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)

A comparison was made of the responses of helical strips of rat ventral tail artery from rats killed by cervical dislocation and rats subjected to poly-drug anesthesia. Anesthetized rats were premedicated with meperidine and atropine. Anesthesia was induced with thiopental and maintained with N2O. The animals were paralyzed with pancuronium and ventilated for 1 h. A mixture of fentanyl and droperidol was administered during anesthesia. Responses of arterial strips from these rats to norepinephrine, 5-hydroxytryptamine, vasopressin, and transmural electrical stimulation were identical with those of similar strips from control rats. Poly-drug anesthesia does not alter responses of isolated strips subsequently studied in vitro.
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PMID:Comparison of responses of helical strips of artery from anesthetized and untreated rats. 712 16

The extramural artery of the human gall bladder (cystic artery), a small artery (outside diameter 1.3 +/- 0.03 mm) with a thick muscular wall and little elastin within the tunica media, has catecholamine fluorescence localized to the adventitia-medial border. Isolated helical strips of the artery are responsive to norepinephrine (NE), 5-hydroxytryptamine (5HT) and vasopressin (VP) at low concentrations, but at the maximal frequency of transmural electrical stimulation used (16 Hz), the response is only 10--20% of the NE maximum response. Phentolamine (2.7 X 10(-6) M) antagonized responses to NE, 5HT and, to a lesser degree, electrical stimulation and these actions are similar to those reported in other mammalian tissue. In vitro use of reserpine (1.6 X 10(-5) M) and guanethidine (4 X 10(-5) M) also produced effects which were predictable from effects observed in other mammalian tissues; except reserpine diminished responsiveness to NE and 5HT and guanethidine enhanced responses to the early administered electrical stimulation.
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PMID:Isolated human cystic artery: responses to common agonist and antagonist drugs. 720 97

In conscious or pentobarbital-anesthetized hypertensive or normotensive rats, N,N-di-n-propyl-dopamine (DPDA) produced sustained decreases in mean systemic arterial blood pressure. In anesthetized normotensive animals, these responses were not significantly changed by vagotomy, desipramine, indomethacin, methylatropine, promethazine or propranolol, were markedly reduced by phenoxybenzamine or phentolamine, were entirely blocked by domperidone, haloperidol or sulpiride and were reverted to an alpha adrenoceptor-mediated pressor response after removal of central sympathetic tone. In phenoxybenzamine-pretreated pithed rats in which the blood pressure was elevated to prepithing levels with vasopressin, DPDA, in contrast to dopamine, produced no hypotensive effect. In the pithed rat, DPDA reduced the pressor responses elicited by electrical stimulation of the spinal cord and this effect was inhibited by haloperidol or sulpiride. DPDA slightly enhanced the pressor effects of norepinephrine but modified neither the blood pressure increases produced by epinephrine, phenylephrine, 5-hydroxytryptamine or angiotension II nor the vasodepressor effects of acetylcholine, histamine or salbutamol. Intracerebroventricular administration of DPDA produced blood pressure decreases which were slightly smaller in magnitude but longer in duration than those elicited by i.v. DPDA. However, DPDA leaked from the cerebroventricular space into the peripheral circulation. These results indicate that in the rat DPDA lowers blood pressure via activation of peripheral dopamine receptors possibly located presynaptically on vascular sympathetic neurons. The stimulation of these receptors induces a decrease in norepinephrine release which in turn is followed by a passive relaxation of the vascular beds under active sympathetic constriction.
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PMID:Blood pressure lowering effects of N,N-di-n-propyl-dopamine in rats: evidence for stimulation of peripheral dopamine receptors leading to inhibition of sympathetic vascular tone. 725 51

1In vitro studies were undertaken on rat aortic strips and portal vein segments to determine whether or not the amine-type anaesthetic, ketamine, can exert direct actions on vascular smooth muscle.2 Ketamine was found to inhibit development of spontaneous mechanical activity and lower basal tension. This action took place with ketamine concentrations found in anaesthetic plasma concentrations, i.e., 1 x 10(-5) to 2 x 10(-4) M.3 Ketamine (10(-5) to 10(-3) M) dose-dependently attenuated contractions induced by adrenaline, noradrenaline, angiotensin II, vasopressin and KCl. These inhibitory actions were observed with ketamine added either before or after the induced contractions.4 Ca(2+)-induced contractions of K(+)-depolarized aortae and portal veins were also attenuated, dose-dependently, by ketamine.5 In contrast to the above inhibitory actions, ketamine (2 x 10(-6) to 1 x 10(-4) M) was found to potentiate specifically 5-hydroxytryptamine(5-HT)-induced contractions of both aortic and venous smooth muscle. However, this was only observed if ketamine was added after 5-HT had initiated a contractile response.6 All of the inhibitory, as well as 5-HT-potentiating, effects were completely, and almost immediately, reversed upon washing out the anaesthetic from the organ baths.7 A variety of pharmacological antagonists failed to mimic or affect the inhibitory effects induced by ketamine.8 These data suggest that rat plasma concentrations of ketamine commonly associated with induction of surgical anaesthesia can induce, directly, relaxation and contractile potentiation of vascular muscle.9 These diverse findings may aid in explaining the well-known biphasic pressor actions of ketamine.
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PMID:Effects of ketamine on vascular smooth muscle function. 742 35

The stainless steel cannula method was applied to isolated and perfused canine basilar arteries to examine the role of endothelium in the responses to intraluminal vasoactive substances. After intraluminal treatment with saponin to remove the endothelium, the monophasic constrictions to potassium chloride and prostaglandin F2 alpha were potentiated, while those to phenylephrine (alpha 1-adrenoceptor agonist) and 5-hydroxytryptamine were not changed. Xylazine (alpha 2-adrenoceptor agonist) and acetylcholine induced a constriction preceded by a small dilation in controls. The response to xylazine was not modified, while the constriction to acetylcholine was augmented after endothelium removal. Bradykinin, substance P and vasopressin caused a dilation in lower doses, and a dilation followed by a secondary constriction in higher doses in controls. The dilations to these peptides were reduced and the constrictions were enhanced after endothelial removal. Adenosine triphosphate produced a biphasic response, i.e., a dilation followed by a constriction, which was occasionally preceded by a small constriction in higher doses, and only the dilation in lower doses was attenuated. The monophasic dilation to adenosine was potentiated, while the papaverine-induced dilation was not influenced by endothelial removal. After extraluminal treatment with oxyhemoglobin, the dilations to calcium ionophore A23187 and thimerosal were attenuated, while the constriction to acetylcholine was enhanced. The dilations to substance P and vasopressin were depressed, and the constrictions were potentiated. The monophasic dilation to sodium nitroprusside was augmented, while that to papaverine was not changed. These results suggest that the endothelium may play important roles not only in producing endothelium-derived relaxing factors but also in modulating the calcium influx into the smooth muscle cells. The mechanisms of altered responsiveness might be implicated in cerebral vasospasm following subarachnoid hemorrhage.
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PMID:Effects of endothelium removal by saponin and of oxyhemoglobin on canine cerebrovascular responses. 783 71

The effects of vasoconstrictors on membrane potential of endothelium of intact rat aorta were investigated using the patch-clamp technique. Norepinephrine, endothelin (ET)-1, 5-hydroxytryptamine (5-HT), vasopressin, and angiotensin II evoked depolarization and oscillations in membrane potential. The alpha 1-adrenoreceptor agonist phenylephrine (PE), but not the alpha 2-agonist clonidine or the beta-agonist isoproterenol, evoked oscillations. The antagonist of 5-HT2-receptors, ketanserin, inhibited 5-HT-evoked oscillations. ET-3, unlike ET-1, did not evoke oscillations. The antagonists of voltage-operated Ca2+ channels, nifedipine and verapamil, inhibited vasoconstrictor-evoked oscillations, and the Ca2+ channel agonist BAY K 8644 enhanced oscillations. Acetylcholine and sodium nitroprusside inhibited PE-evoked oscillations. The inhibitors of NO synthase, N omega-nitro-L-arginine and NG-methyl-L-arginine, as well as methylene blue, enhanced oscillations. The intima of rat aorta with endothelium was removed from underlying smooth muscle. In this preparation, acetylcholine evoked a response similar to that in the intact vessel, but PE and ET-1 were without effect. These data suggest that vasoconstrictors acting on receptors on aortic smooth muscle evoke a response that is transferred to the endothelium and evokes depolarization and oscillations in endothelial membrane potential.
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PMID:Smooth muscle cells affect endothelial membrane potential in rat aorta. 806 36

Arginine8-vasopressin (AVP) has been shown repeatedly to affect learning and memory and to maintain tolerance to ethanol if the brain serotonin and catecholamine systems are intact. In the present study, 5,7-dihydroxytryptamine (5,7-DHT) was injected intracerebroventricularly to disrupt serotonergic projections from the raphe to the forebrain. This resulted in a marked decrease in 5-hydroxytryptamine (5-HT) immunoreactivity in the terminal areas of the septum and the hippocampus, but not in the serotonin-containing neuronal cell bodies in the raphe nuclei. In control rats, tolerance to the motor-impairing effects of ethanol lasted for only 5 days after the cessation of ethanol treatment but could be maintained indefinitely for as long as AVP was given. In the 5,7-dihydroxytryptamine-lesioned rats, AVP was unable to maintain the tolerance. Continuous intracerebroventricular infusion of 5-HT restored the ability of AVP to maintain ethanol tolerance in the lesioned rats. A selective 5-HT2 agonist (alpha-methylserotonin) was equally effective, and a 5-HT3 receptor agonist (2-methylserotonin) was slightly less effective, but the 5-HT1A agonist dipropylaminotetralin (8-hydroxy-dipropylaminotetralin) was totally ineffective in this respect. The results indicate selective involvement of brain 5-HT2 and possibly 5-HT3 receptors in mediating AVP maintenance of tolerance to ethanol but do not pinpoint their specific loci or roles.
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PMID:Selective involvement of central 5-HT2 receptors in the maintenance of tolerance to ethanol by arginine8-vasopressin. 807 72

Experiments were performed on normotensive rats exposed to vitamin D deficient and control diets from the 22nd to the 180th day of age. In 60-120- and 180-day-old rats. The following parameters were evaluated: a) The vasomotor responses elicited by receptor agonists in the absence and in the presence of the respective antagonists [L-norepinephrine (NE) before and 5 min after prazosin; L-isoprenaline (I) before and 5 min after DL-propranolol; L-dopamine (DA) before and 5 min after L-sulpiride or SCH 23390 or chlorpromazine; acetylcholine (Ach) before and 5 min after atropine; histamine (H) before and after chlorpheniramine; 5-hydroxytryptamine (5-HT) before and 5 min after methysergide or ketanserin]; by carotid-sinus baroreceptor stimulation (CO) before and 5 min after hexamethonium, and by electrical stimulation of the vagus peripheral head (V) before and after atropine; b) Reflex tachycardia elicited by bilateral carotid occlusion (CO) (for 40 sec) and by sodium nitroprusside; c) Catecholamine (norepinephrine, epinephrine) and arginine-vasopressin plasma levels; d) Cholesterol, triglyceride and electrolyte (Na+, K+, Cl-, Ca2+) serum levels. Our results showed that vitamin D deficient diets induced a decrease in pressor responses to NE and CO, and an increase in hypotensive responses to I, DA, Ach, H, 5-HT and V. Changes of arterial blood pressure, heart rate, catecholamine and arginine-vasopressin plasma levels were not observed. Cholesterol, triglyceride and electrolyte (Na+, K+, Cl-) serum levels were not modified, while Ca2+ serum levels decreased. In conclusion, our data suggest that vitamin D depletion can induce changes of pressor and depressor vasomotor responses and suppose a direct role for vitamin D in regulating vasomotor reactivity.
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PMID:Effects of dietary vitamin D deficiency on the cardiovascular system. 820 26

Chronic ethanol administration causes hypertension and alterations of vascular reactivity in rats. In several models of hypertension, alterations of vascular reactivity are believed to be secondary to the sustained increase in blood pressure. The present study investigated the effects of serotonin (5-hydroxytryptamine [5-HT]), vasopressin and acetylcholine (ACh) in the isolated perfused mesenteric arteries from Wistar rats submitted to an 8-week course of chronic ethanol intake (8 g/kg.day). No significant differences were observed in the dose-response curves with regard to: pressor effect of 0.04-10.0 nmole 5-HT; relaxant effect of 0.05-50.0 nmole ACh; or the pressor effects of two 1.5-nmole doses of vasopressin between control rats and ethanol-fed rats. These results suggest that modifications in arterial reactivity to endogenous vasoactive substances (observed in other studies involving more prolonged ethanol treatment in rats) may be, in part, secondary to the increase in blood pressure.
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PMID:Effect of high ethanol intake on vascular reactivity to serotonin, vasopressin and acetylcholine in normotensive rats. 829 56

Various endocrine responses to 5-hydroxytryptamine (serotonin, 5-HT) agonists were used to assess serotonergic receptor function after chronic treatment with the antidepressants fluoxetine (10 mg/kg), a 5-HT uptake blocker and the norepinephrine uptake blocker desipramine (DMI, 5 mg/kg). Both were injected (i.p.) once a day for 21 days. DOI (5-HT1C/2 agonist, 0-5 mg/kg i.p.) and 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) (less selective, but predominantly a 5-HT1C agonist, 0-20 mg/kg i.p.) were administered 18 hr after the final antidepressant injection and 30 min before decapitation. Chronic treatment with both fluoxetine and DMI produced a potentiation in most hormone responses to the 5-HT agonists (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-amino-propane HCl (DOI) and MK-212, although there were several differences in individual hormone responses to the two 5-HT agonists. Fluoxetine and DMI potentiated the MK-212- and DOI-induced increase of plasma oxytocin levels and potentiated the effect of DOI on plasma adrenocorticotropic hormone (corticotropin) and prolactin levels. In contrast, the effect of the high dose of MK-212 on plasma prolactin concentration was reduced by both antidepressants. Only MK-212 increased vasopressin levels and this effect was potentiated by fluoxetine, but not by DMI. Fluoxetine also significantly increased the resting level of plasma vasopressin. DMI potentiated the effect of MK-212 on plasma renin concentration. Pretreatment with fluoxetine significantly increased (38%) the Bmax for the 5-HT1C/2 agonist sites ([125I]DOI) in the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Long-term treatment with the antidepressants fluoxetine and desipramine potentiates endocrine responses to the serotonin agonists 6-chloro-2-[1-piperazinyl]-pyrazine (MK-212) and (+-)-1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane HCl (DOI). 839 20


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