UNIPROT:P01185 - FACTA Search

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Query: UNIPROT:P01185 (vasopressin)
23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relative anatomical distributions of vasopressin and the nitric oxide synthase, nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) were examined in the hypothalamo-neurohypophysial system using immunocytochemical and histochemical techniques. Double-labeled neurons were localized predominately to rostral aspects of the hypothalamo-neurohypophysial system. Only scattered double-labeled cells were found throughout the subdivisions of the supraoptic and paraventricular nuclei. Because previous investigations suggest that nitric oxide may play a critical role in neurotransmission and reductions in NADPH-d have been reported in the neural lobe of salt-loaded animals, the present report of its coexistence with the antidiuretic hormone vasopressin in the hypothalamo-neurohypophysial system further supports a role for these neuroactive substances in mechanisms modulating fluid homeostasis.
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PMID:Relationship of vasopressin with NADPH-diaphorase in the hypothalamo-neurohypophysial system. 837 98

Experiments were designed to determine the role of the L-arginine pathway in endothelium-dependent relaxations to vasopressin. The effects of L-arginine analogues NG-nitro-L-arginine (L-NNA), NG-nitro-L-arginine methyl ester (L-NAME), and NG-monomethyl-L-arginine (L-NMMA) on basal and vasopressin-induced activity of nitric oxide synthase were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2-6% CO2 (37 degrees C, pH 7.4). Radioimmunoassay was used to determine the level of guanosine 3',5'-cyclic monophosphate (cGMP). All experiments were performed in the presence of indomethacin, a cyclooxygenase inhibitor. L-NAME and L-NMMA caused endothelium-dependent contractions and inhibited basal production of cGMP. In contrast, L-NNA did not affect basal tone or basal production of cGMP. L-Arginine analogues inhibited relaxations to vasopressin but did not affect relaxations to a nitric oxide donor, molsidomine (SIN-1). The effects of L-NNA, L-NAME, and L-NMMA were reversed in the presence of L-arginine. The relaxations to vasopressin were associated with an increase of cGMP levels in the arterial wall. This effect of vasopressin was inhibited in the presence of L-NNA. These studies suggest that the relaxations to vasopressin are mediated by activation of the endothelial L-arginine pathway, leading to increased production of nitric oxide, with subsequent activation of guanylate cyclase in smooth muscle cells. In canine basilar artery, L-NAME and L-NMMA are nonselective inhibitors of both basal and stimulated production of nitric oxide, whereas L-NNA selectively inhibits vasopressin-induced activation of the L-arginine pathway.
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PMID:Endothelial L-arginine pathway and relaxations to vasopressin in canine basilar artery. 838 55

The present study determined the plasma ACTH and corticosterone responses of the rat to acute local inflammation induced by the im injection of a small volume of turpentine. In response to tissue injury, ACTH and corticosterone concentrations rose rapidly, peaked at 1 h, and returned toward basal values by 3 h after turpentine injection. As acute inflammation developed, plasma interleukin-6 bioactivity increased significantly, and ACTH and corticosterone levels exhibited a secondary rise. These secondary responses were maximum 6-12 h after turpentine administration, persisted for 20-28 h, and were statistically significant regardless of the normal circadian variations in ACTH and corticosterone secretion. Injection of neutralizing anti-CRF antiserum 7 h after turpentine produced a complete reversal, whereas antiarginine vasopressin (anti-AVP) caused a partial (approximately 40%) inhibition, of inflammation-induced ACTH secretion. The cyclooxygenase inhibitor, ibuprofen (10 mg/kg, iv), like CRF antiserum, rapidly and completely reversed turpentine-induced ACTH secretion. In contrast, the nitric oxide synthase inhibitor, Nw-nitro-L-arginine methyl ester (30 mg/kg, iv), produced a significant enhancement of the ACTH response within 30 min of its injection. Measurement of plasma interleukin-6 bioactivity and fever showed that neither anti-CRF, anti-AVP, ibuprofen, nor Nw-nitro-L-arginine methyl ester acutely influenced the local inflammatory process itself, suggesting that these agents interacted directly with the hypothalamo-pituitary-adrenal axis. These data demonstrate that the ACTH response to local inflammation is mediated by synergistic actions of CRF and AVP, and that both stimulatory (PGs) and inhibitory (nitric oxide) intermediates regulate this response.
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PMID:Corticotropin-releasing factor, vasopressin, and prostaglandins mediate, and nitric oxide restrains, the hypothalamic-pituitary-adrenal response to acute local inflammation in the rat. 859 89

Constitutive nitric oxide synthase (cNOS) was immunolocalized to study its role in osmotic regulation. Immunoreactivity was observed in all major hypothalamic osmoregulatory structures, the organum vasculosum laminae terminalis, subfornical organ, median preoptic nucleus, and supraoptic and paraventricular nuclei. These nuclei were compared in normal Long-Evans rats and homozygous Brattleboro rats with hereditary hypothalamic diabetes insipidus and in normal mice and mice with hereditary nephrogenic diabetes insipidus. About 50% of supraoptic neurons in Long-Evans rats and 90% in Brattleboro rats were cNOS immunopositive; a qualitatively similar difference occurred in the paraventricular nucleus. Mice with hereditary nephrogenic diabetes insipidus also showed a greater proportion of cNOS-positive supraoptic neurons (50%) than normal mice (20%). However, the number of cNOS-positive cells in the organum vasculosum laminae terminalis, subfornical organ, and median preoptic nucleus dis not differ significantly between diabetic and normal animals. The similar changes in cNOS in two mutant strains in which the only common feature is chronic osmotic stimulation shows that differences in vasopressin and oxytocin are not involved in the regulation of cNOS. The results suggest strongly that cNOS is involved in long term modulation of the hypothalamo-neurohypophysial system and, hence, body water and electrolyte homeostasis, and that cNOS is itself regulated by body osmotic status.
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PMID:Constitutive nitric oxide synthase in hypothalami of normal and hereditary diabetes insipidus rats and mice: role of nitric oxide in osmotic regulation and its mechanism. 861 10

We studied the effects of vasopressin on isolated rings of human deferential artery and vas deferens (prostatic portion) obtained from patients undergoing radical cystectomy (n = 11) or prostatectomy (n = 10). Ring segments of artery or vas deferens were studied in organ bath experiments at optimal resting tension. In artery rings, vasopressin produced concentration-dependent, endothelium-independent contractions with an EC50 of 4.5 x 10(-10) M. The presence of NG-nitro-L-arginine methyl ester hydrochloride (10(-4) M), an inhibitor of nitric oxide synthase, did not change significantly (P > 0.05) the vasopressin-induced contraction. In ring preparations of the prostatic part of the vas deferens, vasopressin induced phasic contractions with an EC50 of 7.0 x 10(-9) M. The vasopressin V1 receptor antagonist, d(CH2)5Tyr(Me)AVP (10(-8) and 10(-6)), displaced to the right in parallel the control curve to vasopressin in artery and vas deferens rings. These results indicate that vasopressin exerts a powerful constrictor action on human deferential artery and vas deferens by direct stimulation of V1 receptors. It is concluded that the deferential artery may dampen the passage of blood to the vas deferens in circumstances characterized by increased plasma vasopressin levels.
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PMID:Contractile responses of human deferential artery and vas deferens to vasopressin. 873 12

Intact adult male rats fed an alcohol [ethanol (EtOH)] diet for 10 days show blunted adrenocorticotropic hormone (ACTH) release in response to immune signals such as the cytokine interleukin-1 beta (IL-1 beta) and endotoxin [lipopolysaccharide (LPS)], as well as to physical stress (mild electroshocks). The mechanisms responsible for this effect remain poorly understood, but we have recently reported that decreased pituitary responsiveness to vasopressin (VP) might play a role. In naive rats, nitric oxide (NO) exerts a restraining influence on the response of the hypothalamic-pituitary (H-P) axis to cytokines and VP. The ability of long-term EtOH treatment to increase glutamate receptors, and thus NO formation, prompted us to test the hypothesis that abnormally high NO concentrations might modulate the influence of the drug. Blockade of the activity of NO synthase (NOS), the enzyme responsible for NO formation, with the arginine derivative L-N omega nitro-L-arginine-methylester (L-NAME), augmented the ACTH response to IL-1 beta or LPS in both control (C) and EtOH-fed (E) rats. Indeed, after L-NAME treatment, ACTH concentrations were statistically comparable in C and E animals injected with endotoxin or a large dose of IL-1 beta. VP-induced ACTH secretion also became comparable in both experimental groups after blockade of NOS activity. In contrast, the decreased response of the H-P axis of E animals to shocks was only slightly ameliorated, compared with that of C rats. It is therefore possible that changes in the NOergic tone induced by alcohol play a role in the decreased response of the H-P axis to cytokines, possibly in part by altering the stimulatory action of VP on the corticotrophs. On the other hand, in E rats NO seems to exert only a minimal influence on the central nervous system circuits activated by shocks.
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PMID:Adult male rats exposed to an alcohol diet exhibit a blunted adrenocorticotropic hormone response to immune or physical stress: possible role of nitric oxide. 874 13

Experiments were performed to test the hypothesis that renal arteriolar vasoconstrictor responses to angiotensin II (ANG II) are curtailed through a mechanism that involves stimulation of endogenous nitric oxide (NO) synthesis. The in vitro blood-perfused juxtamedullary nephron technique was exploited to monitor arteriolar lumen diameter responses to exogenous ANG II before and during treatment with the NO synthase inhibitor N omega-nitro-L-arginine (L-NNA). Under control conditions, 1 nM ANG II reduced afferent and efferent arteriolar diameters by 13 and 11%, respectively. In the presence of L-NNA, 1 nM ANG II decreased afferent diameter by 26% and efferent diameter by 35%. This augmentation could not be attributed to the L-NNA-induced decrease in baseline diameter. L-NNA also augmented vasopressin responses, indicating a lack of agonist specificity in this interaction. ANG II reactivity during L-NNA treatment was not enhanced when tissue NO activity was fixed at basal levels (exposure to 1 microM sodium nitroprusside). These results indicate that endogenous NO modulates the vasoconstrictive impact of ANG II on both afferent and efferent arterioles of juxtamedullary nephrons and that this process does not require stimulation of NO synthesis.
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PMID:Basal nitric oxide production curtails arteriolar vasoconstrictor responses to ANG II in rat kidney. 877 Jan 68

The enzyme responsible for nitric oxide (NO) formation, NO synthase (NOS), is found in hypothalamic neurons that control ACTH secretion. This led to the hypothesis that brain NO may modulate the response of the hypothalamic-pituitary (HP) axis to various stimuli. We tested this hypothesis by measuring changes in constitutive (c) NOS mRNA levels in the hypothalamus of rats systemically injected with endotoxin, a lipopolysaccharide (LPS) that releases endogenous cytokines, and analyzed these results in the context of the appearance of ACTH-releasing secretagogues such as corticotropin-releasing factor (CRF) and vasopressin (VP), as well as CRF receptors type A (CRF-RA). We purposefully chose doses of LPS thought to only minimally disrupt the blood-brain barrier and not be accompanied by an endotoxin shock, so that the results we obtained did not primarily stem from abnormal passage of compounds into the brain, or non-specific stress. Three to four hours following LPS injection (100 micrograms/kg, i.v.), cNOS mRNA levels increased in the paraventricular nucleus (PVN) of the hypothalamus. LPS treatment also upregulated PVN CRF gene transcription (measured by CRF heteronuclear RNA) and increased steady-state gene expression of the immediate early genes (IEG) c-fos and NGFI-B, with the first changes noted 1-2 h after treatment. Transcripts of CRF receptors type A were present in the hypothalamus 6 h after endotoxin treatment. On the other hand, no alterations in cytoplasmic VP mRNA levels were noted in rats injected with LPS. Because the dose of LPS we used stimulates ACTH secretion within 30 min, our results suggest that systemic LPS acts first within the median eminence, where it stimulates peptidic nerve terminals. Neuronal activation of hypothalamic cell bodies takes place later, and whether this phenomenon is due to the production of brain neurotransmitters and/or cytokines, or whether it primarily results from increased demand on the synthetic machinery, remains to be established. These studies extend prior work showing that systemic LPS increases the neuronal activity of hypothalamic regions known for their involvement in the responses of the HP axis, and bring forth two important additional points. First, increases in CRF primary nuclear transcripts are delayed with regard to the temporal release of ACTH. This suggests, though it does not demonstrate, that under the experimental conditions we used, the first site of action of LPS is the median eminence. Second, the observation of increased cNOS gene expression following LPS treatment, and the presence of this enzyme in neurons that regulate ACTH secretion, bring support to the hypothesis that this gas plays an important function in mediating the HP axis response to an immune challenge.
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PMID:Systemic endotoxin increases steady-state gene expression of hypothalamic nitric oxide synthase: comparison with corticotropin-releasing factor and vasopressin gene transcripts. 882 44

Effects of clonidine on the elevated arterial diastolic blood pressure induced by infusion of alpha 1-adrenoceptor agonists were studied in pithed rats. Intravenous injection of clonidine resulted in a dose-dependent pressor response at a resting state and a further increase in the moderately elevated diastolic blood pressure induced by infusion of lower doses of phenylephrine and methoxamine. However, clonidine produced a depressor response when diastolic blood pressure was elevated by around 100 mmHg during infusion of higher doses of alpha 1-adrenoceptor agonists. The depressor response to clonidine was dose-dependent at a dose range of 10 to 1000 micrograms/kg. On the other hand, clonidine failed to cause the depressor response while diastolic pressure was elevated by infusion of vasopressin by around 100 mmHg. NG-methyl-L-arginine, a nitric oxide synthase inhibitor, and propranolol, a beta-adrenoceptor antagonist, did not affect the depressor response to clonidine. After pretreatment with yohimbine, an alpha 2-adrenoceptor antagonist, the depressor response to clonidine was inhibited, but prazosin, an alpha 1-adrenoceptor antagonist, did not suppress the depressor response. These results demonstrate that clonidine specifically depresses the pressor response to alpha 1-adrenoceptor agonists in pithed rats via a mechanism which is not mediated by beta-adrenoceptors and independent of endothelium-dependent relaxing factor, and suggest that a yohimbine-sensitive mechanism may be related to the clonidine effect.
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PMID:Characteristics of depression by clonidine of the pressor response to alpha 1-adrenoceptor agonists in pithed rats. 882 67

Blood flow in the renal artery, superior mesenteric artery and infra-renal abdominal aorta of conscious rabbits was measured by Doppler ultrasound. Arterial pressure, heart rate and blood flow responses were assessed following 0.2 and 0.8 nmol/kg intravenous endothelin-1. The effects of the following antagonists on these responses were examined: phentolamine, propranolol, scopolamine, captopril, nifedipine, indomethacin, the V1-vasopressin receptor antagonist d(CH2)5Tyr(Me)AVP and the competitive nitric oxide (NO) synthase inhibitor NG-nitro L-arginine (NOLA). Hindlimb resistance and arterial pressure responded in two phases, initial vasodilatation followed by vasoconstriction. Renal and mesenteric vasoconstriction occurred without initial vasodilatation. Following 0.2 nmol/kg endothelin-1, arterial pressure decreased by 18.5 +/- 0.8 mmHg, then increased by 25.2 +/- 1.7 mmHg (n = 27). Heart rate changed reciprocally. Renal resistance increased by 533 +/- 73% (n = 12). Mesenteric resistance increased by 420 +/- 34%. Hindlimb resistance decreased 54 +/- 2% (n = 12, all P < 0.01) then increased slightly (P < 0.05). All changes were greater at 0.8 nmol/kg, particularly the hindlimb vasoconstriction. The only antagonist to alter significantly these responses was NOLA, which in the hindlimb attenuated the vasodilatation and accentuated the vasoconstriction. We conclude that most of the haemodynamic effects of endothelin-1 are direct, but that NO generated by NO synthase causes part of the hindlimb vasodilatation, and that endothelin-1-induced vasoconstriction is attenuated by release of NO.
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PMID:Endothelin-1 produces heterogeneous regional haemodynamic effects in conscious rabbits. 886 98

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