Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

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

The administration of the nitric oxide (NO) synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME, 5 mg/kg s.c.) concurrently with Escherichia coli endotoxin (3 mg/kg i.v.) increased vascular permeability and caused mucosal damage in the rat intestine 1 h later. The vasopressin V1 receptor antagonist, [Mca1,Tyr(Me)2, Arg8]vasopressin (0.01-0.2 microgram/kg s.c., 15 min before endotoxin) dose-dependently reduced this damage. These results suggest a beneficial role of NO, counteracting the injurious vascular actions of endogenous vasopressin, in maintaining intestinal mucosal integrity in acute endotoxaemic states.
...
PMID:Constitutive nitric oxide modulates the injurious actions of vasopressin on rat intestinal microcirculation in acute endotoxaemia. 798 55

The aim of the study was to investigate to what extent inhibition of nitric oxide (NO) formation, cyclooxygenase and converting enzyme activities and vasopressin V1 receptors blockade affects the cardiovascular system in conscious, freely moving normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. The experiments were performed on 33 WKY and on 33 SHR. In series 1 (8 WKY and 8 SHR) animals received bolus injection of N omega-nitro-L-arginine - NLA (10 mg/kg), in series 2 (6 WKY and 6 SHR) bolus injection of indomethacin (10 mg/kg). In series 3 (8 WKY and 8 SHR) the animals received captopril as initial bolus (1 mg/kg) followed by constant infusion (1 mg/kg/min), in series 4 (11 WKY and 11 SHR) vasopressin V1 receptor antagonist 1-(1-mercapto-4-methylcyclohexaneacetic acid)-8-arginine-vasopressin (MeCAAVP) was infused (1.52 micrograms/kg/min). In series 1 in WKY NLA elicited a long-lasting, significant increase in mean blood pressure (max 46 +/- 3 mmHg at 40 min). In SHR mean blood pressure raises were not significant (max 22 +/- 6 mmHg). In series 2, both in WKY and SHR, indomethacin elicited only transient, nonsignificant increases in mean blood pressure. In series 3, the mean blood pressure fall during the captopril infusion was more pronounced in SHR than in WKY (45 +/- 2 mmHg vs 13 +/- 2 mmHg respectively). In series 4 vasopressin V1 receptor blockade caused a nonsignificant fall in mean blood pressure, both in WKY and SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Blood pressure responses to substances interfering with nitric oxide formation, cyclooxygenase and converting enzyme activities and vasopressin V1 receptors blockade in conscious spontaneously hypertensive and normotensive rats. 800 Apr 47

Nitric oxide (NO), which was firstly identified as an endothelium-derived relaxing factor, has recently been demonstrated to be a neurotransmitter in the central and peripheral nervous systems. In the hypothalamus, abundant nitric oxide synthase (NOS) immunoreactivity and its histochemical marker, NADPH-diaphorase activity, have been demonstrated in the hypothalamo-neurohypophyseal system. In the present study, we examined whether NOS is coexpressed with posterior pituitary hormones in the rat hypothalamus by combination of oxytocin and vasopressin immunofluorescence and NADPH-diaphorase histochemistry. Most oxytocin-immunoreactive neurons in the paraventricular and supraoptic nuclei expressed NADPH-diaphorase activity, but virtually no vasopressin-immunoreactive neurons contained NADPH-diaphorase activity. This suggests that oxytocin neurons are the main source of NO production in the hypothalamic-pituitary system.
...
PMID:Coexistence of oxytocin and NADPH-diaphorase in magnocellular neurons of the paraventricular and the supraoptic nuclei of the rat hypothalamus. 808 73

Infusion of arginine vasopressin (AVP) decreases pulmonary artery pressure. To determine whether this is due to stimulated release of endothelium-derived relaxing factor in the pulmonary circulation, the authors studied segments of canine pulmonary artery suspended in organ chambers for measurement of isometric force. In segments in which contraction was induced with phenylephrine (10(-6) mol), AVP (10(-12) to 10(-7) mol) produced concentration-dependent relaxation in segments with endothelium but not in segments without endothelium. Greater concentrations of AVP (3 x 10(-7) to 3 x 10(-5) mol) produced comparable contraction in segments with or without endothelium. Endothelium-dependent vasodilation in response to AVP was inhibited by NG-nitro-L-arginine (10(-4) mol) and NG-monomethyl-L-arginine (L-NMMA) (10(-4) mol), inhibitors of nitric oxide synthesis from L-arginine. The inhibitory effect of L-NMMA was attenuated by L-arginine (10(-4) mol). Endothelium-dependent vasodilation in response to AVP was inhibited reversibly by the vasopressin V1-blocker. Arginine vasopressin induces release of endothelium-derived nitric oxide through action on endothelial V1-receptors. Endothelium-derived nitric oxide mediates vasodilatation, which may explain decreased pulmonary resistance during AVP infusion.
...
PMID:Arginine vasopressin induces endothelium-dependent vasodilatation of the pulmonary artery. V1-receptor-mediated production of nitric oxide. 813 74

Histamine and the guanosine 3',5'-cyclic monophosphate (cGMP)-inducing agent sodium nitroprusside both increased serotonin (5-HT) uptake and cGMP levels in isolated human platelets in vitro. Histaminergic stimulation was observed at concentrations ranging from 10 nM to 0.25 microM [mean effective concentration (EC50) = 0.1 microM histamine]. The inhibition produced by the H2-receptor antagonists tiotidine, metiamide, and cimetidine was 10-10(5) times more potent on histamine receptors regulating 5-HT uptake and cGMP generation in human platelets than on the histaminergic receptors H1, HIC, H2, and H3 in other tissues. The in vitro histamine-induced 5-HT uptake was prevented by preincubation of isolated human platelets in the presence of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine or the cGMP-lowering agent LY-83583. Histamine was ineffective in stimulating cAMP generation in human platelets and did not interact with effector sites known to downregulate 5-HT uptake, including imipramine, gamma-aminobutyric acid A, peripheral type benzodiazepine-binding sites, and V1a vasopressin receptors inducing human platelet shape change and aggregation. These atypical human platelet histaminergic receptors differ from the previously classified histamine receptors by their apparent high affinity to histamine H2-receptor antagonists and their apparent link with the soluble, nitric oxide-dependent guanylate cyclase. These findings suggest that human platelets express a new subtype H2h of histamine receptors.
...
PMID:Increase of human platelet serotonin uptake by atypical histamine receptors. 814 12

Evidence suggests that nitric oxide synthesis within the pulmonary circulation may be attenuated during chronic hypoxia in Wistar rats due to reduced L-arginine availability. In contrast, chronically hypoxic Sprague-Dawley rats exhibit normal endothelium-dependent pulmonary vasodilation. The purpose of the present study was to determine whether 1) Wistar rats demonstrate greater right ventricular (RV) hypertrophy in response to chronic hypoxia than Sprague-Dawley rats and 2) chronic administration of L-arginine would diminish this response in Wistar rats. L-Arginine had no effect on the degree of hypoxia-induced RV hypertrophy or polycythemia in either strain of rat. However, Wistar rats demonstrated greater hypoxia-induced RV hypertrophy and polycythemia compared with Sprague-Dawley rats. To determine whether chronically hypoxic Wistar rats indeed exhibit impaired endothelium-dependent pulmonary vasodilation, isolated lungs from control and chronically hypoxic Wistar rats were administered the endothelium-dependent pulmonary vasodilators A23187 or vasopressin. Vasodilatory responses to either agent were unaffected by chronic hypoxic exposure. We conclude that endothelium-dependent pulmonary vasodilation is maintained in the pulmonary circulation of chronically hypoxic Wistar and Sprague-Dawley rats.
...
PMID:Orally administered L-arginine does not alter right ventricular hypertrophy in chronically hypoxic rats. 814 15

We investigated the differential effect of the intracisternal and intraarterial administration of vasopressin on the regional cerebral blood flow (rCBF) in the parietal cortex of dogs. Regional CBF, velocity and blood volume were assayed by laser flowmetry. The intracisternal injection of 1 nmol vasopressin significantly increased the rCBF and velocity, without affecting blood volume. However, the intravertebral arterial injection of 1 nmol vasopressin significantly decreased the rCBF and velocity. This discrepancy can be explained by a difference in the affected vasculature; large blood vessels in the subarachnoid space vs. whole cerebral vascular system. The intracisternal and intraarterial injection of the nitric oxide inhibitor NG-monomethyl-L-arginine reduced the rCBF from the base line, and significantly suppressed the rCBF elevation induced by vasopressin. The effect of vasopressin may be considered as the summation of the increased flow from the dilated large vessels via the release of nitric oxide from the endothelium, and of the decreased flow from the contracted small vessels.
...
PMID:Differing effects of vasopressin on regional cerebral blood flow of dogs following intracisternal vs. intra-arterial administration. 815 23

Nitric oxide (NO) synthase (NOS), the enzyme responsible for NO formation, is found in hypothalamic neurons containing oxytocin (OT), vasopressin (VP), and to a lesser extent corticotropin-releasing factor (CRF). Because NO is reported to modulate endocrine activity, we have investigated the hypothesis that endogenous NO participates in ACTH released by various secretagogues in the rat. In the adult male rat, the intravenous injection of interleukin-1 beta (IL-1 beta; 0.2-0.3 micrograms/kg), VP (0.3-0.9 micrograms/kg), and OT (30 micrograms/kg) significantly increased plasma ACTH and corticosterone levels. Pretreatment with the L-form, but not the D-form, of N omega nitro-L-arginine-methylester (L-NAME; a specific inhibitor of NOS) markedly augmented the effects of these secretagogues whether it was injected acutely or over a 4 d period. Blockade of NOS activity also caused significant (P < 0.01) extensions of the duration of action of IL-1 beta, VP, and OT. In contrast, L-NAME did not significantly alter the stimulatory action of peripherally injected CRF, or centrally administered IL-1 beta. Administration of L-arginine, but not D-arginine (100 mg/kg), used as a substrate for basal NO synthesis and which did not by itself alter the activity of the hypothalamic-pituitary-adrenal (HPA) axis, blunted IL-1-induced ACTH secretion, and reversed the interaction between L-NAME and IL-1 beta. The stimulatory action of endotoxin, a lipopolysaccharide that releases endogenous cytokines, was also augmented by inhibition of NO formation.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:In the rat, endogenous nitric oxide modulates the response of the hypothalamic-pituitary-adrenal axis to interleukin-1 beta, vasopressin, and oxytocin. 815 53

Nitric oxide (NO), previously identified with endothelium derived relaxing factor (EDRF), is thought to play a role in central neurotransmission: it is characterized by high lipid solubility and short half life, and NO-synthase, the enzyme which generates NO from L-arginine, has been found in the central nervous system (CNS), both in neuronal and glial cells. NO is believed to be involved in many neural events, such as neurotoxicity from N-methyl-D-aspartate (NMDA) receptor overstimulation, brain damage from vascular stroke, fever, nociception, memory and appetite control. Recent evidence implicates NO as a modulator of endocrine secretions, with inhibition of insulin, growth hormone (GH) and oxytocin release and stimulation of vasopressin (AVP), adrenocorticotropin (ACTH) and corticotropin releasing hormone (CRH) release. NO and prostaglandins could mediate neuroendocrine activities of cytokines such as interleukin-1 (IL-1) and interleukin-2 (IL-2), particularly in the CNS.
...
PMID:Nitric oxide: a gas as a modulator of neuroendocrine secretions. 818 Dec 9

The roles of the sympathetic nervous system, angiotensin II, and arginine vasopressin in the cardiovascular-renal responses to nitric oxide synthesis inhibition were examined in eight conscious dogs equipped with arterial and venous catheters and a nonoccluding bladder catheter. Nitric oxide inhibition was achieved by intravenous infusion of NG-nitro-L-arginine methyl ester (L-NAME) at 37.1 nmol/kg per minute for 140 minutes in the control group. The same dogs, after a 1-week recovery, were pretreated for 2 days with either prazosin for alpha 1 blockade, prazosin plus propranolol for alpha 1 plus beta blockade, L-158,809 for angiotensin receptor blockade, or d(CH2)Tyr(Me)arginine vasopressin for vasopressin-V1 blockade, and the L-NAME infusion was repeated. After 140 minutes of L-NAME infusion into the control group, mean arterial pressure and renal vascular resistance had increased 16% and 71%, and renal blood flow, glomerular filtration rate, urine flow, and urinary sodium excretion had decreased 33%, 16%, 61%, and 64%, respectively. The decrement in renal blood flow and glomerular filtration during L-NAME administration was unaffected by any of the neurohumoral blockers. During V1 blockade L-NAME resulted in only a 3% increase in arterial pressure, attenuation of the renal vascular resistance response, and almost total elimination of the decrease in urine flow. During angiotensin blockade the L-NAME-induced increase in arterial pressure was markedly attenuated, and the decrease in urinary sodium excretion was attenuated in the alpha 1 plus beta blockade group.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Mechanisms involved in the cardiovascular-renal actions of nitric oxide inhibition. 820 34


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---