsynaptic excitation by employing the same signalling mechanism as muscarinic cholinergic and V1-vasopressin receptors.
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PMID:Accumulation of inositol phosphates in sympathetic ganglia. Effects of depolarization and of amine and peptide neurotransmitters. 285 52

In this report, we have reviewed recent information gathered by probing with a push-pull cannula (PPC) the in vivo activity of the suprachiasmatic nucleus (SCN), hypothalamus, and anterior pituitary gland of freely moving animals. In male and female rats, probing of the SCN with the PPC revealed distinct oscillatory patterns of 5-hydroxy indole-acetic acid (5-HIAA) output very much dependent on the position of the cannula. In males, it was also possible to demonstrate, for the first time, in vivo output of immunoreactive vasopressin (VP) most likely from the SCN. Interestingly, the output of VP was stimulated by local activation of probable 5-hydroxytryptamine (5-HT) terminals with 5-hydroxytryptophan (5-HTP), a precursor of 5-HT synthesis. Probing the hypothalamus of rats and rabbits revealed that the in vivo release of luteinizing hormone-releasing hormone (LHRH) (frequency and amplitude of the LHRH signal) can be altered by administration of estrogen to ovariectomized rats; in both species, progesterone stimulated the amplitude of the LHRH signal, but only when this steroid was infused in pulses--the physiological mode of circulating progesterone in the rat. Further, in male rabbits, pulses of progesterone did not stimulate LHRH release. Last, probing the anterior pituitary with the PPC revealed that a series of push-pull perfusions could be performed in the same animal under different experimental conditions for nearly 60 days of experimentation. It also resolved the apparent paradox that after castration, decreased instead of increased activity of the neural LHRH apparatus was noticed when the PPC was positioned in the hypothalamus. Moving the PPC to the anterior pituitary revealed that castration was accompanied by an increase in the amplitude and frequency of the LHRH signals arriving in the anterior pituitary of castrated male rats. This mode of operation of the LHRH pulse generator is clearly compatible with the mode of luteinizing hormone (LH) release in gonadectomized animals. Finally, based on these results, a hypothetical model of the operation of the LHRH pulse generator has been proposed.
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PMID:Release of luteinizing hormone-releasing hormone (LHRH) and neuroactive substances in unanesthetized animals as estimated with push-pull cannulae (PPC). 288 90

This report summarizes studies aimed to characterize pharmacologically, hemodynamically and biochemically DA-1 (fenoldopam) and DA-2 (quinpirole) dopamine receptor agonists in anesthetized rats. Fenoldopam (20 micrograms/kg/min i.v. over 15 min) and quinpirole (10 micrograms/kg/min i.v. over 15 min) share the common property of decreasing mean carotid artery blood pressure by lowering peripheral vascular resistance. Fenoldopam increased mesenteric and renal blood flows whereas quinpirole decreased the former blood flow, but enhanced the latter. These effects of quinpirole were antagonized selectively by S-sulpiride, but not SCH 23390; however, with fenoldopam the reverse was found. In chlorisondamine-pretreated rats with blood pressure supported by vasopressin, fenoldopam, but not quinpirole, caused hypotension. In nephrectomized rats, the blood pressure effects of fenoldopam (assessed as area under the infusion time-response curve) were more pronounced than in sham-operated controls. The hypotensive effects due to an i.v. bolus injection of fenoldopam, but not to acetylcholine, histamine, salbutamol or quinpirole, were significantly inhibited in rats pretreated with an infusion of fenoldopam. In pithed rats, quinpirole reduced the pressor responses to electrical stimulation of the spinal cord without affecting those to exogenous norepinephrine, angiotensin II or 5-hydroxytryptamine which, on the contrary, were inhibited by fenoldopam. The plasma renin activity (in intact rats) was reduced by quinpirole, but elevated by fenoldopam. The latter effect also occurred in pithed rats and was blocked by SCH 23390. Quinpirole lowered heart rate, whilst fenoldopam produced tachycardia. These effects of quinpirole and fenoldopam were significantly inhibited by S-sulpiride and SCH 23390, respectively. In chlorisondamine-pretreated rats quinpirole failed to change heart rate whereas fenoldopam still increased it. In conclusion, these results indicate that DA-1 and DA-2 dopamine receptor agonists can be easily discriminated on the basis of their cardiovascular profiles.
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PMID:Cardiovascular characterization of DA-1 and DA-2 dopamine receptor agonists in anesthetized rats. 288 15

The present experiments were carried out to examine the vasodilator mechanism(s) of carvedilol by use of pithed spontaneously hypertensive rats (SHR). Animals were pithed and the dose-pressor response curves to various agonists were obtained 0.5 or 1 hour after oral administration of either carvedilol (30 mg/kg), labetalol (60 mg/kg), prazosin (0.1 mg/kg) or hydralazine (3 mg/kg). These doses of drugs caused approximately equihypotensive responses in the conscious state. Carvedilol significantly shifted the dose-pressor response curve to the right for phenylephrine but not for B-HT 920, angiotensin II and vasopressin. Labetalol and prazosin also significantly shifted the dose-response curve to the right for phenylephrine but not for angiotensin II. The rank order of inhibitory action on the phenylephrine response was prazosin greater than labetalol greater than carvedilol. In addition, carvedilol produced a slight but significant inhibition of the pressor responses to serotonin (5-hydroxytryptamine), which was nearly identical in magnitude to that seen with hydralazine. These results suggest that the vasodilator action of carvedilol is mainly attributed to alpha 1-adrenoceptor blockade, although additional non-adrenergic mechanism(s) of action cannot be excluded.
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PMID:Analysis of the mechanism underlying the vasodilator action of carvedilol in pithed spontaneously hypertensive rats. 290 2

Male rats were treated acutely with nicotine (4 x 2 mg/kg, 30-min time intervals, total treatment time 2 h) or exposed to cigarette smoke from 4 x 1 cigarette (30-min time intervals, total treatment time 2 h). Some rats were pretreated with the D1 dopamine (DA) receptor antagonist SCH 23390 (0.1-3.0 mg/kg, i.p.), or with the D2 DA receptor antagonists remoxipride and raclopride (1 mg/kg, i.p.), or with the 5-hydroxytryptamine 2 (5-HT2) receptor antagonist ketanserin (0.3 mg/kg, i.p.) 5 min before nicotine treatment or the acute intermittent exposure to cigarette smoke. Some rats were treated with the D1 DA receptor agonist SK&F 38393 (1-10 mg/kg, i.p.) 15 min, 30 min or 2 h before decapitation. Hypothalamic and pre-optic catecholamine (CA) levels were measured by quantitative histofluorimetry in discrete DA and noradrenaline (NA) nerve terminal systems. Serum thyroid-stimulating hormone (TSH), prolactin, luteinizing hormone (LH), follicle-stimulating hormone (FSH), vasopressin, corticosterone and testosterone levels were determined by radioimmunoassay procedures. Nicotine treatment and to a minor degree also acute intermittent exposure to cigarette smoke produced a reduction in serum prolactin, LH and TSH but not in serum FSH, vasopressin and testosterone levels. Nicotine treatment also increased serum corticosterone levels. Pretreatment with the D1 DA receptor antagonist SCH 23390 (1-3 mg/kg) counteracted the lowering of serum LH, but not of prolactin and TSH levels induced by nicotine or exposure to cigarette smoke. SCH 23390 alone (1-3 mg/kg) increased serum TSH levels. Remoxipride, raclopride or ketanserin did not counteract any of the neuro-endocrine actions induced by nicotine treatment. However, ketanserin alone lowered serum prolactin levels. SK&F 38393 increased serum TSH, prolactin and LH levels. It was found that nicotine treatment and exposure to cigarette smoke with few exceptions produced a depletion of CA stores in NA and DA nerve terminals of the hypothalamus, pre-optic area and median eminence which was counteracted by SCH 23390 (1 mg/kg) but not by remoxipride, raclopride (1 mg/kg) or ketanserin (0.3 mg/kg). The results indicate that D1 but not D2 DA or 5-HT2 receptors may modulate the NA and DA release in the median eminence, the hypothalamus and the pre-optic area induced by nicotinic cholinoceptor activation. Furthermore, D1 DA receptors in the median eminence may at least in part mediate the inhibitory effects of nicotine on LH but not on TSH and prolactin secretion, although there appears to exist a D1 DA receptor in the median eminence which inhibits TSH secretion.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Involvement of D1 dopamine receptors in the nicotine-induced neuro-endocrine effects and depletion of diencephalic catecholamine stores in the male rat. 297 69

The ability of the five prostaglandins to activate phosphoinositide (PI) metabolism and to induce contraction was studied in rat aorta. All prostaglandins (PG) tested (B2, D2, E2, F1 alpha and F2 alpha) stimulated PI hydrolysis in the range of 0.01-1,000 microM (EC50 s from 0.9 to 47 microM) and elicited contractions in the range of 0.1-100 microM (EC50 s from 0.3 to 22.1 microM). The rank order potency was PGD2 greater than F2 alpha greater than F1 alpha greater than E2 greater than B2 for PI hydrolysis and PGB2 greater than F2 alpha greater than D2 greater than E2 greater than F1 alpha for contraction. The activation of PI hydrolysis by the various prostaglandins was greater than or equal to the effect of 5-hydroxytryptamine, norepinephrine, angiotensin II and [Arg8]vasopressin. The PI hydrolytic activity of PGD2, E2 and F2 alpha correlated with their ability to induce contraction. The results with PGB2 and F1 alpha showed, however, that activation of PI hydrolysis per se is not always a sufficient or necessary condition for rat aortic contraction.
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PMID:Prostaglandins activate phosphoinositide metabolism in rat aorta. 303 68


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