Biomedical subjects

E Colombari

Publications and source records attributed to E Colombari.

33 records · Page 2Linked to original sources

PubMed1995

Denervation supersensitivity to glutamate in the nucleus tractus solitarii after removal of the nodose ganglion.

If L-glutamate (L-Glu) is the transmitter released from cardiovascular vagal afferent nerve fibers in the nucleus tractus solitarii (NTS), then interruption of those afferents should lead to denervation supersensitivity to L-Glu in the NTS. Therefore, we sought to determine if dose-related changes in arterial pressure (AP) and heart rate (HR) elicited by L-Glu microinjected into the NTS evolve after removal of the left nodose ganglion in rats. Twelve rats served as unoperated controls; and eight were studied 5 days, eleven 10 days, and nine 15 days after ganglionectomy. Each rat was anesthetized with halothane (1.5-2.0%) and cannulated for recording AP and HR. After exposure of the brainstem, vehicle or L-Glu (3, 30, 75, 150, 300 and 1500 pmol/50 nl) was microinjected alternately into the right and left dorsomedial NTS. In control animals, and in animals 5 days and 15 days after ganglionectomy, the lowest dose of L-Glu that produced a significant fall of mean AP (-10 +/- 2, -5 +/- 2, -6 +/- 1 mmHg, respectively) was 30 pmoles. The threshold dose with injections on the lesioned side 10 days after ganglionectomy was 3 pmol (-8 +/- 2 mmHg). In rats studied at 10 days, but not in control, 5 or 15 days rats, the dose-responses for injections made on the left were shifted significantly to the left of those made on the right (P < 0.05). In control, 5, and 15 day rats there were no significant differences between dose-related responses elicited from right and left NTS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1995

Evolution of dose-related cardiovascular responses to L-glutamate microinjected into the nucleus tractus solitarii after removal of the nodose ganglion in rat.

1. In this study, we sought to determine if sensitivity to dose-related changes in arterial pressure (AP) and heart rate (HR) elicited by microinjection of L-glutamate (L-GLU) into the nucleus tractus solitarii (NTS) evolves after deafferentation in adult male Sprague-Dawley rats. 2. Twelve rats served as unoperated controls; and eight were studied 5 days, eleven 10 days and nine 15 days after ganglionectomy. Each rat was anaesthetized (halothane 1.5-2.0%) and cannulated for recording AP and HR. Vehicle or L-GLU (3, 30, 75, 150, 300 and 1500 pmole/50 nL) was microinjected into the right and left NTS. Injection sites were confirmed histologically. 3. In control animals and in animals 5 days and 15 days after ganglionectomy, the lowest dose of L-GLU that produced a significant fall of AP was 30 pmole. The threshold dose with injections on the lesioned side 10 days after ganglionectomy was 3 pmole. In rats studied at 10 days, but not in control, 5 or 15 day rats, dose-related responses for injections made on the left were shifted significantly to the left of those made on the right (P < 0.05). 4. In control, 5 and 15 day rats there were no significant differences between dose-related responses elicited from right and left NTS. Responses of HR did not differ between groups of animals or sides of injection. 5. These results suggest that supersensitivity to L-GLU evolves after nodose ganglionectomy and support a role for L-GLU as a transmitter of cardiovascular afferents in the NTS.

Anesthesia↗

PubMed1995

NMDA receptors in NTS are involved in bradycardic but not in pressor response of chemoreflex.

Activation of carotid chemoreceptors with intravenous potassium cyanide (KCN) produces increases in arterial pressure, bradycardia, and tachypnea. In the present study, we activated carotid chemoreceptors with KCN and the neurotransmission of the chemoreceptor reflex into the commissural nucleus tractus solitarii (NTS) was blocked with phosphonovaleric acid (AP-5), an N-methyl-D-aspartate (NMDA)-selective antagonist. The aim of this study was to evaluate the involvement of NMDA receptors in the cardiovascular and respiratory responses produced by chemoreceptor activation in unanesthetized rats. The pressor response to KCN was not changed after microinjection of three different doses of AP-5 into the NTS, whereas the bradycardic response was reduced in a dose-dependent manner. The increase in respiratory frequency in response to carotid chemoreceptor activation was also not affected by AP-5 microinjected into the NTS. The data indicate that the activation of the cardiovagal component of the chemoreflex in the commissural NTS is mediated by NMDA receptors, whereas pressor and ventilatory responses are not.

2-Amino-5-phosphonovalerate↗

PubMed1995

Glycine blocks the pressor response to L-glutamate microinjected into the nucleus tractus solitarii of conscious rats.

Microinjection of L-glutamate into the nucleus tractus solitarii (NTS) of conscious freely moving Wistar rats (240-260 g) produces pressor (+48 +/- 4 mmHg) and bradycardic (-153 +/- 20 bpm) responses. In the present study L-glutamate (2.5 nmol/100 nl) was microinjected before and after microinjection of increasing doses of glycine (10, 25 and 50 nmol/100 nl, N = 6) or saline (vehicle/100 nl, N = 6) into the NTS. Microinjections of increasing doses of glycine into the NTS produced a dose-dependent reduction in the pressor but not in the bradycardic responses to L-glutamate. [10 nmol (+29 +/- 5 mmHg and -110 +/- 18 bpm), 25 nmol (+12 +/- 7 mmHg and -88 +/- 21 bpm) and 50 nmol (+4 +/- 2 mmHg and -100 +/- 31 bpm)] The dose-dependent blockade of the pressor response to L-glutamate by glycine suggests an inhibitory neuromodulatory role for this amino acid in the sympatho-excitatory activity produced by L-glutamate microinjection into the NTS.

Animals↗

PubMed1994

Mechanisms of pressor and bradycardic responses to L-glutamate microinjected into the NTS of conscious rats.

Microinjection of increasing doses of L-glutamate (L-Glu, 0.03-5.0 nmol/100 nl) into the nucleus tractus solitarii (NTS) produced a dose-related pressor and bradycardic response. Prazosin virtually abolished the pressor response but produced no changes in the bradycardic response to L-Glu, indicating that bradycardia is not reflex in origin. The bradycardic response was blocked by atropine. In three different groups of rats, excitatory amino acid receptors in the NTS were blocked by increasing doses of kynurenic acid (0.5, 2.0, and 10.0 nmol/100 nl) and the pressor and bradycardic responses to L-Glu (1 nmol/100 nl) were reduced in a dose-related pattern. Reflex bradycardia induced by an increase in pressure caused by phenylephrine (iv) was also blocked by kynurenic acid. These data show that microinjection of L-Glu into the NTS of conscious rats produced pressor and bradycardic responses, which are due to the activation of two independent autonomic pathways. The data also indicate that the activation of both pathways is mediated by excitatory amino acid receptors. Considering that reflex bradycardia was also blocked by kynurenic acid, we suggest that L-Glu and excitatory amino acid receptors are part of the parasympathetic limb of the baroreceptor reflex. The pressor response to L-Glu is also mediated by excitatory amino acid receptors, but its physiological meaning is still unclear.

Animals↗

PubMed1993

Involvement of the central nervous system in the salivary secretion induced by pilocarpine in rats.

The effect of rats of an anteroventral third ventricle (AV3V) electrolytic lesion on salivary secretion induced by intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) injection of a cholinergic agonist (pilocarpine) was investigated. Sham- or AV3V-lesioned rats anesthetized with urethane and with a stainless steel cannula implanted into the lateral ventricle (LV) were used. The amount of salivary secretion was studied over a seven-minute period after i.c.v. or i.p. injection of pilocarpine. In sham-operated rats, i.p. injection of pilocarpine (1 mg/kg b.w.) (after 6 h, 2, 7, and 15 days) produced salivary secretion (486 +/- 21, 778 +/- 85, 630 +/- 50, and 560 +/- 55 mg/7 min, respectively). This effect was reduced 6 h, 2, and 7 days after an AV3V lesion (142 +/- 22, 113 +/- 32, and 290 +/- 62 mg/7 min, respectively), but not 15 days after an AV3V lesion (516 +/- 19 mg/7 min). I.c.v. injection of pilocarpine (120 micrograms in 1 microL), in sham-operated rats after 6 h, 2, 7, and 15 days also produced salivary secretion (443 +/- 20, 417 +/- 81, 496 +/- 14, and 427 +/- 47 mg/7 min, respectively). The effects of i.c.v. pilocarpine were also reduced 6 h, 2, and 7 days after an AV3V lesion (143 +/- 19, 273 +/- 14, and 322 +/- 17 mg/7 min, respectively), but not after 15 days (450 +/- 28 mg/7 min). The results demonstrate that the central nervous system, and particularly the AV3V region, is important for the effect of pilocarpine on salivary secretion in rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Effect of furosemide treatment on the central and peripheral pressor responses to cholinergic and adrenergic agonists, angiotensin II, hypertonic solution and vasopressin.

The present study was performed to investigate the effect of treatment with furosemide on the pressor response induced by intracerebroventricular (i.c.v.) injections of cholinergic (carbachol) and adrenergic (norepinephrine) agonists, angiotensin II (ANGII) and hypertonic saline (HS, 2 M NaCl). The changes induced by furosemide treatment on the pressor response to intravenous (i.v.) norepinephrine, ANGII and arginine vasopressin (AVP) were also studied. Rats with a stainless-steel cannula implanted into the lateral ventricle (LV) were used. Two injections of furosemide (30 mg/kg b.wt. each) were performed 12 and 1 h before the experiments. Treatment with furosemide reduced the pressor response induced by carbachol, norepinephrine and ANGII i.c.v., but no change was observed in the pressor response to i.c.v. 2 M NaCl. The pressor response to i.v. ANGII and norepinephrine, but not AVP, was also reduced after treatment with furosemide. These results show that the treatment with furosemide impairs the pressor responses induced by central or peripheral administration of adrenergic agonist or ANGII, as well as those induced by central cholinergic activation. The results suggest that the treatment with furosemide impairs central and peripheral pressor responses mediated by sympathetic activation and ANGII, but not those produced by AVP.

Angiotensin II↗

PubMed1992

AV3V lesion suppresses the pressor, dipsogenic and natriuretic responses to cholinergic activation of the septal area in rats.

In the present study we investigated the effect of anteroventral third ventricle (AV3V) lesion on pressor, dipsogenic, natriuretic and kaliuretic responses induced by the injection of carbachol (a cholinergic agonist) into the medial septal area (MSA) of rats. Male rats with sham or AV3V lesion and a stainless-steel cannula implanted into the MSA were used. Carbachol (2 nmol) injected into the MSA in sham lesion rats produced pressor (43 +/- 2 mmHg), dipsogenic (9.6 +/- 1.2 ml/h), natriuretic (531 +/- 82 microEq/120 min) and kaliuretic (164 +/- 14 microEq/120 min) responses. In AV3V-lesioned rats (1-5 days and 14-18 days), the pressor (11 +/- 2 and 14 +/- 2 mmHg, respectively), dipsogenic (1.9 +/- 0.7 and 1.4 +/- 0.6 ml/h), natriuretic (21 +/- 5 and 159 +/- 44 microEq/120 min) and kaliuretic (124 +/- 14 and 86 +/- 13 microEq/120 min) responses induced by carbachol injection into the MSA were reduced. These results show that the AV3V region is essential for the pressor, dipsogenic, natriuretic and kaliuretic responses induced by cholinergic activation of the MSA in rats.

Animals↗

PubMed1992

Cardiovascular effects of central clonidine in conscious rats after hypothalamic lesions.

The central injection of clonidine (an alpha 2-adrenoceptor agonist) in conscious normotensive rats produces hypertensive responses and bradycardia. The present study was performed to investigate the effect of electrolytic lesions in the anteroventral third ventricle (AV3V) region or in the lateral hypothalamus (LH) on the pressor and bradycardic responses induced by central clonidine in rats. Mean arterial pressure and heart rate were recorded in sham or AV3V-lesioned rats with cerebral stainless steel cannulae implanted into the lateral cerebral ventricle (ICV) or LH, and in sham or bilateral LH-lesioned rats with cannulae-implanted ICV. The injection of clonidine (40 nmol) ICV or into the LH of sham rats produced a pressor response (37 +/- 2-48 +/- 3 mmHg) and bradycardia (-45 +/- 10- -93 +/- 6 bpm). After AV3V-lesion (3 and 12 days) or LH-lesion (3 days) the pressor response was abolished and a small hypotensive response was induced by the injection of clonidine (-1 +/- 3- -16 +/- 3 mmHg). The bradycardia (-27 +/- 6- -57 +/- 11 bpm) was reduced, but not abolished by the lesions. These results show that the AV3V region and LH are important cerebral structures that participate in the excitatory pathways involved in the pressor response to central clonidine in rats. They also suggest that, in the absence of these pressor pathways, the hypotensive responses to central clonidine may appear in conscious rats.

Animals↗

PubMed1992

AV3V lesion impairs responses induced by cholinergic activation of SFO in rats.

This study was performed to investigate the effect of lesion of the anteroventral third ventricle (AV3V) region on the pressor, bradycardic, dipsogenic, natriuretic, kaliuretic, and antidiuretic responses induced by cholinergic activation of the subfornical organ (SFO) in rats. Male Holtzman rats with sham or electrolytic AV3V lesion were implanted with a stainless steel cannula directly into the SFO. Microinjection of the cholinergic agonist carbachol (2 nmol) into the SFO of sham rats induced natriuresis (563 +/- 70 mu eq/120 min), kaliuresis (205 +/- 13 mu eq/120 min), antidiuresis (10.4 +/- 0.5 ml/120 min), water intake (9.3 +/- 1.4 ml/h), bradycardia (-42 +/- 11 beats/min), and increased mean arterial pressure (53 +/- 3 mmHg). In AV3V-lesioned rats (1-5 and 14-18 days), there was a reduction of natriuresis (23 +/- 11 and 105 +/- 26 mu eq/120 min, respectively), kaliuresis (92 +/- 16 and 100 +/- 17 mu eq/120 min), water intake (2.5 +/- 0.9 and 1.8 +/- 1.0 ml/h), and arterial pressure increase (17 +/- 2 and 16 +/- 2 mmHg) induced by carbachol into the SFO. Increased antidiuresis (6.0 +/- 1.0 and 5.2 +/- 0.7 ml/120 min, respectively) and tachycardia (39 +/- 4 and 15 +/- 12 beats/min) instead of bradycardia were also observed in both groups of AV3V-lesioned rats. These results show that cholinergic activation of the rat SFO produces marked natriuresis and kaliuresis in addition to the well-known pressor and dipsogenic responses. They also show that the AV3V region plays an important role in the cardiovascular, fluid, and electrolytic changes induced by cholinergic activation of the SFO in rats.

Animals↗

PubMed1990

The anteroventral third ventricle (AV3V) region is essential for pressor, dipsogenic and natriuretic responses to central carbachol.

In the present study we investigated the effect of anteroventral third ventricle (AV3V) lesion on pressor, dipsogenic and natriuretic responses produced by the intracerebroventricular (i.c.v.) injection of a cholinergic agonist (carbachol). Freely moving rats with AV3V or sham lesion (1-2 days and 9-12 days) and a delay cannula implanted into the lateral ventricle were studied. Changes in mean arterial pressure (MAP, 1 h record), water intake (1 h) and Na+ excretion (2 h) were analysed after i.c.v. injection of carbachol (7.5 nmol). In sham rats, i.c.v. injection of carbachol produced an increase in MAP (35 +/- 2 mmHg), water ingestion (7.7 +/- 1.2 ml/h) and Na+ excretion (626 +/- 42 microEq/120 min). The effects of i.c.v. carbachol injection were reduced 1-2 days after AV3V lesion (delta MAP = 6 +/- 2 mmHg, water ingestion = 0.3 +/- 0.3 ml/h and Na+ excretion = 31 +/- 11 microEq/120 min) and 9-12 days (delta MAP = 11 +/- 3 mmHg, water ingestion = 3.3 +/- 0.9 ml/h and Na+ excretion = 37 +/- 11 microEq/120 min). These results show that the AV3V region is essential for the full development of the pressor, dipsogenic and natriuretic responses produced by central cholinergic receptors.

Animals↗

PubMed1990

Role of central alpha 1- and alpha 2-adrenoceptors on the dipsogenic and cardiovascular effect of angiotensin II.

We investigated the effects of previous central treatment with prazosin (an alpha 1-adrenoceptor antagonist) or clonidine (an alpha 2-adrenoceptor agonist) on the dipsogenic, pressor and tachycardic responses produced by intracerebroventricular (ICV) injection of angiotensin II (AII) in conscious rats. Holtzman rats with a chronic cannula implanted in the lateral ventricle were tested for dipsogenic and cardiovascular (arterial pressure and heart rate) responses in separate experiments. Previous ICV treatment with clonidine (20, 40, 80 and 120 nmol) abolished the pressor, tachycardic and dipsogenic effects of ICV AII. After all doses of prazosin (40, 80 and 120 nmol), AII induced bradycardic responses, but only the 80 and 120 nmol doses of prazosin reduced the pressor responses to AII. Prazosin produced no alteration in the dipsogenic effect of AII. The results show that the periventricular alpha 1-adrenoceptors are involved only in the cardiovascular responses produced by central AII, whereas clonidine acting through alpha 2-adrenergic and/or imidazole receptors can modulate all actions of AII.

Angiotensin II↗

PubMed1990

The effect of phentolamine on the pressor response to centrally administered clonidine in rats.

In the present study we investigate the effect of the previous injection of phentolamine (a nonspecific alpha-adrenergic antagonist) into the lateral hypothalamus (LH) and lateral ventricle (LV) on the pressor and bradycardic responses produced by the injection of clonidine (an alpha 2-adrenergic agonist) into these same areas of conscious rats. The injection of clonidine into the LV and LH produced pressor (39 +/- 5 and 38 +/- 3 mmHg, respectively) and bradycardic responses (-65 +/- 16 and -94 +/- 13 bpm, respectively). Previous injection of phentolamine into the LH or LV reduced the pressor response to clonidine injected into the same areas (delta MAP = 13 +/- 6 mmHg for LH and 1 +/- 3 mmHg for LV). No reduction was observed when clonidine was injected into the LV after the injection of phentolamine into the LH. No changes in bradycardic responses were observed after treatment with phentolamine. The present results show the participation of alpha-adrenergic receptors in the pressor response to centrally administered clonidine but not in the bradycardic response. The data also suggest that the pressor effect produced by the injection of clonidine into the LH is due to the activation of alpha-adrenergic receptors located specifically in this area. The pressor response after injection of clonidine into the LV and of phentolamine into the LH is due to the action of clonidine on other cerebral areas.

Animals↗

PubMed1989

Pressor responses of clonidine injected into some prosencephalic areas of conscious rats.

The objective of this investigation was to study the effect of clonidine injection into some prosencephalic areas of unanesthetized rats on mean arterial pressure (MAP) and heart rate (HR). Injection of 40 nmol clonidine in 1.0 lambda 150 mM NaCl into the medial septal area, lateral hypothalamus, lateral preoptic area and lateral ventricle caused the same increase in MAP, 38 +/- 3 to 41 +/- 5 mmHg, and decrease in HR, -65 +/- 10 to -94 +/- 13 bpm (mean +/- SEM, N = 9 to 11 animals). These results show that clonidine can act on several prosencephalic areas to induce a pressor response in the conscious rat.

Animals↗

PubMed1989

Central lesion abolishes the beneficial effect of hypertonic saline on circulatory shock produced by compound 48/80 in rats.

The purpose of the present study was to examine the protective action of a 7.5% hypertonic NaCl solution (HS) on the circulatory shock produced by compound 48/80 (48/80) in rats and to determine the effect of the AV3V lesion on the protective action of HS. Intravenous injection of 48/80 into sham-operated rats resulted in an immediate drop of mean arterial pressure (MAP). In sham-operated rats, intravenous injection of HS prevented the drop of MAP produced by 48/80, but HS was ineffective in AV3V-lesioned rats. These results show that HS had a protective action on the circulatory shock produced by 48/80 and that the AV3V region plays an important role in this protective action.

Animals↗