Biomedical subjects

José V Menani

Publications and source records attributed to José V Menani.

9 recordsLinked to original sources

PubMed2006

AV3V lesions reduce the pressor response to L-glutamate into the RVLM.

Neurons from the rostral ventrolateral medulla (RVLM) directly activate sympathetic pre-ganglionic neurons in the spinal cord. Hypertensive responses and sympathetic activation produced by different stimuli are strongly affected by lesions of the preoptic periventricular tissue surrounding the anteroventral third ventricle (AV3V region). Therefore, in the present study, we investigated the effects of acute (1 day) and chronic (15 days) electrolytic lesions of the AV3V region on the pressor responses produced by injections of the excitatory amino acid L-glutamate into the RVLM of unanesthetized rats. Male Holtzman rats with sham or electrolytic AV3V lesions and a stainless steel cannula implanted into the RVLM were used. The pressor responses produced by injections of L-glutamate (1, 5 and 10 nmol/100 nl) into the RVLM were reduced 1 day (9 +/- 4, 39 +/- 6 and 37 +/- 4 mm Hg, respectively) and 15 days after AV3V lesions (13 +/- 6, 39 +/- 4 and 43 +/- 4 mm Hg, respectively, vs. sham lesions: 29 +/- 3, 50 +/- 2 and 58 +/- 3 mm Hg, respectively). Injections of L-glutamate into the RVLM in sham or AV3V-lesioned rats produced no significant change in the heart rate (HR). Baroreflex bradycardia and tachycardia produced by iv phenylephrine or sodium nitroprusside, respectively, and the pressor and bradycardic responses to chemoreflex activation with iv potassium cyanide were not modified by AV3V lesions. The results suggest that signals from the AV3V region are important for sympathetic activation induced by L-glutamate into the RVLM.

Analysis of Variance↗

PubMed2005

Potassium intake during cell dehydration.

Isotonic NaCl is ingested in addition to water by cell-dehydrated rats in two-bottle tests. The objective of the present work was to find out whether mineral intake in the cell-dehydrated rat is specific to NaCl in a five-bottle test. Adult male Sprague Dawley rats had distilled water and four mineral solutions at palatable concentrations (0.01 M KCl, 0.05 mM CaCl2, 0.15 M NaHCO3, 0.15 M NaCl) simultaneously available for consumption. Cell-dehydration was produced infusing 1.5 ml of NaCl solution (0.15, 0.25, 0.5, 1.0, 2.0, 4.0 M) intravenously for 10 min and intakes were recorded for the next hour. It was observed a NaCl concentration-dependent increase in 0.01 M KCl intake. The ingestion of the other mineral solutions was not significantly altered compared to infusion of 0.15 M NaCl. The ingestion of KCl was not related to changes in serum potassium concentration. The ingestion of KCl was reduced in half and water was the preferred fluid when the five-bottle test was performed with mineral solutions at isomolar (0.15 M) concentrations. There was no increase in intake of other mineral solution in the isomolar test. No preference was observed for palatable or isomolar solutions during early extracellular dehydration until 4 h after subcutaneous injection of furosemide, in spite of the increase in total volume intake. Therefore, mineral intake induced by cell dehydration is not specific for NaCl solution. The type of mineral solution available influences the choice and KCl is the preferred solution of the cell-dehydrated rat in the conditions of the present study.

Analysis of Variance↗

PubMed2004

Cardiovascular responses to microinjection of L-glutamate into the NTS in AV3V-lesioned rats.

The excitatory amino acid L-glutamate injected into the nucleus of the solitary tract (NTS) in unanesthetized rats similar to peripheral chemoreceptor activation increases mean arterial pressure (MAP) and reduces heart rate. In this study, we investigated the effects of acute (1 day) and chronic (15 days) electrolytic lesions of the preoptic-periventricular tissue surrounding the anteroventral third ventricle (AV3V region) on the pressor and bradycardic responses induced by injections of L-glutamate into the NTS or peripheral chemoreceptor activation in unanesthetized rats. Male Holtzman rats with sham or electrolytic AV3V lesions and a stainless steel cannula implanted into the NTS were used. Differently from the pressor responses (28+/-3 mm Hg) produced by injections into the NTS of sham-lesioned rats, L-glutamate (5 nmol/100 nl) injected into the NTS reduced MAP (-26+/-8 mm Hg) or produced no effect (2+/-7 mm Hg) in acute and chronic AV3V-lesioned rats, respectively. The bradycardia to l-glutamate into the NTS and the cardiovascular responses to chemoreflex activation with intravenous potassium cyanide or to baroreflex activation with intravenous phenylephrine or sodium nitroprusside were not modified by AV3V lesions. The results show that the integrity of the AV3V region is essential for the pressor responses to L-glutamate into the NTS but not for the pressor responses to chemoreflex activation, suggesting dissociation between the central mechanisms involved in these responses.

Animals↗

PubMed2004

Central blockade of nitric oxide synthesis reduces moxonidine-induced hypotension.

1. Nitric oxide (NO) and alpha(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 (-42+/-3 mmHg), heart rate (-22+/-7 bpm) and renal (-62+/-15%), mesenteric (-41+/-8%) and hindquarter (-50+/-8%) vascular resistances. 5. Pretreatment with l-NAME (10 nmol into the 4th V) almost abolished central moxonidine-induced hypotension (-10+/-3 mmHg) and renal (-10+/-4%), mesenteric (-11+/-4%) and hindquarter (-13+/-6%) vascular resistance reduction, but did not affect the bradycardia (-18+/-8 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.

Animals↗

PubMed2003

Effect of the gadolinium ion on body fluid regulation.

Both osmoreception and baroreception are thought to involve ion channels that are sensitive to changes in membrane stretch. We investigated the effect of a blocker of stretch-activated ion channels, the Gd3+ ion, on osmoregulatory and cardiovascular responses in the intact rat. Intracerebroventricular injection of 50-100 nmol Gd3+ reduced thirst induced by various treatments. Similar doses also reduced intake of saline induced by various treatments. Intracerebroventricular injection of 100 nmol Gd3+ transiently increased arterial pressure and reduced the pressor response to intracerebroventricular angiotensin II (Ang II). Systemic administration of Gd3+ failed to alter thirst, except for a high dose (270 micromol/kg) that induced illness. This high dose failed to prevent urinary hypertonicity and excretion of a load of hypertonic NaCl. Intravenous infusion of 270 micromol/kg of Gd3+ reduced blood pressure and pressure responses to intravenous phenylephrine, but did not reduce the baroreceptor reflex control of heart rate. We conclude that the effects of Gd3+ on thirst and on the cardiovascular system are probably not due to a direct effect of the drug on stretch-sensitive ion channels. Instead, many of the effects of Gd3+ were compatible with blockade of voltage-gated Ca2+ channels.

Angiotensin II↗

PubMed2002

Ingestion of hypertonic NaCl vs. palatable drinks by sodium-depleted rats.

This work investigated whether the preference for NaCl solution is shifted to more palatable solutions in the adult male sodium-depleted rat (n=6-10 per group). Animals had daily access to three bottles, one containing water, another 1.8% NaCl (300 mM), and a third containing 0.9% NaCl (150 mM), Gatorade (orange--OG or grape flavored--GG), orange juice (sweetened or unsweetened, from concentrate), or 10% sucrose (no sodium). Sodium content in Gatorade and orange juice ranged from 7 to 14 mEq/l. Daily intakes were recorded for at least 5 days prior to sodium depletion. Then, the animals were depleted of sodium (diuretic plus sodium-deficient diet and water for 24 h). Then, the other two bottles were returned to the animals and the intakes were recorded for 120 min (sodium preference test, SPT). Daily intake from the third bottle (except for unsweetened orange juice) at least doubled the daily 1.8% NaCl intake. The average 1.8% NaCl intake (13+/-2 ml) in the SPT was higher than the intake of 10% sucrose (6+/-1 ml) or of any other solution (less than 6 ml). The intakes of 1.8% NaCl and 0.9% NaCl (10+/-3 ml) were similar during the SPT. The animals also preferred 0.9% NaCl (27+/-1 ml) to OG (3+/-1 ml) in the absence of 1.8% NaCl in the SPT. Therefore, the preference for sodium in sodium-depleted rats also applies when palatable and nutritive solutions are simultaneously available.

Animals↗

PubMed2002

Interaction between brain L-type calcium channels and alpha2-adrenoceptors in the inhibition of sodium appetite.

Calcium channels mediate the actions of many drugs. The present work investigated whether diltiazem, an L-type calcium channel blocker, alters the inhibition of sodium appetite induced by noradrenaline and the alpha2-adrenoceptor agonist clonidine. Adult male Holtzman rats (N=4-8) with cannula implanted into the third cerebral ventricle were submitted to sodium depletion (furosemide sc+24-h removal of ambiente sodium). Sodium depleted control animals that received 0.9% NaCl as vehicle injected intracerebroventricularly (i.c.v.) ingested 13.0+/-1.5 ml/120 min of 1.8% NaCl. Intracerebroventricular injection of either noradrenaline (80 nmol) or clonidine (20 nmol) inhibited 1.8% NaCl intake from 70 to 90%. Prior i.c.v. injection of diltiazem (6-48 nmol) inhibited from 50 to 100% the effect of noradrenaline and clonidine in a dose-response manner. Diltiazem alone at 100 nmol inhibited, but at 50 nmol had no effect on, sodium appetite. The results suggest: (1) common ionic mechanisms involving calcium channels for the inhibition that noradrenaline and clonidine exert on sodium appetite and (2) a dual role for the benzothiazepine site of L-type calcium channels in the control of sodium appetite.

Adrenergic alpha-Agonists↗

PubMed2002

Isotonic NaCl intake by cell-dehydrated rats.

Male adult rats that received an intragastric load of 2 ml of 12% NaCl (n=13) ingested both water (4.0+/-0.2 ml/2 h) and 0.9% NaCl (3.7+/-1.0 ml/2 h) when compared with rats that received intragastric load of 2 ml of water (water: 0.1+/-0.1; 0.9% NaCl: 0.5+/-0.3 ml/2 h, n=12) in a two-bottle test. Intragastric sodium load increased plasma sodium concentration and osmolality by 5% and reduced plasma renin activity by half compared to rats that received intragastric load of water. Intravenous infusion of 1.5 ml/10 min of 10% NaCl (n=16) also induced ingestion of water (6.2+/-0.8 ml/2 h) and 0.9% NaCl (2.9+/-0.8 ml/2 h) compared with intravenous infusion of 1.5 ml/10 min of 0.9% NaCl (water: 0.9+/-0.4; 0.9% NaCl: 0.5+/-0.2 ml/2 h, n=14). Therefore, a sodium load that raises natremia and plasma osmolality, and therefore induces cell dehydration, results in both 0.9% NaCl and water ingestion when the rats have a two-bottle choice.

Animals↗

PubMed2002

Water deprivation-induced sodium appetite: humoral and cardiovascular mediators and immediate early genes.

Adult rats deprived of water for 24-30 h were allowed to rehydrate by ingesting only water for 1-2 h. Rats were then given access to both water and 1.8% NaCl. This procedure induced a sodium appetite defined by the operational criteria of a significant increase in 1.8% NaCl intake (3.8 +/- 0.8 ml/2 h; n = 6). Expression of Fos (as assessed by immunohistochemistry) was increased in the organum vasculosum of the lamina terminalis (OVLT), median preoptic nucleus (MnPO), subfornical organ (SFO), and supraoptic nucleus (SON) after water deprivation. After rehydration with water but before consumption of 1.8% NaCl, Fos expression in the SON disappeared and was partially reduced in the OVLT and MnPO. However, Fos expression did not change in the SFO. Water deprivation also 1) increased plasma renin activity (PRA), osmolality, and plasma Na+; 2) decreased blood volume; and 3) reduced total body Na+; but 4) did not alter arterial blood pressure. Rehydration with water alone caused only plasma osmolality and plasma Na+ concentration to revert to euhydrated levels. The changes in Fos expression and PRA are consistent with a proposed role for ANG II in the control of the sodium appetite produced by water deprivation followed by rehydration with only water.

Animals↗