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)

We investigated nitric oxide (NO)-producing neurons in the amygdala which project to the hypothalamic paraventricular nucleus (PVN) of the rat using retrograde tracing and NADPH-diaphorase histochemistry. Numerous NADPH-diaphorase positive neurons with moderate staining were observed mainly in the medial amygdaloid nucleus. We confirmed that these NADPH-diaphorase positive neurons are identical to NO synthase (NOS)-immunoreactive neurons by double staining with NADPH-diaphorase histochemistry and NOS immunocytochemistry. Most neurons containing cholera toxin B subunit (CTb) - which was retrogradely transported from the PVN - were observed in the medial amygdaloid nucleus. In other amygdaloid nuclei, they were observed much less in the central nucleus, basomedial and anterior cortical nucleus. Double labeled neurons by NADPH-diaphorase and CTb were also identified mostly in the medial nucleus. Approximately 40% of the neurons projecting to the PVN were nitrergic neurons and 16% of NADPH-diaphorase positive neurons in the medial nucleus were revealed to project to the PVN. These results suggest that NO-producing neurons in the medial amygdala directly innervate PVN neurons and regulate neuroendocrine systems such as vasopressin and corticotropin releasing factor release.
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PMID:Nitrergic neurons in the medial amygdala project to the hypothalamic paraventricular nucleus of the rat. 944 8

Alterations of the endothelium may play a role in the generation of cerebral vasospasm. The objective of this study was to investigate the involvement of the endothelium and of endogenous endothelin (ET) on the NG-nitro-L-arginine (L-NOARG)-induced contractions in isolated rat basilar arteries. L-NOARG, NG-nitro-L-arginine methyl esther, and methylene blue, but not D-NOARG, induced concentration-dependent contractions and spontaneous vasomotion. The effect of L-NOARG was reversed by L-arginine and submaximally reduced in de-endothelialized arteries. The contractile effect of L-NOARG was completely suppressed by the ET-antagonists BQ 123 and Ro 46-2005 in a part of the basilar arteries. After washout of the respective antagonist, the L-NOARG-induced contraction started, but was not influenced by a second application of the antagonist. In another part of preparations the antagonists failed to influence the L-NOARG-induced contraction. Inconsistent suppressor effects were also observed after preincubation with ketanserin, Manning compound, losartan, or indomethacin. None of these antagonists reversed the established L-NOARG-induced contraction. Thus, endothelium-derived NO suppresses spontaneous contraction and vasomotion in rat basilar arteries. Endogenous ET, 5-HT, vasopressin, angiotensin or cyclooxygenase metabolites do not cause the contraction induced by inhibition of the NO synthase, but may act as 'trigger factors', that may play a role in rat models of cerebral vasospasm or infarction.
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PMID:Contractions induced by NO synthase inhibition in isolated rat basilar artery: role of the endothelium and endogenous vasoconstrictors. 947 Nov 5

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.
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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.
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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.
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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.
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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.
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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.
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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.
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PMID:The contribution of nitric oxide to cardiovascular status and responses to vasodilators in conscious, hypertensive, transgenic ((mRen-2)27) rats. 964 46

1. Nitric oxide (NO) is formed by neuronal NO synthase (nNOS) and acts as a non-conventional neurotransmitter in the brain. A growing body of evidence supports the hypothesis that NO acts to decrease sympathetic output to the periphery; these effects may occur at several autonomic sites. The present review describes studies from our laboratory that address this hypothesis. 2. Restraint stress activates putative NO-producing neurons in many autonomic centres: preoptic area, medial septum, amygdala, hypothalamus, including the paraventricular nucleus (PVN), raphe nuclei, nucleus tractus solitarius (NTS) and ventrolateral medulla (VLM). These results suggest that NO is directly or indirectly involved in regulating sympathetic output to the periphery. 3. Systemic angiotensin II (AngII) activates putative NO-producing neurons in the PVN. These neurons may be activated either by the increases in arterial pressure that accompany AngII injections or due to activation of AngII-containing neural pathways. 4. Hypotension is associated with the activation of putative NO-producing PVN neurons, small numbers of which also project to the NTS or VLM. As the majority of activated neurons is in the magnocellular division, NO production may be related to the production of vasopressin. 5. Adult spontaneously hypertensive rats (SHR) show increased gene expression of nNOS in the hypothalamus, dorsal medulla and caudal VLM. These differences are not present in young prehypertensive SHR, suggesting that the changes in gene expression in adult rats are associated with the increased sympathetic nerve activity found in these rats. 6. Gene expression of nNOS is altered in the hypothalamus and caudal VLM of renal hypertensive rats at 3 and 6 weeks after surgical induction of hypertension. Contrasting results at the two time points may be due to differing underlying physiological processes that characterize the two stages of renal hypertension. 7. Nitric oxide may affect sympathetic output through several possible mechanisms. These include affecting production of the second messenger cGMP and interactions with more classical neurotransmitters or with neurohormonal systems in the brain.
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PMID:Central regulation of autonomic function: no brakes? 967 28


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