Sympathoexcitatory neurotransmission of the chemoreflex in the NTS of awake rats

1999 ◽  
Vol 276 (1) ◽  
pp. R69-R80 ◽  
Author(s):  
Andréa S. Haibara ◽  
Leni G. H. Bonagamba ◽  
Benedito H. Machado

Cardiovascular responses to chemoreflex activation by potassium cyanide (KCN, 20 μg/rat iv) were analyzed before and after the blockade of ionotropic or metabotropic receptors into the nucleus of the solitary tract (NTS) of awake rats. Microinjection of ionotropic antagonists [6,7-dinitroquinoxaline-2,3-dione or kynurenic acid (Kyn)] into the lateral commissural NTS (NTSlat), the midline commissural NTS (NTSmid), or into both (NTSlat+mid), produced a significant increase in basal mean arterial pressure, and the pressor response to chemoreflex activation was only partially reduced, whereas microinjection of Kyn into the NTSmid produced no changes in the pressor response to the chemoreflex. The bradycardic response to chemoreflex activation was abolished by microinjection of Kyn into the NTSlat or into NTSlat+mid but not by Kyn microinjection into the NTSmid. Microinjection of α-methyl-4-carboxyphenylglycine, a metabotropic receptor antagonist, into the NTSlat or NTSmid produced no changes in baseline mean arterial pressure or heart rate or in the chemoreflex responses. These results indicate that 1) the processing of the parasympathetic component (bradycardia) of the chemoreflex seems to be restricted to the NTSlat and was blocked by ionotropic antagonists and 2) the pressor response of the chemoreflex was only partially reduced by microinjection of ionotropic antagonists and not affected by injection of metabotropic antagonists into the NTSlat or NTSmid or into NTSlat+mid in awake rats.

2001 ◽  
Vol 281 (6) ◽  
pp. R2072-R2078 ◽  
Author(s):  
Patrícia M. de Paula ◽  
Benedito H. Machado

The possible involvement of adenosine A1 receptors in neurotransmission of the sympathoexcitatory component of the chemoreflex in the nucleus tractus solitarii (NTS) of awake rats was evaluated. Unilateral microinjection of increasing doses of adenosine (0.01, 0.06, 0.12, 1.25, 2.5, and 5.0 nmol/50 nl) into the lateral aspect of the commissural NTS produced a long-lasting increase in baseline mean arterial pressure (MAP) and no changes in baseline heart rate (HR). Microinjection of adenosine at 1.25 nmol/50 nl (ED50) into the NTS ( n = 9) produced a significant increase in baseline MAP (119 ± 3, 122 ± 4, and 117 ± 4 mmHg at 30 s, 1 min, and 2 min, respectively) compared with control (102 ± 3 mmHg) but no significant changes after previous microinjection of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), an adenosine A1 receptor antagonist (107 ± 3, 107 ± 3, and 106 ± 3 mmHg at 30 s, 1 min, and 2 min, respectively) compared with control (102 ± 3 mmHg). Microinjection of adenosine before and after DPCPX into the same site of the lateral commissural NTS produced no changes in baseline HR. In another group of rats ( n = 8), microinjection of DPCPX (0.285 nmol/50 nl) into lateral and midline aspects of the commissural NTS produced no significant changes in pressor (+46 ± 4 vs. +47 ± 2 mmHg) or bradycardic responses (−216 ± 9 vs. −226 ± 12 beats/min) to chemoreflex activation with intravenous potassium cyanide compared with control responses. These data show that microinjection of adenosine into the NTS produced a small and long-lasting pressor response by activating A1 receptors and that blockade of these receptors produced no changes in cardiovascular responses to chemoreflex activation. We conclude that adenosine A1 receptors are not involved in processing of the chemoreflex afferents at the NTS level.


2003 ◽  
Vol 284 (4) ◽  
pp. R1000-R1009 ◽  
Author(s):  
Franklin F. Pimentel ◽  
Leni G. H. Bonagamba ◽  
Benedito H. Machado

Microinjection of glycine into the rostral (bilateral) and caudal (midline) commissural nucleus of the solitary tract (NTS) using three guide cannulas implanted in the direction of these sites produced an increase in mean arterial pressure (MAP) and abolished the pressor response to chemoreflex activation [potassium cyanide ( n = 7)]. Strychnine, a glycine receptor antagonist, attenuated the increase in MAP, and in this new experimental condition ( n = 5) the pressor response to chemoreflex activation was not altered. Considering that the effect of glycine on the attenuation of the pressor response to chemoreflex activation could be secondary to the increase in baseline MAP, in a third group of rats ( n = 5) sodium nitroprusside infusion (intravenous) after microinjections of glycine into the NTS normalizes MAP. In this case, the pressor response to chemoreflex activation was similar to the control. These data show that glycine when microinjected bilaterally into the lateral commissural NTS as well as into the medial commissural NTS plays no major inhibitory role in the processing of the neurotransmission of the sympathoexcitatory component of the chemoreflex.


1999 ◽  
Vol 276 (6) ◽  
pp. H1902-H1910 ◽  
Author(s):  
João Carlos Callera ◽  
Leni G. H. Bonagamba ◽  
Anne Nosjean ◽  
Raul Laguzzi ◽  
Benedito H. Machado

In the present study we analyzed effects of bilateral microinjections of muscimol (a GABAA agonist) and baclofen (a GABAB agonist) into the nucleus tractus solitarius (NTS) on bradycardic and pressor responses to chemoreflex activation (potassium cyanide, 40 μg/rat iv) in awake rats. Bilateral microinjections of muscimol (25 and 50 pmol/50 nl) into the NTS increased baseline mean arterial pressure (MAP): 119 ± 8 vs. 107 ± 2 mmHg ( n = 6) and 121 ± 8 vs. 103 ± 3 mmHg ( n= 6), respectively. Muscimol at 25 pmol/50 nl reduced the bradycardic response to chemoreflex activation 5 min after microinjection; with 50 pmol/50 nl the bradycardic response to chemoreflex activation was reduced 5, 15, 30, and 60 min after microinjection. Neither muscimol dose produced an effect on the pressor response of the chemoreflex. Effects of muscimol (50 pmol/50 nl) on basal MAP and on the bradycardic response of the chemoreflex were prevented by prior microinjection of bicuculline (a GABAA antagonist, 40 pmol/50 nl) into the NTS. Bilateral microinjections of baclofen (12.5 and 25 pmol/50 nl) into the NTS produced an increase in baseline MAP [137 ± 9 vs. 108 ± 4 ( n= 7) and 145 ± 5 vs. 105 ± 2 mmHg ( n = 7), respectively], no changes in basal heart rate, and no effects on the bradycardic response; 25 pmol/50 nl only attenuated the pressor response to chemoreflex activation. The data show that activation of GABAA receptors in the NTS produces a significant reduction in the bradycardic response, whereas activation of GABAB receptors produces a significant reduction in the pressor response of the chemoreflex. We conclude that 1) GABAA but not GABAB plays an inhibitory role in neurons of the lateral commissural NTS involved in the parasympathetic component of the chemoreflex and 2) attenuation of the pressor response of the chemoreflex by activation of GABAB receptors may be due to inhibition of sympathoexcitatory neurons in the NTS or may be secondary to the large increase in baseline MAP produced by baclofen.


2004 ◽  
Vol 286 (4) ◽  
pp. H1521-H1527 ◽  
Author(s):  
Deoclecio A. Chianca ◽  
Li-Hsien Lin ◽  
Deidre Nitschke Dragon ◽  
William T. Talman

We sought to test the hypothesis that cardiovascular responses to activation of ionotropic, but not metabotropic, glutamate receptors in the nucleus tractus solitarii (NTS) depend on soluble guanylate cyclase (sGC) and that inhibition of sGC would attenuate baroreflex responses to changes in arterial pressure. In adult male Sprague-Dawley rats anesthetized with chloralose, the ionotropic receptor agonists N-methyl-d-aspartate (NMDA) and dl-α-amino-3-hydroxy-5-methylisoxazole-propionic acid (AMPA) and the metabotropic receptor agonist trans-dl-amino-1,3-cyclopentane-dicarboxylic acid (ACPD) were microinjected into the NTS before and after microinjection of sGC inhibitors at the same site. Inhibition of sGC produced significant dose-dependent attenuation of cardiovascular responses to NMDA but did not alter responses produced by injection of AMPA or ACPD. Bilateral inhibition of sGC did not alter arterial pressure, nor did it attenuate baroreflex responses to pharmacologically induced changes in arterial pressure. This study links sGC with NMDA, but not AMPA or metabotropic, receptors in cardiovascular signal transduction through NTS.


1989 ◽  
Vol 256 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
A. Martinez-Arizala ◽  
J. W. Holaday ◽  
J. B. Long

Increases in mean arterial pressure and heart rate have been documented after the intrathecal administration of [Arg8]vasopressin (AVP) in rats. Prior studies in our laboratories with conscious rats indicated that these cardiovascular changes were associated with a marked hindlimb sensorimotor dysfunction. In this study, which represents the first systematic comparison of the effects of intrathecal AVP in conscious and anesthesized rats, we demonstrate that in conscious male Sprague-Dawley rats 1) the motor dysfunction induced by intrathecal AVP is accompanied by a rise in mean arterial pressure that is significantly greater than that produced by an equal intravenous dose of AVP, and 2) both paralytic and pressor effects of intrathecal but not intravenous AVP are blocked by the intrathecal administration of the V1-receptor antagonist d(CH2)5[Tyr(Me)2]AVP (V1-ANT) but are not blocked by intravenous phenoxybenzamine, hexamethonium, or [Sar1, Thr8]angiotensin II, an angiotensin II antagonist. In contrast, in anesthesized rats the arterial pressor response to intrathecal AVP was blocked by intrathecal V1-ANT, intravenous hexamethonium, and intravenous phenoxybenzamine. Furthermore, conscious but not anesthesized rats exhibited a tachyphylaxis to intrathecal AVP. These results indicate that intrathecal AVP produces both the cardiovascular changes and the sensorimotor deficits through interactions with centrally located V1-receptors. In addition, sympathetic catecholaminergic mechanisms mediate the rise in mean arterial pressure produced by intrathecal AVP in anesthesized rats, but they do not in conscious rats.


1992 ◽  
Vol 20 (2) ◽  
pp. 121-126
Author(s):  
K Mikawa ◽  
N Maekawa ◽  
R Goto ◽  
H Yaku ◽  
N Saitoh ◽  
...  

The efficacy of intravenous mexiletine in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation was studied in 30 normotensive patients undergoing elective surgery. The patients were randomly allocated to one of three treatment groups: saline ( n = 10); 2 mg/kg mexiletine ( n = 10); and 3 mg/kg mexiletine ( n = 10). The placebo/mexiletine was administered immediately before induction of anaesthesia using 5 mg/kg thiopentone and tracheal intubation was facilitated with 0.2 mg/kg vecuronium; laryngoscopy lasting 30 s was attempted 2 min after induction of anaesthesia. All groups showed a significant ( P < 0.05) increase in mean arterial pressure and heart rate associated with tracheal intubation. The increase in mean arterial pressure was significantly ( P < 0.05) smaller in patients receiving 3 mg/kg mexiletine compared with those receiving either saline or 2 mg/kg mexiletine. There was no significant attenuation in heart rate in either of the mexiletine treatment groups compared with the saline group. It is concluded that 3 mg/kg mexiletine given intravenously provides a simple and effective method for attenuating the pressor response to laryngoscopy and tracheal intubation.


1981 ◽  
Vol 240 (4) ◽  
pp. H539-H545 ◽  
Author(s):  
J. C. Longhurst ◽  
H. L. Spilker ◽  
G. A. Ordway

Hemodynamic responses to passive gastric distension were examined in alpha-chloralose anesthetized cats. Gastric balloons were distended with 37 degrees C fluid at slow (50 ml/min) and rapid (250 ml/min) infusion rates before and after laparotomy. Passive gastric distension at the slow infusion rate significantly (P less than 0.05) increased mean arterial pressure (MAP) by 28%, dP/dt at 40 mmHg developed pressure by 29%, and systemic vascular resistance (SVR) by 35%. Likewise, the rapid distension rate significantly (P less than 0.05) increased MAP (20%), dP/dt (16%), and SVR (23%). Heart rate, aortic flow, and left ventricular end-diastolic pressure remained unchanged at both distension rates. Cardiovascular responses to passive gastric distension were similar before and after laparotomy. Section of the vagus nerve at the diaphragm did not alter the responses, whereas abdominal splanchnic nerve section significantly (P less than 0.05) reduced the changes in mean arterial pressure and dP/dt. These results indicate that passive gastric distension in the cat elicits cardiovascular reflexes sufficient to increase myocardial oxygen demand. Such a reflex response could potentially contribute to postprandial angina in humans.


2018 ◽  
Vol 36 (4) ◽  
pp. 153-158
Author(s):  
Md Mushfiqur Rahman ◽  
Md Mhbubul Hasan Munir ◽  
Kawsar Sardar ◽  
Abdus Salam Khan ◽  
AKM Nurnobi Chowdhury ◽  
...  

Background: The effects of ProSeal laryngeal mask airway (PLMA) removal and tracheal extubationon cardiovascular responses were studied in elderly hypertensive diabetic patients in a randomize double-blind study.Methods: A total of 60 elderly controlled diabetic hypertensive American Society of Anesthesiologists II & III patients were randomly allocated to two groups (n-30 of each) for PLMA insertion or endotracheal intubation. A standardized anesthetic sequence was used for induction and maintenance of anesthesia. The two groups were then compared for haemodynamic changes at the time of extubation/PLMA removal.Results: In PLMA group, heart rate increased during PLMA removal but remained elevated for only 3 minutes while mean arterial pressure remained elevated for only 2 minutes.The elevations of heart rate and mean arterial pressure were exaggerated in the extubation group and persisted for more than 5 minutes. No complication was observed in any patient and no difficulty was encountered in insertion of PLMA in any patient.Conclusion: Elderly hypertensive diabetic patients are at risk of exaggerated pressor response at the time of extubation. PLMA removal is associated with fewer hemodynamic changes than tracheal extubation and should be preferred wherever possible.J Bangladesh Coll Phys Surg 2018; 36(4): 153-158


1998 ◽  
Vol 85 (5) ◽  
pp. 1957-1965 ◽  
Author(s):  
Todd T. Schlegel ◽  
Edgar W. Benavides ◽  
Donald C. Barker ◽  
Troy E. Brown ◽  
Deborah L. Harm ◽  
...  

We investigated the integrated cardiovascular responses of 15 human subjects to the acute gravitational changes (micro- and hypergravity portions) of parabolic flight. Measurements were made with subjects quietly seated and while subjects performed controlled Valsalva maneuvers. During quiet, seated, parabolic flight, mean arterial pressure increased during the transition into microgravity but decreased as microgravity was sustained. The decrease in mean arterial pressure was accompanied by immediate reflexive increases in heart rate but by absent (or later-than-expected) reflexive increases in total vascular resistance. Mean arterial pressure responses in Valsalva phases IIl, III, and IV were accentuated in hypergravity relative to microgravity ( P < 0.01, P < 0.01, and P < 0.05, respectively), but accentuations differed qualitatively and quantitatively from those induced by a supine-to-seated postural change in 1 G. This study is the first systematic evaluation of temporal and Valsalva-related changes in cardiovascular parameters during parabolic flight. Results suggest that arterial baroreflex control of vascular resistance may be modified by alterations of cardiopulmonary, vestibular, and/or other receptor activity.


2010 ◽  
Vol 2010 ◽  
pp. 1-11 ◽  
Author(s):  
Styliani Goulopoulou ◽  
Bo Fernhall ◽  
Jill A. Kanaley

The purpose of this study was to examine differences in pressor response and cardiovagal modulation during isometric handgrip exercise (IHG) between children and adults. Beat-to-beat heart rate (HR) and blood pressure were measured in 23 prepubertal children and 23 adults at baseline and during IHG. Cardiovagal modulation was quantified by analysis of HR variability. Mean arterial pressure responses to IHG were greater in adults compared to children (P<.05) whereas there were no group differences in HR responses (P>.05). Children had a greater reduction in cardiovagal modulation in response to IHG compared to adults (P<.05). Changes in mean arterial pressure during IHG were correlated with baseline cardiovagal modulation and force produced during isometric contraction (P<.05). In conclusion, differences in pressor reflex response between children and adults cannot be solely explained by differences in autonomic modulation and appear to be associated with factors contributing to the force produced during isometric contraction.


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