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

The effects of fluid intake on basal and vasopressin-responsive urinary PGE excretion (UPGEV) were examined in conscious rats under conditions of 1) ad libitum water intake, 2) water deprivation, and 3) water diuresis induced by ad libitum intake of 5% dextrose in water. UPGEV fell progressively during 40 h of water deprivation. Water diuresis after water deprivation increased UPGEV transiently (8 h). Vasopressin (Pitressin tannate in oil, 5 U/kg subcutaneously) increased UPGEV and decreased urine volume (V) in rats on ad libitum water intake but did not alter UPGEV during water deprivation. Indomethacin suppressed UPGEV (70-90%), increased basal urine osmolality (Uosmol), and potentiated the antidiuretic response to Pitressin in rats on ad libitum water intake. Indomethacin accelerated by 8 h the onset of maximal antidiuresis in water-deprived rats but did not significantly alter water balance. During water diuresis, UPGEV declined in the first 8 h after Pitressin. Thereafter, UPGEV increased markedly, concurrent with early vasopressin escape. Indomethacin or meclofenamate inhibited the rise in UPGEV, the decline in Uosmol, and the increase in V of the escape phase. Indomethacin or meclofenamate also impaired the excretion of an acute water load (5% body wt) given during escape. The spontaneous decline in UPGEV during hydropenia may serve to maximize physiologic antidiuresis. Conversely, the marked increase in UPGEV induced by administration of vasopressin during water diuresis may serve to suppress the antidiuretic response and thus play a role in the mediation of escape from physiologically inappropriate antidiuresis.
 ...
PMID:Effects of fluid intake on basal and vasopressin-responsive urinary prostaglandin E. 686 38

The present experiments examined the role of prostaglandin biosynthesis in the increase in urine flow rate seen in rats with hypercalcemia induced by the administration of 1,25-dihydroxycholecalciferol. In a first group, rats receiving the vitamin D metabolite developed hypercalcemia, polyuria, and increased urine prostaglandin E excretion. Indomethacin resulted in a fall in urine prostaglandin E excretion. A second group was fluid restricted to ascertain whether increased thirst could be an etiologic mechanism of the polyuria. This resulted in a trivial fall in urine flow rate despite a fall in body weight and a rise in both urine and plasma osmolality. In a final group, prostaglandin inhibition restored the vasopressin sensitivity of the hypercalcemic kidney. Accordingly, the polyuria seen in hypercalcemic rats after the administration of 1,25-dihydroxycholecalciferol is associated with an increase in urine prostaglandin E excretion and can be reversed by inhibition of prostaglandin synthesis. In addition, this polyuria can occur independent of the thirst mechanism. Finally, there is evidence that the vasopressin resistance of the hypercalcemic kidney could be reversed by prostaglandin inhibition.
 ...
PMID:Prostaglandin-dependent polyuria in hypercalcemia. 689 50

The effect of prostaglandin on diffusional water permeability has been studied in collecting ducts in an isolated rat papilla. PGE2 increased water permeability. The effect was significant at a concentration of 10(-8) mol 1(-1) and was maximal with a concentration of 10(-6) mol 1(-1). The maximal increment of 0.94 +/- 0.10 (SEM) micron s-1 was approximately half that produced by maximal stimulation with antidiuretic hormone (2.18 +/- 0.12 micron s-1). A concentration of 10(-8) mol 1(-1) produced an increase in basal water permeability and 24 mu unit ml-1 ADH, which without PGE2 present gave a similar increase, had no incremental effect. ADH 100 mu unit ml-1 increased permeability to a value similar to that observed in the absence of PGE2. Thus PGE2 and ADH both increase water permeability but the increments are not additive. Indomethacin in a concentration that inhibited prostaglandin production altered the response of the collecting duct to ADH. The dose response curve was shifted to the left and the maximal increase in water permeability and the lowest dose at which a response occurred took place at concentrations less than 1/2 those required in its absence. Prostaglandins influence the action of ADH and it is likely that in life they regulate and modulate the change in water permeability induced by anti-diuretic hormone.
 ...
PMID:The effect of prostaglandin E2 and ADH on diffusional water permeability in collecting duct of an isolated rat papilla. 694 74

1. The effect of 3 days' treatment with indomethacin on the renal response to infused vasopressin was assessed in eight healthy volunteer subjects. 2. Indomethacin produced significant weight gain and an increase in serum potassium without a change in creatinine clearance. 3. Although indomethacin reduced maximum free water clearance in five subjects, the anti-diuresis produced by an incremental infusion of physiological amounts of vasopressin was no different whether indomethacin had been taken or not. 4. Indomethacin, in the dose we have used, is known to reduce prostaglandin production and we therefore conclude that endogenous prostaglandins do not inhibit the effect of physiological amounts of vasopressin on water clearance, which makes it unlikely that prostaglandins are important in the day-to-day modulation of response to vasopressin.
 ...
PMID:The effect of indomethacin on vasopressin-induced antidiuresis in man. 728 99

Indomethacin (40 mg kg-1 in a single dose) was applied by stomach tube to inhibit the synthesis of prostaglandins during extracellular fluid volume expansion with isotonic saline in normal and acutely (2 h) hypophysectomized Wistar rats and hydropaenic diabetes insipidus Brattleboro rats. In the normal rats indomethacin reduced urine output due to decreased free water excretion. In the rats deprived of antidiuretic hormone (ADH) by acute hypophysectomy or due to hereditary eror in ADH synthesis indomethacin also decreased the urine output and clearance of osmotically free water. It is concluded that also other mechanisms besides the established competition between ADH and prostaglandins for ADH receptors may be responsible for the indomethacin effect on the osmotic movement of water in the distal nephron.
 ...
PMID:Decreased free water excretion after indomethacin in the absence of antidiuretic hormone in saline loaded hypophysectomized Wistar and hydrapaenic Brattleboro rats. 737 6

1 The response of the dog anococcygeus muscle to field stimulation and to some drugs has been studied. The results are compared with those reported previously in the rat, cat and rabbit. 2 Field stimulation produced frequency-dependent contractions which were inhibited by guanethidine and phentolamine. When the tonus of the muscle was increased with guanethidine, field stimulation always produced frequency-dependent relaxation. The relaxation was not prevented by propranolol. 3 The muscle was contracted by noradrenaline, tyramine, acetylcholine, histamine (H1), 5-hydroxy-tryptamine, prostaglandin E2 and vasopressin. Phentolamine, atropine, promethazine (but not cimetidine) and methysergide inhibited the effect of the respective agonists. 4 After increasing the tonus of the muscle, it was relaxed by low concentrations of isoprenaline. The relaxation was antagonized by propranolol. 5 The response to adenosine triphosphate (ATP) was variable. In some preparations, it relaxed the muscle, in others it contracted the muscle prior to relaxation, in others still it only contracted the muscle. Indomethacin did not prevent ATP-induced contraction. 6 It is concluded that the anococcygeus of the dog, like that of rat, cat and rabbit, has an adrenergic motor innervation and an inhibitory innervation, the transmitter of which is not identified.
 ...
PMID:Pharmacological study of the anococcygeus muscle of the dog. 747 Jul 46

The present study was designed to investigate the possible role of endothelium-derived vasodilators, nitric oxide and prostaglandins, in the regulation of blood pressure during the presence and absence of the major pressor systems. Conscious rats were infused with a cocktail of inhibitors of the sympathetic nervous system, renin-angiotensin system, and V1 vascular receptor to vasopressin (achieved with hexamethonium, captopril, phentolamine, propranolol, and the V1 vasopressin (AVP) antagonist des-(CH2)5Tyr(Me)-AVP). The cocktail of vasoconstrictor inhibitors induced a marked fall of mean arterial pressure (MAP) from 109 +/- 2 to 52 +/- 2 mmHg (1 mmHg = 133.3 Pa) (n = 24). In animals with blockade, the specific inhibitor of nitric oxide synthesis, NG-nitro-L-arginine methyl ester (L-NAME), induced a significant increase of MAP from 51 +/- 1 to 84 +/- 2 mmHg (n = 6). In the presence of indomethacin, a cyclooxygenase inhibitor, the pressor response to L-NAME was from 52 +/- 2 to 126 +/- 4 mmHg (n = 6). Neither indomethacin (n = 6) nor vehicle (n = 6) alone altered MAP. In intact animals without blockade, L-NAME caused a similar increase of MAP when it was injected alone (from 107 +/- 3 to 144 +/- 4 mmHg, n = 7) or with indomethacin (from 113 +/- 3 to 144 +/- 3, n = 6). Indomethacin alone (n = 8) did not change MAP. In conclusion, in the absence of the major pressor systems, the pressor effect of the inhibition of the production of endogenous nitric oxide and vasodilator prostanoid synthesis appears to be synergistic. These results suggest that these two endogenous vasodilators are involved in the maintenance of blood pressure.
 ...
PMID:Role of nitric oxide and prostaglandins in the regulation of blood pressure in conscious rats. 758 39

To assess the central role of interleukin 1-beta (IL-1 beta) in the release of ACTH, vasopressin (AVP) and atrial natriuretic peptide (ANP) and in the regulation of blood pressure and thermogenesis, 3 ng (0.173 pM) x 100-1 x BW-1 (LIL), 30 ng (1.73 pM) x 100g-1 x BW-1 (MIL), and 150 ng (8.63 pM) x 100g-1 x BW-1 (HIL) of human IL-1 beta dissolved in sterile saline were injected intracerebroventricularly to conscious rats. In the control rats, saline alone (5 microliters) was administered. In three other groups, rats were pretreated with indomethacin, a cyclooxygenase inhibitor, given i.v. (1 mg x 100g-1 x BW-1); medium and high doses of IL-1 beta or its vehicle were given. In the LIL group, IL-1 beta increased blood pressure, body temperature and plasma AVP and ANP without any changes in heart rate (HR) and plasma ACTH. In the MIL group, plasma ACTH was increased, and changes in the other parameters were similar to those in the LIL group. In the HIL group, however, the pressor and thermogenetic responses were attenuated; plasma AVP, ACTH, and ANP were increased; and HR was unchanged. In the control (CON) group, none of these parameters was changed throughout the studies. Indomethacin abolished the AVP and ACTH responses to IL-1 beta, but potentiated the pressor and hypothermic responses and increased plasma ANP. These data suggest that the actions of IL-1 beta on AVP and ACTH release and thermogenesis, but not on blood pressure and the release of ANP, are modulated by the stimulated central production of prostaglandins.
 ...
PMID:Central effects of interleukin-1 on blood pressure, thermogenesis, and the release of vasopressin, ACTH, and atrial natriuretic peptide. 839 69

Endothelium-dependent relaxation of mesenteric resistance arteries of spontaneously hypertensive rats (SHRs) and normotensive Wistar-Kyoto (WKY) rats was studied. Acetylcholine-induced relaxation of SHR vessels precontracted with 10 microM norepinephrine was endothelium dependent and attenuated compared with WKY vessels. The impaired response of SHR vessels was normalized by inhibition of cyclooxygenase with indomethacin. Blockade of nitric oxide synthetase with NG-nitro L-arginine methyl ester (L-NAME) or inhibition of guanylate cyclase with methylene blue attenuated acetylcholine-induced relaxation of norepinephrine-contracted SHR vessels but had no effect on WKY vessels. When vessels were precontracted with 30 nM arginine vasopressin, acetylcholine induced similar degrees of relaxation in both strains. A similar response was detected when lysine vasopressin was used to induce tone. Indomethacin had no effect on relaxation responses of SHR and WKY vessels precontracted with either form of vasopressin. L-NAME and methylene blue partially inhibited acetylcholine-induced relaxation of vasopressin-contracted vessels from both strains. Acetylcholine added at baseline did not induce contraction of vessels from either strain. It is concluded that endothelium-dependent relaxation of SHR resistance arteries is not impaired under all circumstances. Acetylcholine-induced relaxation may be suppressed in SHR resistance arteries when norepinephrine is used to induce contraction as a result of catecholamine-induced production of an endothelium-derived contracting factor. Vasopressin, on the other hand, does not elicit production of this contracting factor and may enhance the vasorelaxant action of acetylcholine in resistance arteries of both strains via actions on endothelial or vascular smooth muscle cells.
 ...
PMID:Endothelium-dependent relaxation of hypertensive resistance arteries is not impaired under all conditions. 841 84

1. The effects of pregnancy on mesenteric arterial function were examined in constantly perfused (5 ml min-1) mesenteric arterial beds isolated from 21-day pregnant rats. The function of sympathetic and sensory-motor perivascular nerves, endothelium and smooth muscle was examined. The role of nitric oxide and prostaglandins in vasoconstrictor function was tested by use of NG-nitro-L-arginine methyl ester (L-NAME; 100 microM) and indomethacin (10 microM), respectively. 2. Electrical field stimulation (EFS; 4-32 Hz, 1 ms, 90V, 30s) at basal tone elicited frequency-dependent vasoconstriction which was markedly reduced in preparations from pregnant rats at all frequencies. Vasoconstrictor responses to vasopressin and endothelin were also reduced in pregnancy and there was a trend towards a reduction in maximal responses to noradrenaline (NA). In contrast, there was no difference in vasoconstrictor responses to ATP, 5-hydroxytryptamine (5-HT) or angiotension II. 3. L-NAME (100 microM) augmented responses to EFS, NA, ATP and vasopressin in control mesenteric arterial preparations. In contrast, L-NAME augmented responses only to EFS in pregnancy, having no significant effect on responses to NA, ATP and vasopressin. 4. Indomethacin (10 microM) attenuated responses to NA and vasopressin, but not to EFS, in controls and in pregnancy. Responses to ATP were attenuated by indomethacin in controls but not in pregnancy. 5. Mesenteric preparations from pregnant rats were resistant to having tone raised by continuous perfusion with methoxamine. Despite an approximately 10 fold greater concentration of methoxamine, there was a significantly smaller increase in tone in preparations from pregnant, 34.27 +/- 4.8 mmHg (n = 11) compared to control, 65.92 +/- 5.4 mmHg (n = 11), rats. EFS (4-12 Hz, 60 V, 0.1 ms, 30s) in the presence of guanethidine (5 microM) to block sympathetic neurotransmission elicited frequency-dependent vasodilatation due to activation of sensory-motor nerves. Percentage relaxations were similar in preparations from pregnant and non-pregnant rats. 6. Dose-dependent endothelium-dependent vasodilatations to acetylcholine and ATP were similar in preparations from pregnant and non-pregnant rats. Endothelium-independent vasodilatation to sodium nitroprusside and to calcitonin gene-related peptide were also similar between the two groups. 7. There was no significant difference in the basal perfusion pressure of mesenteric arterial beds from control (21.3 +/- 1.0 mmHg, n = 24) and pregnant (20.2 +/- 1.2 mmHg, n = 23) rats. However, a step-wise increase in perfusate flow from 5 to 10, 15, 20 and 24ml min-1 produced smaller increases in perfusion pressure in pregnancy compared to the controls. L-NAME (100 microM) or indomethacin (10 microM) had no significant effect on the relationship between flow and perfusion pressure. 8. The present results show that prejunctional changes are involved in blunted sympathetic vasoconstriction of rat mesenteric arteries in pregnancy. Non-specific postjunctional changes are implicated in the reduced constrictor responses to applied methoxamine, vasopressin and endothelin, but not to ATP. In contrast, sensory-motor nerves and endothelium-dependent and -independent vasodilatation was unchanged. The decrease in receptor-mediated mesenteric arterial constrictor responsiveness in pregnancy does not appear to be due to acute modulation by NO or prostaglandins, but may involve changes in the distensibility of the bed and/or changes in wall thickness.
 ...
PMID:Mesenteric arterial function in the rat in pregnancy: role of sympathetic and sensory-motor perivascular nerves, endothelium, smooth muscle, nitric oxide and prostaglandins. 873 Jul 40


<< Previous 1 2 3 4 5 6 7 Next >>