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

Cravo, Sérgio L.; Lopes, Oswaldo Ubrı́aco; Pedrino, Gustavo Rodrigues

doi:10.1590/s0100-879x2011007500092

Cited by 6 publications

(9 citation statements)

References 58 publications

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“…Previous studies have indicated that A2 neurons are involved in the regulation of body fluid homeostasis [10]–[14], [22]–[25]. However, there was previously no evidence to support the contribution of these neurons to the autonomic control of the circulating volume composition.…”

Section: Discussionmentioning

confidence: 94%

“…Studies have shown the importance of medullary noradrenergic neurons in the integration of the mechanisms involved in the autonomic, cardiovascular and respiratory systems [3], [10]–[15], [22], [24], [25], [27], [33]–[36]. With regard to the A1 noradrenergic cluster, several authors have shown that these neurons are important for the response induced by changes in the circulating volume [3], [12], [15], [22], [27], [33]–[37].…”

Section: Discussionmentioning

confidence: 99%

“…With regard to the A1 noradrenergic cluster, several authors have shown that these neurons are important for the response induced by changes in the circulating volume [3], [12], [15], [22], [27], [33]–[37]. Studies have demonstrated that increases in the sodium plasma concentration induce the expression of c-Fos in these noradrenergic neurons, indicating their activation [15], [23].…”

Section: Discussionmentioning

confidence: 99%

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A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats

et al. 2012

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Renal vasodilation and sympathoinhibition are recognized responses induced by hypernatremia, but the central neural pathways underlying such responses are not yet entirely understood. Several findings suggest that A2 noradrenergic neurons, which are found in the nucleus of the solitary tract (NTS), play a role in the pathways that contribute to body fluid homeostasis and cardiovascular regulation. The purpose of this study was to determine the effects of selective lesions of A2 neurons on the renal vasodilation and sympathoinhibition induced by hypertonic saline (HS) infusion. Male Wistar rats (280–350 g) received an injection into the NTS of anti-dopamine-beta-hydroxylase-saporin (A2 lesion; 6.3 ng in 60 nl; n = 6) or free saporin (sham; 1.3 ng in 60 nl; n = 7). Two weeks later, the rats were anesthetized (urethane 1.2 g⋅kg−1 b.wt., i.v.) and the blood pressure, renal blood flow (RBF), renal vascular conductance (RVC) and renal sympathetic nerve activity (RSNA) were recorded. In sham rats, the HS infusion (3 M NaCl, 1.8 ml⋅kg−1 b.wt., i.v.) induced transient hypertension (peak at 10 min after HS; 9±2.7 mmHg) and increases in the RBF and RVC (141±7.9% and 140±7.9% of baseline at 60 min after HS, respectively). HS infusion also decreased the RSNA (−45±5.0% at 10 min after HS) throughout the experimental period. In the A2-lesioned rats, the HS infusion induced transient hypertension (6±1.4 mmHg at 10 min after HS), as well as increased RBF and RVC (133±5.2% and 134±6.9% of baseline at 60 min after HS, respectively). However, in these rats, the HS failed to reduce the RSNA (115±3.1% at 10 min after HS). The extent of the catecholaminergic lesions was confirmed by immunocytochemistry. These results suggest that A2 noradrenergic neurons are components of the neural pathways regulating the composition of the extracellular fluid compartment and are selectively involved in hypernatremia-induced sympathoinhibition.

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Section: Discussionmentioning

confidence: 94%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats

et al. 2012

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“…In the 1980s, important study revealed that HSI was able to quickly restore blood pressure and cardiac output [ 5 ]. Although these hemodynamic responses to HSI in animals with hemorrhagic shock are already well established in the literature [ 6 – 9 ], there is still dearth of information about the involvement of central nervous system (CNS) in HSI induced resuscitation.…”

Section: Introductionmentioning

confidence: 99%

Median Preoptic Nucleus Mediates the Cardiovascular Recovery Induced by Hypertonic Saline in Hemorrhagic Shock

Amaral

Naves

Ferreira-Neto

et al. 2014

The Scientific World Journal

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Changes in plasma osmolarity, through central and peripheral osmoreceptors, activate the median preoptic nucleus (MnPO) that modulates autonomic and neuroendocrine adjustments. The present study sought to determine the participation of MnPO in the cardiovascular recovery induced by hypertonic saline infusion (HSI) in rats submitted to hemorrhagic shock. The recordings of mean arterial pressure (MAP) and renal vascular conductance (RVC) were carried out on male Wistar rats (250–300 g). Hemorrhagic shock was induced by blood withdrawal over 20 min until the MAP values of approximately 60 mmHg were attained. The nanoinjection (100 nL) of GABAA agonist (Muscimol 4 mM; experimental group (EXP)) or isotonic saline (NaCl 150 mM; control (CONT)) into MnPO was performed 2 min prior to intravenous overload of sodium through HSI (3 M NaCl, 1.8 mL/kg, b.wt.). Hemorrhagic shock reduced the MAP in control (62 ± 1.1 mmHg) and EXP (61 ± 0.4 mmHg) equipotently. The inhibition of MnPO impaired MAP (CONT: 104 ± 4.2 versus EXP: 60 ± 6.2 mmHg) and RVC (CONT: 6.4 ± 11.4 versus EXP: -53.5 ± 10.0) recovery 10 min after HSI. The overall results in this study demonstrated, for the first time, that the MnPO plays an essential role in the HSI induced resuscitation during hypovolemic hemorrhagic shock.

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“…The present study demonstrated that OT induced a concentration-dependent relaxation in renal arteries both in vivo and in vitro. The complex mechanisms involved in the genesis and maintenance of the renal vasodilation induced by increases plasma sodium concentration are poorly understood and seem to involve hormonal and autonomic mechanisms [8] , [10] , [14] , [41] , [42] . Our in vitro results show that OT can act on oxytocin receptors in the renal vasculature to promote vasodilatation.…”

Section: Discussionmentioning

confidence: 99%

Efferent Pathways in Sodium Overload-Induced Renal Vasodilation in Rats

et al. 2014

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Hypernatremia stimulates the secretion of oxytocin (OT), but the physiological role of OT remains unclear. The present study sought to determine the involvement of OT and renal nerves in the renal responses to an intravenous infusion of hypertonic saline. Male Wistar rats (280–350 g) were anesthetized with sodium thiopental (40 mg. kg−1, i.v.). A bladder cannula was implanted for collection of urine. Animals were also instrumented for measurement of mean arterial pressure (MAP) and renal blood flow (RBF). Renal vascular conductance (RVC) was calculated as the ratio of RBF by MAP. In anesthetized rats (n = 6), OT infusion (0.03 µg • kg−1, i.v.) induced renal vasodilation. Consistent with this result, ex vivo experiments demonstrated that OT caused renal artery relaxation. Blockade of OT receptors (OXTR) reduced these responses to OT, indicating a direct effect of this peptide on OXTR on this artery. Hypertonic saline (3 M NaCl, 1.8 ml • kg−1 b.wt., i.v.) was infused over 60 s. In sham rats (n = 6), hypertonic saline induced renal vasodilation. The OXTR antagonist (AT; atosiban, 40 µg • kg−1 • h−1, i.v.; n = 7) and renal denervation (RX) reduced the renal vasodilation induced by hypernatremia. The combination of atosiban and renal denervation (RX+AT; n = 7) completely abolished the renal vasodilation induced by sodium overload. Intact rats excreted 51% of the injected sodium within 90 min. Natriuresis was slightly blunted by atosiban and renal denervation (42% and 39% of load, respectively), whereas atosiban with renal denervation reduced sodium excretion to 16% of the load. These results suggest that OT and renal nerves are involved in renal vasodilation and natriuresis induced by acute plasma hypernatremia.

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

Cited by 6 publications

References 58 publications

A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats

A2 Noradrenergic Lesions Prevent Renal Sympathoinhibition Induced by Hypernatremia in Rats

Median Preoptic Nucleus Mediates the Cardiovascular Recovery Induced by Hypertonic Saline in Hemorrhagic Shock

Efferent Pathways in Sodium Overload-Induced Renal Vasodilation in Rats

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