Drinking and blood pressure responses to central injection of L-NAME in conscious rats

Camargo

et al. 1999

Braz J Med Biol Res

The drinking behavior responses to centrally administered N G -nitro-L-arginine methyl ester (L-NAME; 10, 20 or 40 µg/µl), an inhibitor of nitric oxide synthase, were studied in satiated rats, with cannulae stereotaxically implanted into the lateral ventricle (LV) and subfornical organ (SFO). Water intake increased in all animals after angiotensin II (ANG II) injection into the LV, with values of 14.2 ± 1.4 ml/ h. After injection of L-NAME at doses of 10, 20 or 40 µg/µl into the SFO before injection of ANG II (12 ng/µl) into the LV, water intake decreased progressively and reached basal levels after treatment with 0.15 M NaCl and with the highest dose of L-NAME (i.e., 40 µg). The water intake obtained after 40 µg/µl L-NAME was 0.8 ± 0.01 ml/h. Also, the injection of L-NAME, 10, 20 or 40 µg/µl, into the LV progressively reduced the water intake induced by hypertonic saline, with values of 5.3 ± 0.8, 3.2 ± 0.8 and 0.7 ± 0.01 ml/h, respectively. These results indicate that nitric oxide is involved in the regulation of drinking behavior induced by centrally administered ANG II and cellular dehydration and that the nitric oxide of the SFO plays an important role in this regulation.

Section: Discussionsupporting

confidence: 92%

Effect of injection of L-NAME on drinking response

Camargo

et al. 1999

Braz J Med Biol Res

European Journal of Endocrinology

“…Therefore, if AV3V PGE 2 contributes to the AVP and pressor responses to the plasma hypertonicity, NO might also be implicated in these effects. In agreement with this view, Liu et al (23) have reported that the intracerebroventricular (i.c.v.) injection of a potent NOS inhibitor (24,25), N G -nitro-L-arginine methyl ester (L-NAME) ± a treatment that may allow the drug to act on the AV3V (26) ± attenuated the effect of an osmotic stimulus on the water intake of rats.…”

Section: Introductionmentioning

confidence: 55%

“…The fact that the AV3V infusion of L-NAME in¯uenced neither the effects of plasma hypertonicity nor those of PGE 2 , one cerebral factor engaged in the osmotic responses (18,37), suggests that NOS activity in the AV3V may not have an essential role in regulating AVP release and arterial pressure in the hyperosmotic state. In contrast to this view, Liu et al (23) have reported inhibition of osmotic drinking by i.c.v. L-NAME, suggesting a possible role of periventricular NOS activity in the osmosensitivity.…”

Section: Discussionmentioning

confidence: 86%

See 1 more Smart Citation

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

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.

“…The vasodilatation induced by moxonidine was almost totally blocked by central L-NAME, while the bradycardia was not affected; this suggests that different central mechanisms are activated by moxonidine to induce vasodilatation and bradycardia. It is well accepted that NO either peripherally or centrally has an important role in the maintenance of blood pressure (Calver et al, 1993;Zanzinger et al, 1995;Liu et al, 1996). Inhibition of peripheral NOS results in increased arterial pressure, an indication that NO produced at its basal rate by the vascular endothelium causes vasodilatation (Rees et al, 1989).…”

Section: Ts Moreira Et Al Moxonidine-induced Hypotension: Possible mentioning

confidence: 99%

Central blockade of nitric oxide synthesis reduces moxonidine‐induced hypotension

Moreira

Takakura

Menani

et al. 2004

British J Pharmacology

1 Nitric oxide (NO) and a 2 -adrenoceptor and imidazoline agonists such as moxonidine may act centrally to inhibit sympathetic activity and decrease arterial pressure. 2 In the present study, we investigated the effects of pretreatment with L-NAME (NO synthesis inhibitor), injected into the 4th ventricle (4th V) or intravenously (i.v.), on the hypotension, bradycardia and vasodilatation induced by moxonidine injected into the 4th V in normotensive rats. 3 Male Wistar rats with a stainless steel cannula implanted into the 4th V and anaesthetized with urethane were used. Blood flows were recorded by use of miniature pulsed Doppler flow probes implanted around the renal, superior mesenteric and low abdominal aorta. 4 Moxonidine (20 nmol), injected into the 4th V, reduced the mean arterial pressure (À4273 mmHg), heart rate (À2277 bpm) and renal (À62715%), mesenteric (À4178%) and hindquarter (À5078%) vascular resistances. 5 Pretreatment with L-NAME (10 nmol into the 4th V) almost abolished central moxonidineinduced hypotension (À1073 mmHg) and renal (À1074%), mesenteric (À1174%) and hindquarter (À1376%) vascular resistance reduction, but did not affect the bradycardia (À1878 bpm). 6 The results indicate that central NO mechanisms are involved in the vasodilatation and hypotension, but not in the bradycardia, induced by central moxonidine in normotensive rats.