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 neuroanatomical distribution of nitric oxide synthase-immunoreactive neurons was investigated in post mortem hypothalami of 10 patients suffering from schizophrenia, eight patients with depression and 13 matched control cases. Neuronal nitric oxide synthase containing nerve cells were detected in several hypothalamic nuclei including the medial preoptic region, the ventromedial, infundibular and suprachiasmatic nuclei and the lateral hypothalamus. The vast majority of hypothalamic nitric oxide synthase-immunoreactive neurons was found to be located in the paraventricular nucleus. Both magno and parvocellular paraventricular neurons contained the enzyme. A small subset of immunoreactive parvocellular paraventricular neurons co-expresses corticotropin-releasing hormone. The supraoptic nucleus did not contain nitric oxide synthase-immunoreactive neurons. Cell counts of paraventricular nitric oxide synthase-positive neurons in controls, schizophrenics and depressed patients revealed a statistically significant reduction of cell density in the right paraventricular nucleus of depressed patients and schizophrenics as compared to controls. The total amount of nitric oxide synthase-immunoreactive paraventricular neurons was smaller in depressive and schizophrenic patients than in normal cases. The putative pathophysiologic significance of the reduced expression of paraventricular nitric oxide synthase in depressive patients might be related to the supposed regulatory function of nitric oxide in the release of corticotropin-releasing hormone and arginine-vasopressin and/or oxytocin, which have been reported to be over-expressed in the so-called endogenous psychoses, especially in depression.
 ...
PMID:Nitric oxide synthase-containing neurons in the human hypothalamus: reduced number of immunoreactive cells in the paraventricular nucleus of depressive patients and schizophrenics. 948 70

To investigate the role of nitric oxide (NO) and its interaction with oxygen radicals in fever, we injected conscious rabbits intravenously (i.v.) with 1 microgram/kg bacterial lipopolysaccharide (LPS) and measured body temperatures, and circulatory and respiratory parameters. We estimated plasma levels of antidiuretic hormone (ADH); nitrate as a measure of NO metabolism under aerobic conditions; prostaglandin E2 (PGE2) and prostaglandin PGF2 alpha (PGF2 alpha); and tumor necrosis factor alpha (TNF alpha). We studied the effects of LPS before and after treatment with oxygen radical scavengers superoxide dismutase and catalase (SOD/CAT), before and after treatment with NG-monomethyl-L-arginine (L-NMMA), a specific blocker of nitric oxide synthase (NOS), before and after treatment with methylene blue (MB). N-methyl-D-aspartate (NMDA) receptors were blocked with ketamine. LPS increased core temperature by 1.1 +/- 0.1 degree C within 3 h, associated with a rapid increase of plasma TNF alpha, PGE2 and PGF2 alpha, and a fall of nitrate. The decrease of nitrate following LPS was augmented in rabbits pretreated with SOD/CAT, associated with a rise of core temperature of 1.6 +/- 0.1 degree C within 3 h. The lowest levels of nitrate were observed in rabbits pretreated with L-NMMA, associated with a rise of core temperature of 3.0 +/- 0.1 degree C within 3 h. Treating the same rabbits with a continuous i.v. infusion of 5 mg/kg/h MB, starting 30 min before injection of LPS, caused an immediate increase in nitrate and completely prevented fever. The rise of TNF alpha and ADH after LPS, however, was not significantly different from the control fever, and plasma PGE2 levels were nearly twice as elevated. MB also prevented fever in NMMA-treated rabbits, but only as long as nitrate levels remained elevated. MB induced an immediate rise of core temperature in ketamine-treated rabbits. We conclude that an undisturbed or elevated synthesis of NO in the central nervous system prevents fever, possibly via positive feedback action of NO on presynaptic glutaminergic neurons.
 ...
PMID:Antipyretic role of nitric oxide during endotoxin-induced fever in rabbits. 950 19

Intracerebroventricular (I.C.V.) administration of an inhibitor of nitric oxide synthase (NOS) increases oxytocin but not vasopressin secretion, in dehydrated rats [38]. Surprisingly, central injection of L-arginine, the substrate for NOS, caused a similar effect. Kyotorphin (L-tyrosyl-L-arginine), a dipeptide formed from L-arginine by kyotorphin synthetase in the brain may mediate this magnocellular response. Therefore, the dose and time responses of hormone release were compared following I.C.V. injection of kyotorphin and L-arginine to conscious rats that were normally hydrated or deprived of water for 24 h. In water-sated rats, both L-arginine and kyotorphin increased blood pressure and plasma glucose levels coincident with elevating circulating levels of oxytocin, but not vasopressin. In dehydrated animals, both L-arginine and kyotorphin increased plasma oxytocin levels with a similar time course but only kyotorphin decreased vasopressin release. D-arginine, like L-arginine, stimulated secretion of oxytocin, indicating a nonstereospecific effect. A kyotorphin receptor antagonist (L-leucyl-L-arginine) given I.C.V. to dehydrated animals elevated plasma oxytocin and prevented the decrease in vasopressin levels after kyotorphin. Thus, kyotorphin, but not L-arginine, appears to attenuate release of vasopressin either directly from magnocellular neurons or indirectly via modulating compensatory reflexes activated by the pressor response. On the other hand, an excess of L-arginine and kyotorphin within the CNS may mimic the stress response by augmenting release of oxytocin and activating the sympathetic nervous system to increase blood pressure and plasma glucose levels.
 ...
PMID:Effects of central injection of kyotorphin and L-arginine on oxytocin and vasopressin release and blood pressure in conscious rats. 952 14

The thick ascending limb of Henle's loop (TAL) is involved in the urinary dilution/concentration process by actively reabsorbing NaCl through a complex mechanism. Some years ago, compelling evidence was provided that cAMP stimulates NaCl reabsorption through the activation of adenylyl cyclase by several hormones other than antidiuretic hormone (ADH). Synthesis of cyclic AMP is inhibited by prostaglandin E2 (PGE2) and arachidonic acid per se, via the pertussis toxin-sensitive protein Gi activation. Cyclic GMP cascade down-regulates NaCl reabsorption, through activation of both guanylyl cyclase receptors (by ANF and urodilatin), and soluble guanylyl cyclase (by nitric oxide, NO). In TAL, NO is produced by the cytokine-inducible form of NO synthase, but not by the constitutive one. Agonists known to activate protein kinase C (PKC) in TAL elicit opposite effects on NaCl reabsorption. Five PKC isoforms belonging to the conventional, novel, and atypical enzyme subclasses have been recently defined in TAL and might differently regulate NaCl flux. Increments in intracellular calcium ([Ca2+]i) inhibit NaCl reabsorption via three pathways: (i) a possible direct effect on ion channels, (ii) a PLA2-mediated production of arachidonic acid derivatives (20-HETE), and (iii) inhibition of the ADH-induced cAMP accumulation. This last effect results from activation of phosphodiesterase (common to the agents that increase [Ca2+]i), and inhibition of adenylyl cyclase (only elicited by Ca2+c). Finally, the apical localization of some agonists effects is documented.
 ...
PMID:Transducing pathways involved in the control of NaCl reabsorption in the thick ascending limb of Henle's loop. 955 29

Recently, we have demonstrated a decreased neuronal isoform of nitric oxide synthase (nNOS) message in the hypothalamus of rats with heart failure (HF). The purpose of this study was to determine the changes in NADPH-diaphorase (a commonly used marker for neuronal NOS activity) positive neurons in specific hypothalamic sites of rats with HF. After a standard histochemical protocol, NOS positive neurons were measured in paraventricular nucleus (PVN), supraoptic nucleus (SON), median preoptic area (MePO), subfornical organ (SFO), organum vasculosum of the lamina terminalis (OVLT) and lateral hypothalamus (LH) of rats with coronary artery ligation (HF group; n=8) and sham-operated control rats (n=9). A total of 4 months after coronary ligation, the rats in the HF group displayed infarcts greater than at least 35% of the left ventricular wall (n = 8). Sham-operated rats had no observable damage to the myocardium. Rats with HF had a significantly lower number of NOS positive cells in the PVN (36% less) compared to sham rats. The number of NOS positive cells remained unaltered in the SON, MePO and LH in rats with HF. Conversely there was an increased number of NOS positive cells in the SFO (42% greater) and OVLT (100% greater). These data support the conclusion that the NO system within the hypothalamus involved in controlling autonomic outflow is altered during HF and may contribute to the elevated levels of vasopressin and sympatho-excitation commonly observed in HF.
 ...
PMID:Altered number of diaphorase (NOS) positive neurons in the hypothalamus of rats with heart failure. 955 24

NG-nitro-L-arginine methyl ester (L-NAME; 250 micrograms/5 microliters), an inhibitor of NO synthase, or the vehicle artificial cerebrospinal fluid (aCSF; 5 microliters) was administered intracerebroventricularly to conscious rats hemorrhaged (0.7 ml/min) to a 20% volume depletion. Hypotension was maximal 5 min after hemorrhage ended, with compensatory recovery to basal levels 20 min later, regardless of drug treatment. L-NAME, however, elevated (P < 0.05) blood pressure (vs. aCSF controls) 40-45 min after intracerebroventricular administration. In normovolemic rats, L-NAME produced a significant pressor response and increased plasma levels of vasopressin (VP) and oxytocin (OT). After hemorrhage, both hormone levels increased, but only OT was further enhanced by L-NAME. Thus centrally produced NO tonically inhibits OT and VP secretion under basal normovolemic conditions and selectively inhibits OT release during hypovolemia. Hemorrhage increased the rates of glucose utilization in the neural lobe, indicative of enhanced efferent neural functional activity. L-NAME further enhanced the metabolic activity in the entire hypothalamoneurohypophysial system of hemorrhaged animals. Several other brain structures involved in the regulation of blood pressure and the stress response were also metabolically affected by the hemorrhage and L-NAME.
 ...
PMID:Effects of L-NAME on cerebral metabolic, vasopressin, oxytocin, and blood pressure responses in hemorrhaged rats. 957 71

To assess the interaction of endothelin (ET) with nitric oxide (NO) and the effects on venous circulation and handling of renal water and electrolytes, ET (1.0 ng/kg/min) or saline was administered with or without three doses (0.27, 2.7 and 27 ng/kg/min for 40 min) of N omega-nitro-L-arginine methyl ester (L-NAME), and NO synthase inhibitor, in anesthetized dogs. ET increased total peripheral resistance (TPR), pulmonary capillary wedge pressure (PCWP), urine flow (UF), and urinary K excretion (UKV), and decreased cardiac output (CO), urinary osmolality (Uosm), renal plasma flow (RPF), and glomerular filtration rate (GFR). L-NAME increased blood pressure (BP), TPR, PCWP, right atrial pressure (RAP), and mean circulatory filling pressure (MCFP), and decreased CO, RPF, and GFR, ET plus L-NAME markedly increased TPR, resistance to venous return, and plasma atrial natriuretic peptide (ANP), but not BP and MCFP, and curtailed the ET-induced responses in UF, UKV, and Uosm. Plasma aldosterone (ALD) was decreased in all groups, but plasma vasopressin (AVP) and renin activity (PRA) were not altered in any group. These results indicate that ET-induced NO formation might mitigate increases in venous as well as arterial vascular resistance and changes in renal handling of water and electrolytes, and might also play an inhibitory role in ANP release but not in PRA or AVP and ALD release.
 ...
PMID:Effects of endothelin-induced nitric oxide on venous circulation and renal water-electrolyte handling. 959 20

Intracerebroventricular (i.c.v.) injection of the inhibitor of NO synthase (NOS), N(G)-nitro-L-arginine methyl ester (L-NAME) (250 microg/5 microL) attenuated the drinking response in rats deprived of water for 24 h. Moreover, oxytocin (OT) levels in plasma increased after 2 min, whereas both oxytocin and vasopressin levels were elevated at 120 min after intracerebroventricular injection. The delayed effect of L-NAME on both hormones was not observed in dehydrated animals allowed to drink water. Blood pressure remained stable after injection of artificial cerebrospinal fluid (aCSF) in dehydrated rats not allowed to drink. In rats having access to water, however, there was an immediate but transient pressor response (0-5 min) with a delayed hypotension from 45 to 120 min. L-NAME consistently increased blood pressure in a biphasic mode, whether the animals drank or not, with an early peak at 5 min that decayed after 15-30 min and a second pressor response beginning at 30-45 min and remaining elevated at 120 min when the experiment ended. These pressor responses were independent of the adrenal glands. Thus, centrally produced nitric oxide facilitates drinking, inhibits release of vasopressin and oxytocin from the magnocellular system, and maintains resting arterial blood pressure in normally hydrated and dehydrated rats.
 ...
PMID:Nitric oxide control of drinking, vasopressin and oxytocin release and blood pressure in dehydrated rats. 961 97

Although two-way communication between the hypothalamus and the immune system in now well established, particularly for the hypothalamo-pituitary-adrenal axis, the role of the gaseous neurotransmitters nitric oxide (NO) and carbon monoxide (CO) is much less well understood in terms of hypothalamic function. These agents are an important part of the peripheral inflammatory response; and their synthetic enzymes, NO synthase (NOS) and heme oxygenase (HO), respectively, have been localized to the hypothalamic PVN and SON. The induced generation of both NO and CO leads to the suppression of CRH and vasopressin, the major stimulators of the HPA. Thus, the addition of hemin to hypothalamic explants is maximally active at 1 microM in attenuating the release of CRH and vasopressin, and this dose is also most effective in generating biliverdin and associated CO. CO generation is also able to stimulate cyclooxygenase to produce prostaglandin E2, an established intermediary in the cytokine-stimulated activation of the HPA. Finally, inducible NOS mRNA is specifically induced in the hypothalalmus in response to endotoxin, in parallel to interleukin-1. These data provide increasing evidence in favor of NO and CO as counterregulatory agents in the HPA response to immune activation.
 ...
PMID:Acute and subacute effects of endotoxin on hypothalamic gaseous neuromodulators. 962 53

1. The aim of the study was to measure the regional haemodynamic responses to vasodilators, and the effects of nitric oxide (NO) synthase inhibition, in conscious, hypertensive, transgenic ((mRen-2)27) rats (TG rats) and normotensive, Hannover Sprague-Dawley (SD) rats. 2. The hypotensive response to acetylcholine was greater in TG than in SD rats, but the renal vasodilator responses were not different. 3. The responses to bradykinin were similar in the two strains, except that hindquarters vasodilatation occurred only in SD rats. 4. Salbutamol caused smaller renal and hindquarters vasodilatation in TG rats than in SD rats, and there was mesenteric vasodilatation only in the latter strain. 5. The hypotensive response to sodium nitroprusside was smaller, but the accompanying mesenteric vasodilatation was greater, in SD than in TG rats. 6. The contribution of NO to the vasodilator responses was taken as the difference between the responses in the presence of the NO synthase inhibitor, NG-nitro-L-arginine methylester (L-NAME), compared to those in the presence of a co-infusion of angiotensin II and vasopressin (to match the haemodynamic effects of L-NAME). 7. In TG rats, L-NAME caused a greater absolute pressor effect, but a smaller mesenteric vasoconstriction, than in SD rats. 8. L-NAME affected the vasodilator responses to all the challenges similarly in the two strains. 9. Collectively, the results provide no direct evidence for impaired NO-mediated vasodilator mechanisms in TG rats. It is feasible that the reduced hindquarters response to bradykinin and the reduced renal and hindquarters responses to salbutamol, in TG rats are due to abnormal beta2-adrenoceptor-mediated processes.
 ...
PMID:The contribution of nitric oxide to cardiovascular status and responses to vasodilators in conscious, hypertensive, transgenic ((mRen-2)27) rats. 964 46


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