Baroreceptor activation or glutamate coinjection facilitates depressor responses to ANF microinjection into NTS

1989 ◽  
Vol 257 (2) ◽  
pp. R405-R409
Author(s):  
D. J. McKitrick ◽  
F. R. Calaresu

As microinjection of atrial natriuretic factor (ANF) into the nucleus of the solitary tract (NTS) has been shown to elicit depressor responses [D. J. McKitrick and F. R. Calaresu. Am. J. Physiol. 255 (Regulatory Integrative Comp. Physiol. 24): R182-R187, 1988], we investigated the possibility that these responses might be facilitated either by electrical stimulation of arterial baroreceptor fibers in the aortic depressor nerve (ADN) or by simultaneous microinjection of L-glutamate (Glu) into the same sites in the NTS. Male Wistar rats (n = 51) were anesthetized with urethan (1.4 g/kg ip), artificially ventilated, and the dorsal medulla was exposed. The ADN was isolated, cut distally, and the central end was placed on bipolar stimulating electrodes. Threshold doses of 10(-7) M ANF microinjected into the NTS were combined with threshold electrical stimulation of the ADN (n = 37) or threshold doses of 0.13-0.5 M Glu (n = 14) microinjected into the NTS. There was a significant interaction between ANF microinjection and ADN stimulation in producing changes in mean arterial pressure (MAP) and heart rate [HR; P less than 0.05; -20.2 +/- 2.3 (SE) mmHg and -30.8 +/- 6.9 (SE) beats/min, respectively; n = 18]. There was also a significant interaction between ANF and Glu in producing changes in MAP and HR [P less than 0.05; -16.3 +/- 1.8 (SE) mmHg and -15.0 +/- 3.0 (SE) beats/min, respectively; n = 8]. These results indicate that ANF influences neurons in the NTS, which are also influenced by activation of arterial baroreceptors, and ANF and Glu interact in the NTS to produce facilitated cardiovascular responses.

2016 ◽  
Vol 310 (7) ◽  
pp. R612-R618 ◽  
Author(s):  
Tomás O. C. Teixeira Pinto ◽  
Renata M. Lataro ◽  
Jaci A. Castania ◽  
Marina T. Durand ◽  
Carlos A. A. Silva ◽  
...  

Chronic heart failure (CHF) is characterized by autonomic dysfunction combined with baroreflex attenuation. The hypotensive and bradycardic responses produced by electrical stimulation of the aortic depressor nerve (ADN) were examined in conscious CHF and control male Wistar rats (12–13 wk old). Furthermore, the role of parasympathetic and sympathetic nervous system in mediating the cardiovascular responses to baroreflex activation was evaluated by selective β1-adrenergic and muscarinic receptor antagonists. CHF was induced by myocardial infarction. After 6 wk, the subjects were implanted with electrodes for ADN stimulation. Twenty-four hours later, electrical stimulation of the ADN was applied for 20 s using five different frequencies (5, 15, 30, 60, and 90 Hz), while the arterial pressure was recorded by a catheter implanted into the femoral artery. Electrical stimulation of the ADN elicited progressive and similar hypotensive and bradycardic responses in control ( n = 12) and CHF ( n = 11) rats, while the hypotensive response was not affected by methylatropine. Nevertheless, the reflex bradycardia was attenuated by methylatropine in control, but not in CHF rats. Atenolol did not affect the hypotensive or bradycardic response in either group. The ADN function was examined under anesthesia through electroneurographic recordings. The arterial pressure-ADN activity relationship was attenuated in CHF rats. In conclusion, despite the attenuation of baroreceptor function in CHF rats, the electrical stimulation of the ADN elicited a stimulus-dependent hypotension and bradycardia of similar magnitude as observed in control rats. Therefore, electrical activation of the aortic baroreflex overcomes both the attenuation of parasympathetic function and the sympathetic overdrive.


Life Sciences ◽  
2016 ◽  
Vol 148 ◽  
pp. 99-105 ◽  
Author(s):  
Fernanda Brognara ◽  
Daniel P. Martins Dias ◽  
Jaci A. Castania ◽  
Rubens Fazan ◽  
Stephen J. Lewis ◽  
...  

1980 ◽  
Vol 239 (1) ◽  
pp. R137-R142 ◽  
Author(s):  
J. Ciriello ◽  
F. R. Calaresu

To investigate the role of the paraventricular (PAH) and supraoptic (SON) nuclei in regulation of the cardiovascular system experiments were done in 26 cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. Electrical stimulation of histologically verified sites in the region of the PAH and SON elicited increases in arterial pressure in bilaterally vagotomized animals and increases in heart rate both in spinal (C2) animals and in animals bilaterally vagotomized, In addition, stimulation of either the PAH or SON inhibited the reflex vagal bradycardia elicited by stimulation of the carotid sinus nerve (CSN) and bilateral lesions of these areas increased the magnitude of the response. On the other hand, stimulation and lesions of these hypothalamic regions did not alter the magnitude of the cardiovascular responses to stimulation of the aortic depressor nerve. These results demonstrate that stimulation of the PAH and SON elicit cardiovascular responses due to reciprocal changes in activity of the parasympathetic and sympathetic nervous systems and that these structures maintain a tonic inhibitory influence on the heart rate component of the CSN reflex.


1985 ◽  
Vol 63 (9) ◽  
pp. 1122-1132 ◽  
Author(s):  
J. A. Armour ◽  
W. C. Randall

Electrical stimulation of a canine vagosympathetic complex or a cardiopulmonary nerve can elicit a variety of negative chronotropic and inotropic cardiac responses, with or without alterations in systemic arterial pressure. In the period immediately following cessation of such a stimulation "rebound" tachycardia, increased inotropism above control values in one or more regions of the heart, and (or) elevation in systemic arterial pressure can occur. These "rebound" phenomena are abolished by propranolol or ipsilateral chronic sympathectomy. It is proposed that "vagal" poststimulation "rebound" of the canine cardiovascular system is primarily the result of activation of sympathetic neural elements present in the vagosympathetic complexes or cardiopulmonary nerves.


2017 ◽  
Vol 10 (1) ◽  
pp. 116-125 ◽  
Author(s):  
D. Martínez-Vargas ◽  
A. Valdés-Cruz ◽  
V.M. Magdaleno-Madrigal ◽  
R. Fernández-Mas ◽  
S. Almazán-Alvarado

2002 ◽  
Vol 282 (4) ◽  
pp. H1278-H1287 ◽  
Author(s):  
Pedro Boscan ◽  
Julian F. R. Paton

We determined the activity of neurons within the nucleus of the solitary tract (NTS) after stimulation of the cornea and assessed whether this input affected the processing of baroreceptor and peripheral chemoreceptor inputs. In an in situ, unanesthetized decerebrate working heart-brain stem preparation of the rat, noxious mechanical or electrical stimulation was applied to the cornea, and extracellular single unit recordings were made from NTS neurons. Cornea nociceptor stimulation evoked bradycardia and an increase in the cycle length of the phrenic nerve discharge. Of 90 NTS neurons with ongoing activity, corneal stimulation excited 51 and depressed 39. There was a high degree of convergence to these NTS neurons from either baroreceptors or chemoreceptors. The excitatory synaptic response in 12 of 19 baroreceptive and 10 of 15 chemoreceptive neurons was attenuated significantly during concomitant electrical stimulation of the cornea. This inhibition was GABAA receptor mediated, being blocked by pressure ejection of bicuculline. Thus the NTS integrates information from corneal receptors, some of which converges onto neurons mediating reflexes from baroreceptors and chemoreceptors to inhibit these inputs.


1993 ◽  
Vol 71 (5-6) ◽  
pp. 365-373 ◽  
Author(s):  
Stefanie Roder ◽  
John Ciriello

Experiments were done in α-chloralose anesthetized rats to investigate the effect of stimulating the intermediate region of the ventrolateral medulla (VLM) on the response of single units in nucleus of the solitary tract (NTS) that altered their rate of discharge during aortic baroreceptor stimulation. Of 178 units recorded within NTS, 65 responded orthodromically to VLM stimulation. An additional 16 units were activated antidromically by VLM stimulation. The interaction between the aortic depressor nerve and VLM orthodromic inputs was investigated in 38 units that received converging inputs from VLM and the aortic depressor nerve. A conditioning stimulus applied to VLM, regardless of whether the NTS unit was excited by (n = 13) or did not respond to (n = 9) VLM stimulation, decreased the excitatory response of the unit to aortic depressor nerve stimulation. These data suggest that VLM neurons are involved in the modulation of aortic baroreceptor afferent information at the level of the NTS and that this interaction of inputs in NTS may involve both postsynaptic and presynaptic mechanisms.Key words: ventrolateral medulla, aortic depressor nerve, A1 noradrenergic cell group, C1 adrenergic cell group, baroreceptor reflex, vagal bradycardia, central regulation of circulation.


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