Mechanisms mediating NG-nitro-l-arginine methyl ester-induced hypophagia in mice

Hui, Siu‐Chun G.; Chan, Tak-Yuen

doi:10.1016/0014-2999(95)00312-9

Cited by 19 publications

(14 citation statements)

References 32 publications

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“…The decrease in body weight in this group may be mainly caused by L-NAME treatment because NO seems to be involved in the regulation of appetite in mice. 14 During the baroreflex testing and consistent with observations in rats, 3-5 L-NAME-treated mice showed an attenuated pressor response to phenylephrine because, at least in part, the basal values of arterial pressure were already elevated. In contrast, it is conceivable that the exaggerated nitroprussideinduced hypotension in L-NAME mice could be caused by both the high basal arterial pressure levels and the direct donation of NO to the vessels.…”

Section: Discussionsupporting

confidence: 82%

Cardiovascular Neural Reflexes in L-NAME–Induced Hypertension in Mice

2001

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Abstract-The mouse is the most used animal for studying the genetic basis of cardiovascular diseases. However, the mechanisms of regulation of cardiovascular function in this animal are not yet well understood. The goal of this study was to evaluate the baroreflex, the Bezold-Jarisch cardiopulmonary reflex (BJR), and the chemoreflex in mice with hypertension induced by inhibition of NO using N-nitro-L-arginine-methyl ester (L-NAME). Basal mean arterial pressure (MAP) measured under anesthesia (urethane, 1 mg/g IP) was significantly higher in L-NAME (400 g/g IP for 7 days)-treated (HT) mice (nϭ7) compared with vehicle-treated (NT; nϭ10) animals (126Ϯ9 versus 79Ϯ2 mm Hg) without differences in heart rate (HR). Baroreflex sensitivity, evaluated using phenylephrine (1 g/g IV) was enhanced in HT mice compared with NT mice (Ϫ9.8Ϯ1.4 versus Ϫ4.9Ϯ0.5 bpm/mm Hg). The BJR, induced by phenylbiguanide (40 ng/g IV), was significantly attenuated in HT animals (MAP, Ϫ13Ϯ5%; HR, Ϫ39Ϯ6%) compared with NT animals (MAP, Ϫ38Ϯ5%; HR, Ϫ66Ϯ2%). The chemoreflex, induced by potassium cyanide (0.26 g/g IV), was significantly attenuated in HT animals (MAP, ϩ14Ϯ4%; HR, Ϫ8Ϯ2%) compared with NT animals (MAP, ϩ29Ϯ4%; HR, Ϫ15Ϯ4%). As has been observed in rats, chronic inhibition of NO synthase in mice results in arterial hypertension. Enhancement of baroreflex sensitivity and attenuation of BJR and chemoreflex seem to be mainly caused by inhibition of NO synthesis because individual analyses did not show positive correlation between changes in these reflexes and MAP levels in the HT group. Key Words: hypertension, experimental Ⅲ mice Ⅲ L-NAME Ⅲ baroreflex Ⅲ reflex M olecular biology techniques have permitted the development of genetically altered animals, in which genes controlling a specific function are overexpressed or disrupted to enable study of the contribution of the respective gene product to a specific disease. For practical reasons, the mouse has been the most genetically altered animal. Although transgenic mice are increasingly available to be used in cardiovascular research, knowledge about the normal physiological and pathophysiological characteristics of the murine cardiovascular system is still limited.After the first demonstration that chronic administration of the NO synthase inhibitor N-nitro-L-arginine methyl ester (L-NAME) causes arterial hypertension in rats 1 and our demonstration that the sympathetic nervous system plays a major role in L-NAME-induced hypertension in rats, 2 many interesting data have been obtained in this model of experimental hypertension. It has also been shown that L-NAME hypertension in rats is characterized by changes in baroreflex control of cardiovascular function 3-5 and a profound enhancement of the Bezold-Jarisch cardiopulmonary reflex. 6 Although it has been demonstrated that chronic administration of L-NAME also leads to arterial hypertension in mice, 7 no previous studies have systematically evaluated the effects of chronic inhibition of NO synthase on the neural reflex control of cardiovas...

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Section: Discussionsupporting

confidence: 82%

Cardiovascular Neural Reflexes in L-NAME–Induced Hypertension in Mice

2001

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“…Vasodilatory activity of Barnidipine was demonstrated in several types of vessels, including coronary, aorta and mesenteric arteries (Inagaki et al, 1999;Nakayama et al, 1989;van der Lee et al, 1998). In addition, several favourable effects on renal functions have been documented with Barnidipine in different animal models of hypertension (Hashimoto et al, 1999;Kaizu et al, 1995;Kawashima et al, 1991;Kimura et al, 1998;Saitoh et al, 1995).…”

Section: Introductionmentioning

confidence: 95%

Barnidipine ameliorates the vascular and renal injury in l-NAME-induced hypertensive rats

Yıldırım

Kizilay

Ergin

et al. 2015

European Journal of Pharmacology

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“…Some studies have suggested an interaction between NO and other neurotransmitters such as dopamine (DA) [18,28,37,51], noradrenaline [51], GABA [63], acetylcholine (Ach) [56,62] and 5-HT [11,23,38,66]. In the medial preoptic area, NO has been shown by a microdialysis method to increase 5-HT and DA levels [38].…”

Section: Considerable Relationship Between Nadph-d-positive Neurons Amentioning

confidence: 99%

Distribution of NADPH-Diaphorase-Positive Neurons in the Mouse Brain: Differences from Previous Findings in the Rat Brain and Comparison with the Distribution of Serotonergic Neurons.

Matsushita

Takeuchi

Kawata

et al. 2001

Acta Histochem. Cytochem

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Mechanisms mediating NG-nitro-l-arginine methyl ester-induced hypophagia in mice

Cited by 19 publications

References 32 publications

Cardiovascular Neural Reflexes in L-NAME–Induced Hypertension in Mice

Cardiovascular Neural Reflexes in L-NAME–Induced Hypertension in Mice

Barnidipine ameliorates the vascular and renal injury in l-NAME-induced hypertensive rats

Distribution of NADPH-Diaphorase-Positive Neurons in the Mouse Brain: Differences from Previous Findings in the Rat Brain and Comparison with the Distribution of Serotonergic Neurons.

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