NG-Monomethyl-l-arginine co-injection attenuates the thermogenic and hyperthermic effects of E2 prostaglandin microinjection into the anterior hypothalamic preoptic area in rats

Amir, Shimon; Blasio, Emma De; English, Ann M.

doi:10.1016/0006-8993(91)90561-9

Cited by 45 publications

(18 citation statements)

References 17 publications

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“…Therefore, it appears that NOS in the AV3V may not be involved in the AVP and cardiovascular responses to PGE 2 . Although POA application of L-NAME has been reported to block the febrile response to PGE 2 (22), cerebral mechanisms underlying the thermogenic action of PGE 2 may be different from those implicated in the AVP and cardiovascular responses to the prostanoid. Similarly, AV3V application of L-NAME was without signi®cant effect on the responses of AVP and arterial pressure to i.v.…”

Section: Discussionmentioning

confidence: 97%

“…It is known that there may be a functional correlation between PGE 2 and NO. For example, NO can activate cyclooxygenase to promote generation of PGE 2 (20,21), and the febrile response to the application of PGE 2 to the POA was blocked by an NOS inhibitor administered concomitantly (22). Therefore, if AV3V PGE 2 contributes to the AVP and pressor responses to the plasma hypertonicity, NO might also be implicated in these effects.…”

Section: Introductionmentioning

confidence: 99%

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Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats

Yamaguchi

Watanabe²,

Yamaya³

2000

European Journal of Endocrinology

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Objective: To examine local actions of nitric oxide (NO) on the neural mechanisms controlling the release of vasopressin (AVP) and the cardiovascular system in the anteroventral third ventricular region (AV3V), a pivotal area for autonomic functions, and to pursue the problem of whether it may have any role in the AVP and cardiovascular responses evoked by plasma hypertonicity or by increased prostaglandin E 2 (PGE 2 ) in the AV3V ± one possible factor implicated in osmotic responses. Methods: We infused NO-related agents into the AV3V, its adjacent area, the nucleus of the vertical limb of the diagonal band (VDB), or into the lateral cerebral ventricle of conscious rats, monitoring effects on plasma AVP, osmolality, sodium, potassium and chloride, arterial pressure and heart rate in the presence or absence of an osmotic or PGE 2 stimulus. The infusion sites were determined histologically. Results: Infusion of L-arginine, the substrate of NO synthase (NOS), into the AV3V structures such as the median preoptic nucleus and periventricular nucleus produced dose-related increases in plasma AVP, arterial pressure and heart rate 5 or 15 min later, whereas infusion of D-arginine (which is not a substrate for NO synthesis) was without signi®cant effect on these variables. Plasma osmolality or electrolytes were not changed by these treatments. The AV3V infusion of sodium nitroprusside (SNP), a spontaneous releaser of NO, also induced dose-dependent augmentations of plasma AVP, without evoking remarkable alteration in the cardiovascular parameters. The infusion of L-or D-arginine into the VDB affected none of the variables signi®cantly. When applied intracerebroventricularly, Larginine caused only increases in plasma AVP, whereas SNP caused only reductions in arterial pressure, leaving other variables at stable values. The effects of AV3V L-arginine on plasma AVP and the cardiovascular variables were abolished by N G -nitro-L-arginine methyl ester (L-NAME), a potent inhibitor of NOS, applied 15 min before. In contrast, infusion of L-NAME to the AV3V did not exert a signi®cant effect on the responses of plasma AVP or cardiovascular variables to AV3V application of PGE 2 or i.v. infusion of hypertonic NaCl. The infusion of L-NAME alone did not affect plasma variables including AVP, although it tended to increase basal arterial pressure and heart rate. Conclusion: These results suggest that NO generated in or near the AV3V may act to enhance AVP release, arterial pressure and heart rate, but it may not play an essential role in eliciting the responses of these variables to osmotic or PGE 2 stimuli.

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Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats

Yamaguchi

Watanabe²,

Yamaya³

2000

European Journal of Endocrinology

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“…Initially recognized for a primary role in the relaxation of peripheral vasculature, NO has since been implicated in the control of several activities that are at least partially mediated by the preoptic area or hypothalamus (1,3,14). Nitric oxide may influence these behaviors through release of a variety of neurotransmitters and hormonesamong them, dopamine (13).…”

mentioning

confidence: 99%

A Nitric Oxide Synthesis Inhibitor Administered Into the Medial Preoptic Area Increases Seminal Emissions in an Ex Copula Reflex Test

Moses

Hull

1999

Pharmacology Biochemistry and Behavior

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“…L-NAME attenuates the hypothermia produced by insulin, -opioids, hypoxia, and arginine vasopressin, suggesting that NO production is necessary for the development of hypothermia (Steiner et al, 1998;Almeida and Branco, 2001;Benamar et al, 2002). Conversely, NO generation facilitates the hyperthermic actions of morphine, prostaglandin E2, and lipopolysaccharide (Amir et al, 1991;Lin and Lin, 1996;Minano et al, 1997;Benamar et al, 2001).…”

Section: Discussionmentioning

confidence: 99%

“…An accumulating body of evidence suggests that NO participates in thermoregulation. Some studies provide strong evidence that NO production is involved in the hyperthermia evoked by prostaglandin E2, lipopolysaccharide, and morphine (Amir et al, 1991;Minano et al, 1997;Benamar et al, 2001). Furthermore, the injection of L-NAME, a NOS inhibitor, abolishes the fever produced by interleukin-1␤ and lipopolysaccharide (Roth et al, 1998a).…”

mentioning

confidence: 99%

l-NAME (N^ω-Nitro-l-Arginine Methyl Ester), a Nitric-Oxide Synthase Inhibitor, and WIN 55212-2 [4,5-dihydro-2-methyl-4(4-morpholinylmethyl)-1-(1-naphthalenyl-carbonyl)-6H-pyrrolo[3,2,1ij]quinolin-6-one], a Cannabinoid Agonist, Interact to Evoke Synergistic Hypothermia

Tallarida¹,

Gray²,

Geller³

et al. 2003

J Pharmacol Exp Ther

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Cannabinoids evoke profound hypothermia in rats by activating central CB 1 receptors. Nitric oxide (NO), a prominent second messenger in central and peripheral neurons, also plays a crucial role in thermoregulation, with previous studies suggesting pyretic and antipyretic functions. Dense nitric-oxide synthase (NOS) staining and CB 1 receptor immunoreactivity have been detected in regions of the hypothalamus that regulate body temperature, suggesting that intimate NO-cannabinoid associations may exist in the central nervous system. The present study investigated the effect of N -nitro-L-arginine methyl ester (L-NAME), a NO synthase inhibitor, on the hypothermic response to WIN 55212-2 [4,5-dihydro-2-methyl-4(4-morpholinylmethyl)-1-(1-naphthalenylcarbonyl)-6H-pyrrolo[3,2,1ij]quinolin-6-one], a selective cannabinoid agonist, in rats. WIN 55212-2 (1-5 mg/kg, i.m.) produced dose-dependent hypothermia that peaked 45 to 90 min postinjection. L-NAME (10 -100 mg/kg, i.m.) by itself did not significantly alter body temperature. However, a nonhypothermic dose of L-NAME (50 mg/kg) potentiated the hypothermia caused by WIN 55212-2 (0.5-5 mg/kg). The augmentation was strongly synergistic, indicated by a 2.5-fold increase in the relative potency of WIN 55212-2. The inactive enantiomer of WIN 55212-2, WIN 55212, did not produce hypothermia in the absence or presence of L-NAME (50 mg/kg), confirming that cannabinoid receptors mediated the synergy. The present data are the first evidence that drug combinations of NOS blockers and cannabinoid agonists produce synergistic hypothermia. Thus, NO and cannabinoid systems may interact to induce superadditive hypothermia.Cannabis and its derivative compounds, collectively called cannabinoids, evoke an array of pharmacological symptoms in rodents, including hypothermia, analgesia, catalepsy, and hypolocomotion. The discovery of endogenous ligands, such as anandamide and 2-arachidonyl glycerol, which act at cannabinoid receptors, has intensified the interest in the therapeutic potential of cannabinoids (Bisogno et al., 1997). CB 1 receptors are located primarily in the central nervous system (Howlett, 1995), whereas CB 2 receptors are expressed by peripheral immune cells (Dragic et al., 1996).The development of cannabinoid agonists and antagonists has facilitated the characterization of cannabinoid receptor subtypes and their pharmacological profiles. One such agonist is the aminoalkylindole, WIN 55212-2, which exhibits high selectivity for cannabinoid receptors and interacts negligibly with other neurotransmitter systems and ion channels (Martin et al., 1991;Compton et al., 1992). Several reports indicate that WIN 55212-2 elicits hypothermia in rodents via a CB 1 receptor mechanism (Compton et al., 1992;Fan et al., 1994;Fox et al., 2001). Recently, our laboratory confirmed those results by demonstrating that the systemic injection of WIN 55212-2 produces hypothermia that is dependent on CB 1 , but not CB 2 , receptors (Rawls et al., 2002a). Moreover, the injection of WIN 55212-2 ...

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NG-Monomethyl-l-arginine co-injection attenuates the thermogenic and hyperthermic effects of E2 prostaglandin microinjection into the anterior hypothalamic preoptic area in rats

Cited by 45 publications

References 17 publications

Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats

Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats

A Nitric Oxide Synthesis Inhibitor Administered Into the Medial Preoptic Area Increases Seminal Emissions in an Ex Copula Reflex Test

l-NAME (N^ω-Nitro-l-Arginine Methyl Ester), a Nitric-Oxide Synthase Inhibitor, and WIN 55212-2 [4,5-dihydro-2-methyl-4(4-morpholinylmethyl)-1-(1-naphthalenyl-carbonyl)-6H-pyrrolo[3,2,1ij]quinolin-6-one], a Cannabinoid Agonist, Interact to Evoke Synergistic Hypothermia

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NG-Monomethyl-l-arginine co-injection attenuates the thermogenic and hyperthermic effects of E2 prostaglandin microinjection into the anterior hypothalamic preoptic area in rats

Cited by 45 publications

References 17 publications

Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats

Evaluation for roles of nitric oxide generated in the anteroventral third ventricular region in controlling vasopressin secretion and cardiovascular system of conscious rats

A Nitric Oxide Synthesis Inhibitor Administered Into the Medial Preoptic Area Increases Seminal Emissions in an Ex Copula Reflex Test

l-NAME (Nω-Nitro-l-Arginine Methyl Ester), a Nitric-Oxide Synthase Inhibitor, and WIN 55212-2 [4,5-dihydro-2-methyl-4(4-morpholinylmethyl)-1-(1-naphthalenyl-carbonyl)-6H-pyrrolo[3,2,1ij]quinolin-6-one], a Cannabinoid Agonist, Interact to Evoke Synergistic Hypothermia

Contact Info

Product

Resources

About

l-NAME (N^ω-Nitro-l-Arginine Methyl Ester), a Nitric-Oxide Synthase Inhibitor, and WIN 55212-2 [4,5-dihydro-2-methyl-4(4-morpholinylmethyl)-1-(1-naphthalenyl-carbonyl)-6H-pyrrolo[3,2,1ij]quinolin-6-one], a Cannabinoid Agonist, Interact to Evoke Synergistic Hypothermia