Role of nitrosyl factors in the hindlimb vasodilation elicited by baroreceptor afferent nerve stimulation

Possas, Olga S.; Johnson, Alan Kim; Lewis, Stephen J.

doi:10.1152/ajpregu.00660.2005

Cited by 16 publications

(19 citation statements)

References 28 publications

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“…This suggests that L-NAME did not interfere with the central actions of 5-HT or the central processing of autonomic outflow. We have also provided evidence that the systemic injection of a 25 µmol/kg dose of L-NAME did not interfere with central processing aortic depressor nerve or superior laryngeal afferent input (Possas et al, 1997, 2006). As such, it is unlikely that the ability of L-NAME to abolish the hindquarter vasodilation elicited by i.c.v.…”

Section: Discussionmentioning

confidence: 69%

“…injection of 5-HT in rats pretreated systemically with a 25 µg/kg dose of the NO synthesis inhibitor, N G -nitro-L-arginine methylester (L-NAME) (Moncada et al, 1991). This dose of L-NAME elicits robust hemodynamic responses, most likely by actions within microvasculature (see Davisson et al, 1996a), but does not appear to act in the brain since it did not interfere with central processing of afferent input regulating hemodynamic function (Possas et al, 1997, 2006). …”

Section: Introductionmentioning

confidence: 99%

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Effects of intracerebroventricular injections of 5-HT on systemic vascular resistances of conscious rats

Davisson

Bates

Johnson

et al. 2014

Microvascular Research

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The aims of this study were to determine (i) the effects of intracerebroventricular (i.c.v.) injections of 5-hydroxytryptamine (5-HT, 10 µg) on mean arterial blood pressure (MAP), heart rate (HR) and mesenteric (MR), renal (RR) and hindquarter (HQR) vascular resistances of conscious rats, (ii) the central 5-HT receptor subtype which mediates these effects, and (iii) the role of nitric oxide (NO) in the expression of these responses. The i.c.v. injection of 5-HT had minor effects on MAP but produced a decrease in HR (−18 ± 4%), which lasted for 20 min. The i.c.v. injection of 5-HT elicited marked increases in MR (+50 ± 7%) and reductions in HQR (−31 ± 3%). These responses occurred promptly and lasted for 25–35 min. 5-HT also produced a transient decrease in RR (−26 ± 8% at 10 min). All of these responses were prevented by the prior i.c.v. injection of the 5-HT1/5-HT2-receptor antagonist, methysergide (10 µg). The intravenous injection of the NO synthesis inhibitor, L-NAME (25 µmol/kg), produced a sustained pressor response, bradycardia and increases in MR, RR and HQR. Subsequent i.c.v. injection of 5-HT produced a minor pressor response (+7 ± 2%), bradycardia (−18 ± 3%), an increase in MR (+52 ± 8%) but no decreases in RR or HQR. This study demonstrates that i.c.v. 5-HT differentially affects peripheral vascular resistances by activation of central 5-HT1/5-HT2-receptors. It appears that L-NAME did not interfere with the central actions of 5-HT as it did not prevent the 5-HT-induced bradycardia or mesenteric vasoconstriction. Since the 5-HT-induced falls in RR and HQR were abolished by L-NAME, it is possible that these responses are mediated by an active neurogenic process involving the release of NO within the vasculature.

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Section: Discussionmentioning

confidence: 69%

Section: Introductionmentioning

confidence: 99%

Effects of intracerebroventricular injections of 5-HT on systemic vascular resistances of conscious rats

Davisson

Bates

Johnson

et al. 2014

Microvascular Research

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“…Although the reasons for this discrepancy are unclear, it might be suggested that sympathetic withdrawal is not the sole mechanism of baroreflex vasodilatations in the hindlimb circulation and that active phenomena are also involved. It has indeed been shown that the hindlimb circulation of the rat receives a nitroxidergic innervation (8) that might be, at least partly, under baroreflex control (26). During stimulation of the aortic depressor nerve, both sympathetic withdrawal and active neurogenic vasodilatation could act in concert, evoking stronger vasodilatory effects in the hindlimbs than in the kidney.…”

Section: Discussionmentioning

confidence: 99%

Baroreflex control of lumbar and renal sympathetic nerve activity in conscious rats

Kanbar

Chapuis²,

Oréa³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Kanbar R, Chapuis B, Oréa V, Barrès C, Julien C. Baroreflex control of lumbar and renal sympathetic nerve activity in conscious rats. Am J Physiol Regul Integr Comp Physiol 295: R8 -R14, 2008. First published April 30, 2008 doi:10.1152/ajpregu.00147.2008This study compared the baroreflex control of lumbar and renal sympathetic nerve activity (SNA) in conscious rats. Arterial pressure (AP) and lumbar and renal SNA were simultaneously recorded in six freely behaving rats. Pharmacological estimates of lumbar and renal sympathetic baroreflex sensitivity (BRS) were obtained by means of the sequential intravenous administration of sodium nitroprusside and phenylephrine. Sympathetic BRS was significantly (P Ͻ 0.05) lower for lumbar [3.0 Ϯ 0.4 normalized units (NU)/mmHg] than for renal (7.6 Ϯ 0.6 NU/mmHg) SNA. During a 219-min baseline period, spontaneous lumbar and renal BRS were continuously assessed by computing the gain of the transfer function relating AP and SNA at heart rate frequency over consecutive 61.4-s periods. The transfer gain was considered only when coherence between AP and SNA significantly differed from zero, which was verified in 99 Ϯ 1 and 96 Ϯ 3% of cases for lumbar and renal SNA, respectively. When averaged over the entire baseline period, spontaneous BRS was significantly (P Ͻ 0.05) lower for lumbar (1.3 Ϯ 0.2 NU/mmHg) than for renal (2.3 Ϯ 0.3 NU/mmHg) SNA. For both SNAs, spontaneous BRS showed marked fluctuations (variation coefficients were 26 Ϯ 2 and 28 Ϯ 2% for lumbar and renal SNA, respectively). These fluctuations were positively correlated in five of six rats (R ϭ 0.44 Ϯ 0.06; n ϭ 204 Ϯ 8; P Ͻ 0.0001). We conclude that in conscious rats, the baroreflex control of lumbar and renal SNA shows quantitative differences but is modulated in a mostly coordinated way. arterial pressure; baroreceptor reflex; sympathetic nervous system; transfer function THE ARTERIAL BARORECEPTOR reflex plays a major role in the short-term control of arterial pressure (AP) mainly through the modulation of efferent sympathetic nerve activity (SNA) to regional circulations (12). In rats, studies aimed at characterizing the baroreflex control of SNA under physiological conditions, i.e., in the conscious state, have been based mostly on recordings of renal SNA (RSNA;3,5,7,10,13,16,20,23,25), mainly because of the purely postganglionic nature of this activity. Most often, authors implicitly assumed that RSNA provided a reliable reflection of other regional SNAs. In the meantime, evidence has accumulated suggesting a differential baroreflex control of regional SNAs in several animal species (22). In the rat, the comparison of the baroreflex control of regional SNAs has been carried out in urethane-chloralose anesthetized animals by using the vasoactive drug injection technique, i.e., the so-called pharmacological method (29,30). In these studies, it was reported that the characteristics of the baroreflex function curves differed between RSNA, lumbar SNA (LSNA), and adrenal SNA. In conscious rats, this information has not...

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“…Accordingly, the vasodilation in the hindquarter bed of our pentobarbital-anesthetized rats may involve the relatively more pronounced down-regulation of α-adrenoreceptor-mediated vasoconstriction. It is also possible that the hindquarter vasodilation involves the activation of a unique neurogenic vasodilator pathway, which may release preformed pools of nitric oxide factors (Davisson et al, 1996a,b, 1997; Possas et al, 2006), with the capacity to directly dilate resistance arteries and blunt α-adrenoreceptor-mediated vasoconstriction (Nozik-Grayck et al, 2006). …”

Section: Discussionmentioning

confidence: 99%

Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

Whalen

Johnson

Lewis

2014

Microvascular Research

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Purpose The objectives of this study were (i) to characterize the hemodynamic responses caused by controlled hemorrhage (HEM) in pentobarbital-anesthetized rats, and (ii) to determine the responses elicited by systemic bolus injections of isotonic saline (0.15 M) or hypertonic saline (3 M) given 5 min after completion of HEM. Results Controlled HEM (4.3 ± 0.2 ml/rat at 1.5 ml/ min) resulted in a pronounced and sustained fall in mean arterial blood pressure (MAP) to about 40 mmHg. The fall in MAP was associated with a reduction in hindquarter vascular resistance (HQR) but no changes in renal (RR) or mesenteric (MR) vascular resistances. Systemic injections of isotonic saline (96–212 µmol/kg iv, in 250–550 µl) did not produce immediate responses but promoted the recovery of MAP to levels below pre-HEM values. Systemic injections of hypertonic saline (750–3000 µmol/kg, i.v., in 250–550 µl) produced immediate and pronounced falls in MAP, RR, MR and especially HQR of 30–120 sec in duration. However, hypertonic saline prompted a full recovery of MAP, HQR and RR to pre-HEM levels and an increase in MR to levels above pre-HEM values. Conclusions This study demonstrates that (i) HEM induced a pronounced fall in MAP which likely involved a fall in cardiac output and HQR, (ii) isotonic saline did not fully normalize MAP, and (iii) hypertonic saline produced dramatic initial responses, and promoted normalization of MAP probably by restoring blood volume and cardiac output through sequestration of fluid from intracellular compartments.

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Role of nitrosyl factors in the hindlimb vasodilation elicited by baroreceptor afferent nerve stimulation

Cited by 16 publications

References 28 publications

Effects of intracerebroventricular injections of 5-HT on systemic vascular resistances of conscious rats

Effects of intracerebroventricular injections of 5-HT on systemic vascular resistances of conscious rats

Baroreflex control of lumbar and renal sympathetic nerve activity in conscious rats

Hemodynamic responses elicited by systemic injections of isotonic and hypertonic saline in hemorrhaged rats

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