Cardiovascular adjustments induced by hypertonic saline in hemorrhagic rats: Involvement of carotid body chemoreceptors

Pedrino, Gustavo Rodrigues; Rossi, M; Schoorlemmer, Guus H. M.; Lopes, Oswaldo Ubrı́aco; Cravo, Sérgio L.

doi:10.1016/j.autneu.2010.11.009

Cited by 12 publications

(21 citation statements)

References 29 publications

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“…Previous studies demonstrated the involvement of carotid and aortic afferents in endocrine and renal responses induced by acute hypernatremia . Furthermore, Dibona et al .…”

Section: Discussionmentioning

confidence: 92%

Involvement of sinoaortic afferents in renal sympathoinhibition and vasodilation induced by acute hypernatremia

Silva

Sera

Mourão

et al. 2015

Clin Exp Pharma Physio

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Despite the abundance of evidence that supports the important role of aortic and carotid afferents to short-term regulation of blood pressure and detection of variation in the arterial PO2 , PCO2 and pH, relatively little is known regarding the role of these afferents during changes in the volume and composition of extracellular compartments. The present study sought to determine the involvement of these afferents in the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Sinoaortic-denervated and sham male Wistar rats were anaesthetised with intravenous (i.v.) urethane (1.2 g/kg body weight (bw)) prior to the measurement of the mean arterial pressure (MAP), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA). In the sham group, the HS infusion (3 mol/L NaCl, 1.8 mL/kg bw, i.v.) induced transient hypertension (12 ± 4 mmHg from baseline, peak at 10 min; P < 0.05), an increase in RVC (127 ± 9% and 150 ± 13% from baseline, at 20 and 60 min respectively; P < 0.05) and a decrease in RSNA (-34 ± 10% and -29 ± 5% from baseline, at 10 and 60 min respectively; P < 0.05). In sinoaortic-denervated rats, HS infusion promoted a sustained pressor response (30 ± 5 and 17 ± 6 mmHg of baseline values, at 10 and 30 min respectively; P < 0.05) and abolished the increase in RVC (85 ± 8% from baseline, at 10 min) and decrease in RSNA (-4 ± 3% from baseline, at 10 min). These results suggest that aortic and carotid afferents are involved in cardiovascular and renal sympathoinhibition responses induced by acute hypernatremia.

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“…Previous studies demonstrated the involvement of carotid and aortic afferents in endocrine and renal responses induced by acute hypernatremia . Furthermore, Dibona et al .…”

Section: Discussionmentioning

confidence: 92%

Involvement of sinoaortic afferents in renal sympathoinhibition and vasodilation induced by acute hypernatremia

Silva

Sera

Mourão

et al. 2015

Clin Exp Pharma Physio

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“…The baroreflex and chemoreflex are important mechanisms that are used to recover homeostasis after changes in extracellular volume and composition occur [10], [26], [57]. Previous studies demonstrated that the hypertension that was induced by HS was significantly higher in sinoaortic,denervated rats [10].…”

Section: Discussionmentioning

confidence: 99%

“…The central nervous system (CNS) detects variations in the volume, tonicity, and composition of the extracellular compartment through various peripheral and central receptors [2]–[5]. Once detected,these changes trigger a set of responses that reestablish physiological conditions.…”

Section: Introductionmentioning

confidence: 99%

A1 Noradrenergic Neurons Lesions Reduce Natriuresis and Hypertensive Responses to Hypernatremia in Rats

et al. 2013

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Noradrenergic neurons in the caudal ventrolateral medulla (CVLM; A1 group) contribute to cardiovascular regulation. The present study assessed whether specific lesions in the A1 group altered the cardiovascular responses that were evoked by hypertonic saline (HS) infusion in non-anesthetized rats. Male Wistar rats (280–340 g) received nanoinjections of antidopamine-β-hydroxylase-saporin (A1 lesion, 0.105 ng.nL−1) or free saporin (sham, 0.021 ng.nL−1) into their CVLMs. Two weeks later, the rats were anesthetized (2% halothane in O2) and their femoral artery and vein were catheterized and led to exit subcutaneously between the scapulae. On the following day, the animals were submitted to HS infusion (3 M NaCl, 1.8 ml • kg−1, b.wt., for longer than 1 min). In the sham-group (n = 8), HS induced a sustained pressor response (ΔMAP: 35±3.6 and 11±1.8 mmHg, for 10 and 90 min after HS infusion, respectively; P<0.05 vs. baseline). Ten min after HS infusion, the pressor responses of the anti-DβH-saporin-treated rats (n = 11)were significantly smaller(ΔMAP: 18±1.4 mmHg; P<0.05 vs. baseline and vs. sham group), and at 90 min, their blood pressures reached baseline values (2±1.6 mmHg). Compared to the sham group, the natriuresis that was induced by HS was reduced in the lesioned group 60 min after the challenge (196±5.5 mM vs. 262±7.6 mM, respectively; P<0.05). In addition, A1-lesioned rats excreted only 47% of their sodium 90 min after HS infusion, while sham animals excreted 80% of their sodium. Immunohistochemical analysis confirmed a substantial destruction of the A1 cell group in the CVLM of rats that had been nanoinjected withanti-DβH-saporin. These results suggest that medullary noradrenergic A1 neurons are involved in the excitatory neural pathway that regulates hypertensive and natriuretic responses to acute changes in the composition of body fluid.

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“…We subsequently examined the role of carotid body chemoreceptors in the effect of hypertonic saline, inactivating the carotid body chemoreceptors by ligation of the carotid body arteries. That study indicated that the nervous organ glomus caroticum has a prominent and determinant role in the effect of hyperosmotic saline (26). When the function of carotid body chemoreceptors was blocked, leaving all nerves in the area functional, hyperosmotic saline failed to restore arterial pressure.…”

Section: Role Of Carotid Afferents In Responses To Ecf Changesmentioning

confidence: 92%

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

Cravo

Lopes

Pedrino

2011

Braz J Med Biol Res

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Water deprivation and hypernatremia are major challenges for water and sodium homeostasis. Cellular integrity requires maintenance of water and sodium concentration within narrow limits. This regulation is obtained through engagement of multiple mechanisms and neural pathways that regulate the volume and composition of the extracellular fluid. The purpose of this short review is to summarize the literature on central neural mechanisms underlying cardiovascular, hormonal and autonomic responses to circulating volume changes, and some of the findings obtained in the last 12 years by our laboratory. We review data on neural pathways that start with afferents in the carotid body that project to medullary relays in the nucleus tractus solitarii and caudal ventrolateral medulla, which in turn project to the median preoptic nucleus in the forebrain. We also review data suggesting that noradrenergic A1 cells in the caudal ventrolateral medulla represent an essential link in neural pathways controlling extracellular fluid volume and renal sodium excretion. Finally, recent data from our laboratory suggest that these structures may also be involved in the beneficial effects of intravenous infusion of hypertonic saline on recovery from hemorrhagic shock.

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Cardiovascular adjustments induced by hypertonic saline in hemorrhagic rats: Involvement of carotid body chemoreceptors

Cited by 12 publications

References 29 publications

Involvement of sinoaortic afferents in renal sympathoinhibition and vasodilation induced by acute hypernatremia

Involvement of sinoaortic afferents in renal sympathoinhibition and vasodilation induced by acute hypernatremia

A1 Noradrenergic Neurons Lesions Reduce Natriuresis and Hypertensive Responses to Hypernatremia in Rats

Involvement of catecholaminergic medullary pathways in cardiovascular responses to acute changes in circulating volume

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