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N Belova

Publications and source records attributed to N Belova.

11 recordsLinked to original sources
PubMed1995

Role of nitric oxide in control of prolactin release by the adenohypophysis.

Nitric oxide synthase-containing cells were visualized in the anterior pituitary gland by immunocytochemistry. Consequently, we began an evaluation of the possible role of NO in the control of anterior pituitary function. Prolactin is normally under inhibitory hypothalamic control, and in vitro the gland secretes large quantities of the hormone. When hemipituitaries were incubated for 30 min in the presence of sodium nitroprusside, a releaser of NO, prolactin release was inhibited. This suppression was completely blocked by the scavenger of NO, hemoglobin. Analogs of arginine, such as NG-monomethyl-L-arginine (NMMA, where NG is the terminal guanidino nitrogen) and nitroarginine methyl ester, inhibit NO synthase. Incubation of hemipituitaries with either of these compounds significantly increased prolactin release. Since in other tissues most of the actions of NO are mediated by activation of soluble guanylate cyclase with the formation of cyclic GMP, we evaluated the effects of cyclic GMP on prolactin release. Cyclic GMP (10 mM) produced an approximately 40% reduction in prolactin release. Prolactin release in vivo and in vitro can be stimulated by several peptides, which include vasoactive intestinal polypeptide and substance P. Consequently, we evaluated the possible role of NO in these stimulations by incubating the glands in the presence of either of these peptides alone or in combination with NMMA. In the case of vasoactive intestinal polypeptide, the significant stimulation of prolactin release was augmented by NMMA to give an additive effect. In the case of substance P, there was a smaller but significant release of prolactin that was not significantly augmented by NMMA. We conclude that NO has little effect on the stimulatory action of these two peptides on prolactin release. Dopamine (0.1 microM), an inhibitor of prolactin release, reduced prolactin release, and this inhibitory action was significantly blocked by either hemoglobin (20 micrograms/ml) or NMMA and was completely blocked by 1 mM nitroarginine methyl ester. Atrial natriuretic factor at 1 microM also reduced prolactin release, and its action was completely blocked by NMMA. In contrast to these results with prolactin, luteinizing hormone (LH) was measured in the same medium in which the effect of nitroprusside was tested on prolactin release, there was no effect of nitroprusside, hemoglobin, or the combination of nitroprusside and hemoglobin on luteinizing hormone release. Therefore, in contrast to its inhibitory action on prolactin release NO had no effect on luteinizing hormone release. Immunocytochemical studies by others have shown that NO synthase is present in the folliculostellate cells and also the gonadotrophs of the pituitary gland. We conclude that NO produced by either of these cell types may diffuse to the lactotropes, where it can inhibit prolactin release. NO appears to play little role in the prolactin-releasing action of vasoactive intestinal polypeptide and substance P, but mediates the prolactin-inhibiting activity of dopamine and atrial natriuretic factor.

Amino Acid Oxidoreductases↗
PubMed1995

Effect of lesions to the supramammillary area of the posterior hypothalamus on atrial natriuretic peptide release following acute blood volume expansion in conscious Wistar rats.

Acute blood volume expansion (AVE) is a potent stimulus for atrial natriuretic peptide (ANP) release. Since several central nervous structures are well known for their involvement in the regulation of fluid and electrolyte homeostasis and in the secretion of central ANP, we carried our experiments on 33 conscious Wistar rats in order to determine if the integrity of the supramammillary (SMA) hypothalamic area is essential for the peripheral ANP response to AVE. We performed stereotaxic electrolytic lesions of SMA in part of the animals. To obtain AVE we administered 2 mL saline/100 g b.m. for 2 minutes into v. jugularis through the chronically implanted venous catheters. Plasma ANP was assayed radioimmunologically. AVE significantly increased plasma ANP both in the intact animals and in the lesioned rats. This concluded that SMA is not involved in the regulation of peripheral ANP release during AVE.

Animals↗
PubMed1994

Blockade by interleukin-1-alpha of nitricoxidergic control of luteinizing hormone-releasing hormone release in vivo and in vitro.

Nitric oxide (NO) synthase (NOS), the enzyme that converts arginine into citrulline plus NO, the latter a highly active free radical, occurs in a large number of neurons in the brain, including certain neurons in the hypothalamus. Our previous experiments have shown that norepinephrine (NE)-induced prostaglandin E2 (PGE2) release from medial basal hypothalamic explants (MBH) is mediated by NO. Because release of luteinizing hormone (LH)-releasing hormone (LHRH) is also driven by NE and PGE2, we hypothesized that NO controls pulsatile release of LHRH in vivo, which in turn induces pulsatile LH release. Indeed, in vivo and in vitro experiments using an inhibitor of NOS (NG-monomethyl-L-arginine; NMMA) demonstrated that pulsatile LH release is mediated by NO; LHRH release in vitro is also mediated by this free radical. Cytokines that are released from cells of the immune system during infection also inhibit LHRH release. We compared the action of one such cytokine, interleukin-1 alpha (IL-1 alpha), on LHRH release with that of substances which inhibit or induce NO release. Microinjection of IL-1 alpha (0.06 pmol in 2 microliters) into the third cerebral ventricle (3V) of conscious, castrated male rats had an action similar to that of 3V microinjection of NMMA (1 mg in 5 microliters): it blocked pulsatile LH, but not follicle-stimulating hormone (FSH) release. The only difference between the responses to NMMA and IL-1 alpha was that the latency to onset was greater with IL-1 alpha.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effect of dopamine receptor blockade on the renal excretory response to acute volume expansion (AVE) in conscious Brattleboro rats.

UNLABELLED: All the studies were performed on chronically cannulated, conscious Brattleboro rats, housed in metabolic cages under standard conditions. The renal excretory indices: diuresis (V), sodium (UNa.V), potassium (UK.V), chloride (UCl.V) and osmotic (Uosm.V) excretion were measured under the following experimental protocol: (1) controls, (2) 2% volume expansion (AVE)-0.9% NaCl i.v. for 2 min, (3) Dopamine (DA) receptor antagonist Flupentixol (FLU) 0.5 mg.kg-1 i.v., and (4) AVE 10 min after i.v. application of FLU. All the indices studied, given as cumulative curves, showed a firm linearity with time during the whole experimental period (5 h) in groups 1 and 2 (p < 0.05), while such a relationship was not found significantly in groups 3 and 4. AVE quickly, strongly and significantly (p < 0.01) increased V and especially UNa.V, UCl.V and Uosm.V. Pretreatment with FLU potently suppressed the effect of AVE on the renal excretion. FLU alone decreased almost equally V and saliuresis. IN CONCLUSION: the DA antagonist FLU blocks the diuretic and saliuretic response to AVE probably by affecting tubular processes.

Animals↗
PubMed1993

Role of nitric oxide in the control of luteinizing hormone-releasing hormone release in vivo and in vitro.

Nitric oxide (NO) synthase, the enzyme which converts arginine into citrulline plus NO, a highly active free radical, has been found in many neurons in the brain, including neurons in the hypothalamus. Our previous experiments showed that norepinephrine-induced prostaglandin E2 release from hypothalamic explants incubated in vitro is mediated by NO. Since the release of luteinizing hormone-releasing hormone (LHRH) is also driven by norepinephrine and prostaglandin E2, we hypothesized that NO might also control pulsatile release of LHRH in vivo, resulting in turn in pulsatile release of luteinizing hormone (LH). To ascertain the role of NO in control of pulsatile LH release in vivo, an inhibitor of NO synthase, NG-monomethyl-L-arginine (NMMA), was microinjected into the third cerebral ventricle (1 mg/5 microliters) of conscious castrate male rats at time 0 and 60 min later; blood samples were taken every 10 min during this period. NMMA blocked pulsatile LH release within 20 min, and plasma LH concentration declined further without pulses after the injection at 60 min. Pulsatile release of LH was not altered in diluent-injected controls. NMMA did not alter pulsatile release of follicle-stimulating hormone, which suggests that its release does not require NO. Incubation of medial basal hypothalami with norepinephrine (10 microM) induced an increase in LHRH release that was inhibited by NMMA (300 microM). NMMA alone did not alter basal LHRH release, whereas it was augmented by sodium nitroprusside (100 microM), which releases NO spontaneously. This augmentation was prevented by hemoglobin (2 micrograms/ml), which binds the NO released by nitroprusside. Our previous experiments showed that norepinephrine-induced release of prostaglandin E2 is mediated by NO. Nitric oxidergic neurons were visualized in the median eminence adjacent to the LHRH terminals. The combined in vivo and in vitro results indicate that the pulsatile release of LHRH induced by norepinephrine is brought about by alpha 1-adrenergic activation of NO synthase. NO then induces prostaglandin E2 release that activates exocytosis of LHRH secretory granules into the portal vessels to induce pulsatile LH release.

Amino Acid Oxidoreductases↗
PubMed1991

Renal excretory function, atrial natriuretic peptide (ANP) and plasma renin activity (PRA) during long-term sodium loading in rats.

The effect of chronic sodium loading on the level of plasma atrial natriuretic peptide (ANP) and on plasma renin activity (PRA), as well as on the renal excretory function was studied. Fifty-six standardly bred Long Evans rats were divided into three experimental groups: controls, rats drinking 170 mmol NaCl/l solution instead of water, and rats consuming food with high sodium content (850 mmol NaCl/kg) for 21 days. During the study, we measured the amount of fluid intake, the parameters of the renal function: diuresis (VU); sodium, potassium and cloride excretion (UNa V, UKV and UClV), and the dynamics of body mass. On the 21st day the animals were sacrificed by decapitation. Plasma ANP and PRA were determined radioimmunologically. Packed cells volume and plasma Na and Cl concentrations were measured. The data showed a full compensation in sodium balance: the body mass dynamics in the three groups was similar; no changes in packed cells volume and plasma electrolytes were seen; UNaV and UClV were significantly increased in the groups with high sodium intake. PRA was significantly depressed in the two groups while ANP did not show any real changes. We concluded that it is PRA and not ANP that might participate in the regulation of chronic sodium balance.

Animals↗
PubMedDate not supplied

Inhibition of nitric oxide synthase in the hypothalamus blocks the increase in plasma prolactin induced by intraventricular injection of interleukin-1 alpha in the rat.

Injection of interleukin-1 (IL-1) into the third cerebral ventricle (3V) of conscious rats increases plasma prolactin (PRL) concentration. Nitric oxide (NO) is involved in control of corticotropin-releasing factor (CRF) and luteinizing hormone-releasing hormone (LHRH) release. Consequently, we evaluated its role in the PRL-releasing action of IL-1. In the present experiment, NG-mono-methyl-L-arginine (NMMA) (1 mg in 5 microliters of 0.9% NaCl (saline)], an inhibitor of NO synthase, or 5 microliter of saline was microinjected into the 3V of conscious, castrate male rats and blood samples were removed from jugular catheters just prior to and at 10-min intervals after injection. A second injection of NMMA or saline was given 60 min after the first. Five minutes after the injection of NMMA or saline, IL-1 alpha (0.6 pmol in 2 microliter saline), or an equal volume of saline, was injected into the 3V. Plasma PRL concentrations were increased within 10-20 min after injection of IL-1 alpha and a second pulse of PRL usually occurred at 60-70 min following its injection. The maximal increase in plasma PRL from the initial value in the animals injected with IL-1 alpha was highly significant, whereas there was no significant increase in the animals injected with NMMA plus IL-1 alpha or in the animals injected with saline or NMMA. The area under the plasma PRL curve was significantly elevated in the animals injected with IL-1 alpha above that of rats injected with NMMA plus IL-1 alpha during the first hour after injection.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Role of nitric oxide in control of growth hormone release in the rat.

Previous experiments in this and other laboratories have revealed that nitric oxids (NO) plays a role in controlling the release of corticotropin-releasing hormone (CRH) and luteinizing-hormone-releasing hormone (LHRH). Therefore, we have investigated its role in control of growth hormone (GH) release in conscious rats by microinjecting NG-monomethyl-L-arginine (NMMA), an inhibitor of NO synthase (NOS), into the third ventricle (3V) of conscious, freely moving castrate male rats. An initial blood sample (0.3 ml) was drawn from an indwelling intra-atrial catheter just prior to injection of NMMA [1 mg in 5 microliters of 0.9% NaCl (saline)] into the 3V. To maintain the inhibitory action on NOS, a second injection of NMMA was administered into the 3V 60 min after the first. Additional blood samples (0.3 ml) were removed at 10 min intervals for 120 min. Other animals received injections of the diluent at the same times and volumes as NMMA. Interleukin (IL)-1 alpha (0.06 pmol in 2 microliters saline) was injected into the 3V immediately after the first injection of NMMA, whereas other animals received the NMMA diluent followed by IL-1 alpha. The effects of IL-1 alpha were almost identical to those of NMMA in that there was a dramatic lowering of plasma GH achieved primarily by a reduction in height of the GH pulses without a significant reduction in their number.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗