Pressor response to chemoreflex activation in awake rats: role of vasopressin and adrenal medulla

2005 ◽  
Vol 84 (1) ◽  
pp. 39-44 ◽  
Author(s):  
Luciano G. Fernandes ◽  
Vagner R. Antunes ◽  
Leni G.H. Bonagamba ◽  
Benedito H. Machado
Keyword(s):  
Adrenal Medulla ◽  
Pressor Response ◽  
Awake Rats

Role of adrenal medulla in hemodynamic response to hemorrhage and naloxone

1988 ◽  
Vol 254 (3) ◽  
pp. R559-R565 ◽  
Author(s):  
J. C. Schadt ◽  
R. R. Gaddis
Keyword(s):  
Adrenal Medulla ◽  
Pressor Response ◽  
Sympathetic Nerves ◽  
Hemodynamic Response ◽  
Plasma Norepinephrine ◽  
Plasma Catecholamine ◽  
Intact Group ◽  
New Zealand White Rabbits ◽  
Possible Cause

We tested the hypothesis that enkephalins or some other compound(s) released by the adrenal medulla during hemorrhage were responsible for the resultant hypotension. We compared the hemodynamic and plasma catecholamine responses to hemorrhage and subsequent opioid receptor blockade with naloxone in intact, adrenal-denervated (ADD), and adrenalectomized (ADX) rabbits. The studies were done in conscious, chronically prepared, male New Zealand White rabbits. The hemodynamic response to hemorrhage was not different among the three groups. Plasma norepinephrine (NE) increased early in hemorrhage in all groups. In the ADD and ADX animals, NE decreased significantly at the transition to hypotension, suggesting decreased release of NE by peripheral sympathetic nerves as a possible cause of the decrease in pressure. In the intact group, NE did not decrease but reached a plateau possibly due to the release of some NE by the adrenal medulla, which obscured the decreased release by sympathetic nerves. The pressor response to naloxone, though present in all groups, was attenuated by adrenalectomy or adrenal denervation. The plasma NE response to naloxone was similar in all groups and involved a two- to threefold increase after naloxone. We conclude that enkephalins or any other compounds released by the adrenal gland are not responsible for the acute hemodynamic changes during hemorrhage in the conscious rabbit. However, some substance(s) released by the adrenal medulla, perhaps epinephrine, does play a role in naloxone's pressor effect, since this is reduced by adrenalectomy or adrenal denervation.

Modulation of respiratory responses to chemoreflex activation by l-glutamate and ATP in the rostral ventrolateral medulla of awake rats

2011 ◽  
Vol 300 (6) ◽  
pp. R1476-R1486 ◽  
Author(s):  
Davi J. A. Moraes ◽  
Leni G. H. Bonagamba ◽  
Daniel B. Zoccal ◽  
Benedito H. Machado
Keyword(s):  
Kynurenic Acid ◽  
Pressor Response ◽  
Respiratory Arrest ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Bötzinger Complex ◽  
Respiratory Chemoreflex ◽  
Peripheral Chemoreflex ◽  
Awake Rats

Presympathetic neurons in the different anteroposterior aspects of rostral ventrolateral medulla (RVLM) are colocalized with expiratory [Bötzinger complex (BötC)] and inspiratory [pre-Bötzinger complex (pre-BötC)] neurons of ventral respiratory column (VRC), suggesting that this region integrates the cardiovascular and respiratory chemoreflex responses. In the present study, we evaluated in different anteroposterior aspects of RVLM of awake rats the role of ionotropic glutamate and purinergic receptors on cardiorespiratory responses to chemoreflex activation. The bilateral ionotropic glutamate receptors antagonism with kynurenic acid (KYN) (8 nmol/50 nl) in the rostral aspect of RVLM (RVLM/BötC) enhanced the tachypneic (120 ± 9 vs. 180 ± 9 cpm; P < 0.01) and attenuated the pressor response (55 ± 2 vs. 15 ± 1 mmHg; P < 0.001) to chemoreflex activation ( n = 7). On the other hand, bilateral microinjection of KYN into the caudal aspect of RVLM (RVLM/pre-BötC) caused a respiratory arrest in four awake rats used in the present study. Bilateral P2X receptors antagonism with PPADS (0.25 nmol/50 nl) in the RVLM/BötC reduced chemoreflex tachypneic response (127 ± 6 vs. 70 ± 5 cpm; P < 0.001; n = 6), but did not change the chemoreflex pressor response. In addition, PPADS into the RVLM/BötC attenuated the enhancement of the tachypneic response to chemoreflex activation elicited by previous microinjections of KYN into the same subregion (188 ± 2 vs. 157 ± 3 cpm; P < 0.05; n = 5). Our findings indicate that: 1) l-glutamate, but not ATP, in the RVLM/BötC is required for pressor response to peripheral chemoreflex and 2) both transmitters in the RVLM/BötC are required for the processing of the ventilatory response to peripheral chemoreflex activation in awake rats.

Involvement of the paraventricular nucleus of the hypothalamus in the pressor response to chemoreflex activation in awake rats

2001 ◽  
Vol 895 (1-2) ◽  
pp. 167-172 ◽  
Author(s):  
Marcelo V. Olivan ◽  
Leni G.H. Bonagamba ◽  
Benedito H. Machado
Keyword(s):  
Paraventricular Nucleus ◽  
Pressor Response ◽  
Awake Rats

Increased Pressor Responsiveness to Enkephalin in Spontaneously Hypertensive Rats: The Role of Vasopressin

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Pressor Response ◽  
Cardiovascular Effects ◽  
Hypertensive Rats ◽  
Methionine Enkephalin ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto Rats ◽  
Wistar Kyoto

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.

Involvement of NMDA receptors in the pressor response to microinjection of 5-HT3 agonist into the NTS of awake rats

2002 ◽  
Vol 98 (1-2) ◽  
pp. 2-6 ◽  
Author(s):  
Ricardo V Reges ◽  
Leni G.H Bonagamba ◽  
Anne Nosjean ◽  
Raul Laguzzi ◽  
Benedito H Machado
Keyword(s):  
Nmda Receptors ◽  
Pressor Response ◽  
Awake Rats

Role of the Splanchnic Nerve and the Adrenal Medulla in the Genesis of ‘Preoptic Pulmonary Edema’

1956 ◽  
Vol 184 (2) ◽  
pp. 351-355 ◽  
Author(s):  
Frederick W. Maire ◽  
Harry D. Patton
Keyword(s):  
Body Weight ◽  
Protective Effect ◽  
Pulmonary Edema ◽  
Adrenal Medulla ◽  
Adrenal Glands ◽  
Splanchnic Nerve ◽  
Lung Edema ◽  
Splanchnic Nerves ◽  
Intact Rats

The pulmonary edema which follows preoptic lesions in rats is prevented by antecedent bilateral section of the splanchnic nerves. Intravenous epinephrine in doses exceeding 0.0125 mg/100 gm body weight causes fatal lung edema in rats comparable to that produced by preoptic lesions. Moreover, extracted pressor amines from rat adrenal glands cause lung edema, often fatal, when injected into the donor or into intact rats. However, adrenal demedullation does not prevent lung edema following preoptic lesions. Hence the protective effect of splanchnectomy against preoptic lesions is not wholly due to adrenal denervation. It is tentatively suggested that preoptic lung edema results from overloading of the pulmonary circuit owing to splanchnic mediated constriction of visceral venous reservoirs. Liver and spleen weights of animals dying from preoptic lung edema were significantly less than normal.

Direct effect of hypothalamic neuropeptides on the release of catecholamines by adrenal medulla in sheep – study ex vivo

2017 ◽  
Vol 20 (2) ◽  
pp. 339-346 ◽  
Author(s):  
D. Wrońska ◽  
B.F. Kania ◽  
M. Błachuta
Keyword(s):  
Adrenal Gland ◽  
Adrenal Medulla ◽  
Noradrenaline Release ◽  
Adrenocorticotropic Hormone ◽  
Ex Vivo ◽  
Adrenal System ◽  
Adrenaline Release ◽  
Hormone Control

Abstract Stress causes the activation of both the hypothalamic-pituitary-adrenocortical axis and sympatho-adrenal system, thus leading to the release from the adrenal medulla of catecholamines: adrenaline and, to a lesser degree, noradrenaline. It has been established that in addition to catecholamines, the adrenomedullary cells produce a variety of neuropeptides, including corticoliberine (CRH), vasopressin (AVP), oxytocin (OXY) and proopiomelanocortine (POMC) – a precursor of the adrenocorticotropic hormone (ACTH). The aim of this study was to investigate adrenal medulla activity in vitro depending, on a dose of CRH, AVP and OXY on adrenaline and noradrenaline release. Pieces of sheep adrenal medulla tissue (about 50 mg) were put on 24-well plates and were incubated in 1 mL of Eagle medium without hormone (control) or supplemented only once with CRH, AVP and OXY in three doses (10−7, 10−8 and 10−9 M) in a volume of 10 μL. The results showed that CRH stimulates adrenaline and noradrenaline release from the adrenal medulla tissue. The stimulating influence of AVP on adrenaline release was visible after the application of the two lower doses of this neuropeptide; however, AVP reduced noradrenaline release from the adrenal medulla tissue. A strong, inhibitory OXY effect on catecholamine release was observed, regardless of the dose of this hormone. Our results indicate the important role of OXY in the inhibition of adrenal gland activity and thus a better adaptation to stress on the adrenal gland level.

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