Differential control of renal vs. adrenal sympathetic nerve activity by NTS A2a and P2x purinoceptors

1998 ◽  
Vol 275 (6) ◽  
pp. H2130-H2139 ◽  
Author(s):  
Tadeusz J. Scislo ◽  
Donal S. O’Leary
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Receptor Activation ◽  
Differential Inhibition ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Cgs 21680 ◽  
Sprague Dawley Rats ◽  
Sympathetic Responses ◽  
Differential Control

Activation of adenosine A2a and ATP P2x purinoceptors in the subpostremal nucleus tractus solitarii (NTS) via microinjection of the selective agonists CGS-21680 and α,β-methylene ATP (α,β-MeATP), respectively, elicits large dose-dependent decreases in arterial pressure and heart rate, differential regional vasodilation, and differential inhibition of regional sympathetic outputs. With marked hypotensive hemorrhage, preganglionic adrenal sympathetic nerve activity (pre-ASNA) increases, whereas renal (RSNA) and postganglionic adrenal sympathetic nerve activity (post-ASNA) decrease. In this setting, adenosine levels in the brain stem increase. Therefore, we investigated whether stimulation of specific purinoceptors in the NTS may evoke differential sympathetic responses. RSNA was recorded simultaneously with pre-ASNA or post-ASNA in chloralose-urethan-anesthetized male Sprague-Dawley rats. CGS-21680 (2 and 20 pmol in 50 nl) inhibited RSNA and post-ASNA, whereas pre-ASNA increased markedly. α,β-MeATP (25 and 100 pmol in 50 nl) inhibited all sympathetic outputs. Sinoaortic denervation plus vagotomy markedly prolonged the responses to P2x-purinoceptor stimulation. Glutamate (100 pmol in 50 nl) caused differential inhibition of all sympathetic outputs similar to that evoked by α,β-MeATP. We conclude that NTS A2a-purinoceptor activation evokes differential sympathetic responses similar to those observed during hemorrhage, whereas P2x-purinoceptor and glutamate-receptor activation evokes differential inhibition of sympathetic outputs similar to arterial baroreflex responses.

scholarly journals Arcuate nucleus injection of an anti-insulin affibody prevents the sympathetic response to insulin

2013 ◽  
Vol 304 (11) ◽  
pp. H1538-H1546 ◽  
Author(s):  
Brittany S. Luckett ◽  
Jennifer L. Frielle ◽  
Lawrence Wolfgang ◽  
Sean D. Stocker
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Arcuate Nucleus ◽  
Insulin Receptors ◽  
Ventromedial Hypothalamus ◽  
Intracerebroventricular Injection ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Sympathetic Response ◽  
Sprague Dawley Rats

Accumulating evidence suggests that insulin acts within the hypothalamus to alter sympathetic nerve activity (SNA) and baroreflex function. Although insulin receptors are widely expressed across the hypothalamus, recent evidence suggests that neurons of the arcuate nucleus (ARC) play an important role in the sympathoexcitatory response to insulin. The purpose of the present study was to determine whether circulating insulin acts directly in the ARC to elevate SNA. In anesthetized male Sprague-Dawley rats (275–425 g), the action of insulin was neutralized by microinjection of an anti-insulin affibody (1 ng/40 nl). To verify the efficacy of the affibody, ARC pretreatment with injection of the anti-insulin affibody completely prevented the increase in lumbar SNA produced by ARC injection of insulin. Next, ARC pretreatment with the anti-insulin affibody attenuated the lumbar sympathoexcitatory response to intracerebroventricular injection of insulin. Third, a hyperinsulinemic-euglycemic clamp increased lumbar, but not renal, SNA in animals that received ARC injection of a control affibody. However, this sympathoexcitatory response was absent in animals pretreated with the anti-insulin affibody in the ARC. Injection of the anti-insulin affibody in the adjacent ventromedial hypothalamus did not alter the sympathoexcitatory response to insulin. The ability of the anti-insulin affibody to prevent the sympathetic effects of insulin cannot be attributed to a general inactivation or nonspecific effect on ARC neurons as the affibody did not alter the sympathoexcitatory response to ARC disinhibition by gabazine. Collectively, these findings suggest that circulating insulin acts within the ARC to increase SNA.

Glucocorticoids reduce responses to AMPA receptor activation and blockade in nucleus tractus solitarius

2003 ◽  
Vol 284 (5) ◽  
pp. H1751-H1761 ◽  
Author(s):  
Sylvan S. Shank ◽  
Deborah A. Scheuer
Keyword(s):  
Arterial Pressure ◽  
Ampa Receptors ◽  
Sympathetic Nerve Activity ◽  
Nucleus Tractus Solitarius ◽  
Receptor Activation ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Sprague Dawley Rats ◽  
Renal Sympathetic

We tested the hypothesis that glucocorticoids attenuate changes in arterial pressure and renal sympathetic nerve activity (RSNA) in response to activation and blockade of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors within the nucleus of the solitary tract (NTS). Experiments were performed in Inactin-anesthetized male Sprague-Dawley rats treated for 7 ± 1 days with a subcutaneous corticosterone (Cort) pellet or in control rats. Baseline mean arterial pressure (MAP) was significantly higher in Cort-treated rats (109 ± 2 mmHg, n = 39) than in control rats (101 ± 1 mmHg, n = 48, P < 0.05). In control rats, microinjection of AMPA (0.03, 0.1, and 0.3 pmol/100 nl) into the NTS significantly decreased MAP at all doses and decreased RSNA at 0.1 and 0.3 pmol/100 nl. Responses to AMPA in Cort-treated rats were attenuated at all doses of AMPA ( P < 0.05). Responses to the AMPA-kainate receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) were also significantly reduced in Cort-treated rats relative to control rats. Blockade of glucocorticoid type II receptors with mifepristone significantly enhanced responses to CNQX in both control and Cort rats. We conclude that glucocorticoids attenuate MAP and RSNA responses to activation and blockade of AMPA receptors in the NTS.

Peripheral endotoxin increases splenic sympathetic nerve activity via central prostaglandin synthesis

1997 ◽  
Vol 273 (2) ◽  
pp. R609-R614 ◽  
Author(s):  
B. J. MacNeil ◽  
A. H. Jansen ◽  
L. J. Janz ◽  
A. H. Greenberg ◽  
D. M. Nance
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Prostaglandin Synthesis ◽  
Intermediate Step ◽  
Intracerebroventricular Injection ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Intravenous Injections ◽  
Sprague Dawley Rats ◽  
The Central Nervous System

We tested whether prostaglandin synthesis mediates the lipopolysaccharide (LPS)-induced increase in splenic sympathetic nerve activity. Sprague-Dawley rats were pretreated with intravenous or intracerebroventricular injections of indomethacin, and splenic nerve activity was recorded after intravenous injections of LPS. In vehicle-pretreated rats, 100 micrograms LPS induced a 62.8 +/- 5.6% increase in splenic nerve activity beginning 22.7 +/- 2.7 min postinjection. All vehicle-pretreated animals responded to high (100 micrograms, 5 of 5 animals) and low (10 micrograms, 8 of 8 animals) doses of LPS. Both intravenous (15 mg/kg) and intracerebroventricular (50 micrograms) pretreatments with indomethacin delayed (F1.19 = 30.66, P < 0.001) the increase in nerve activity after 100 micrograms LPS. When given intravenously, 50 micrograms indomethacin (the intracerebroventricular dose) did not delay the response to intravenous LPS, indicating that the effects of intracerebroventricular indomethacin pretreatment were restricted to the central nervous system. Importantly, intracerebroventricular indomethacin reduced (2 of 7 animals) or completely blocked (5 of 7 animals) the splenic nerve response to the low dose of LPS (10 micrograms, iv). The indomethacin effects could not be accounted for by central release of vasopressin because intracerebroventricular injection of indomethacin did not alter baseline nerve activity or blood pressure, whereas intracerebroventricular injection of vasopressin rapidly increased both measures. Additionally, central injection of LPS did not elevate splenic nerve activity, whereas intracerebroventricular injection of prostaglandin E2 induced a rapid (2.2 +/- 2.7 min) increase in splenic nerve activity. These data indicate that central prostaglandin synthesis is an intermediate step whereby systemic LPS elicits an increase in sympathetic outflow to an immune organ.

Differential role of ionotropic glutamatergic mechanisms in responses to NTS P2x and A2a receptor stimulation

2000 ◽  
Vol 278 (6) ◽  
pp. H2057-H2068 ◽  
Author(s):  
Tadeusz J. Scislo ◽  
Donal S. O'Leary
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Slow Component ◽  
Glutamate Release ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Receptor Stimulation ◽  
Cgs 21680 ◽  
Fast Responses ◽  
Stimulation Of

Activation of ATP P2x receptors in the subpostremal nucleus tractus solitarii (NTS) via microinjection of α,β-methylene ATP (α,β-MeATP) elicits fast initial depressor and sympathoinhibitory responses that are followed by slow, long-lasting inhibitory effects. Activation of NTS adenosine A2a receptors via microinjection of CGS-21680 elicits slow, long-lasting decreases in arterial pressure and renal sympathetic nerve activity (RSNA) and an increase in preganglionic adrenal sympathetic nerve activity (pre-ASNA). Both P2x and A2a receptors may operate via modulation of glutamate release from central neurons. We investigated whether intact glutamatergic transmission is necessary to mediate the responses to NTS P2x and A2areceptor stimulation. The hemodynamic and neural (RSNA and pre-ASNA) responses to microinjections of α,β-MeATP (25 pmol/50 nl) and CGS-21680 (20 pmol/50 nl) were compared before and after pretreatment with kynurenate sodium (KYN; 4.4 nmol/100 nl) in chloralose-urethan-anesthetized male Sprague-Dawley rats. KYN virtually abolished the fast responses to α,β-MeATP and tended to enhance the slow component of the neural responses. The depressor responses to CGS-21680 were mostly preserved after pretreatment with KYN, although the increase in pre-ASNA was reduced by one-half following the glutamatergic blockade. We conclude that the fast responses to stimulation of NTS P2x receptors are mediated via glutamatergic ionotropic mechanisms, whereas the slow responses to stimulation of NTS P2x and A2a receptors are mediated mostly via other neuromodulatory mechanisms.

NTS A2a purinoceptor activation elicits hindlimb vasodilation primarily via a β-adrenergic mechanism

2000 ◽  
Vol 278 (6) ◽  
pp. H1775-H1782 ◽  
Author(s):  
Amy M. Kitchen ◽  
Tadeusz J. Scislo ◽  
Donal S. O'Leary
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Responses ◽  
Receptor Activation ◽  
Adrenergic Blockade ◽  
Nerve Activity ◽  
Lumbar Sympathectomy ◽  
Cgs 21680 ◽  
Adrenergic Mechanism ◽  
Stimulation Of

Previously, we have shown that activation of adenosine A2a receptors in the subpostremal nucleus tractus solitarii (NTS) via microinjection of the selective A2a receptor agonist CGS-21680 elicits potent, dose-dependent decreases in mean arterial pressure and preferential, marked hindlimb vasodilation. Although A2a receptor activation does not change lumbar sympathetic nerve activity, it does markedly enhance the preganglionic adrenal sympathetic nerve activity, which will increase epinephrine release and could subsequently elicit hindlimb vasodilation via activation of β2-adrenergic receptors. Therefore we investigated whether this hindlimb vasodilation was due to neural or humoral mechanisms. In chloralose-urethan-anesthetized male Sprague-Dawley rats, we monitored cardiovascular responses to stimulation of NTS adenosine A2a receptors (CGS-21680, 20 pmol/50 nl) in the intact control animals; after pretreatment with propranolol (2 mg/kg iv), a β-adrenergic antagonist; after bilateral lumbar sympathectomy; after bilateral adrenalectomy; and after combined bilateral lumbar sympathectomy and adrenalectomy. After β-adrenergic blockade, stimulation of NTS adenosine A2a receptors produced a pressor response and a hindlimb vasoconstriction. Lumbar sympathectomy reduced the vasodilation seen in the intact animals by ∼40%, and adrenalectomy reduced it by ∼80%. The combined sympathectomy and adrenalectomy virtually abolished the hindlimb vasodilation evoked by NTS A2a receptor activation. We conclude that the preferential, marked hindlimb vasodilation produced by stimulation of NTS adenosine A2a receptors is mediated by both the efferent sympathetic nerves directed to the hindlimb and the adrenal glands via primarily a β-adrenergic mechanism.

Age-related central and baroreceptor impairment in female Sprague-Dawley rats

1989 ◽  
Vol 256 (5) ◽  
pp. H1399-H1406 ◽  
Author(s):  
S. Tanabe ◽  
R. D. Bunag
Keyword(s):  
Heart Rate ◽  
Sodium Nitroprusside ◽  
Sympathetic Nerve ◽  
Baroreflex Sensitivity ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Reflex Responses ◽  
Sprague Dawley Rats ◽  
Old Rats

To determine whether baroreflex sensitivity changes with age, we compared drug-induced reflex responses in 2- and 9-mo-old female Sprague-Dawley rats anesthetized with urethan-chloralose. Baroreflexes were stimulated by elevating or lowering blood pressure with intravenous infusions of phenylephrine or sodium nitroprusside. Reflex responses in heart rate and sympathetic nerve activity during phenylephrine infusions were weaker in 9- than in 2-mo-old rats, as were reflex tachycardia during sodium nitroprusside infusion and decreases in heart rate and sympathetic nerve activity elicited by electrical stimulation of the left aortic depressor nerve. Afferent aortic nerve activity was also appreciably lower in 9-mo-old rats at pressures greater than 130 mmHg but did not differ between rat groups at normotensive pressures. These results suggest that baroreflex sensitivity in 9-mo-old rats can be characterized as follows: 1) impaired at pressures greater than 130 mmHg but still adequate at normotensive pressures, and 2) all reflex arc components may be impaired.

Contrasting effects of vasopressin on baroreflex inhibition of lumbar sympathetic nerve activity

1985 ◽  
Vol 249 (5) ◽  
pp. H922-H928 ◽  
Author(s):  
F. M. Sharabi ◽  
G. B. Guo ◽  
F. M. Abboud ◽  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Urinary Osmolality ◽  
Arterial Baroreceptors ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
High Level

Baroreflex inhibition of lumbar sympathetic nerve activity (LSNA) during intravenous infusions of phenylephrine and vasopressin is contrasted in rats and rabbits. In rabbits, vasopressin caused smaller increases in arterial pressure and greater inhibition of LSNA than phenylephrine. In Sprague-Dawley rats, however, both vasopressin and phenylephrine caused equivalent increases in arterial pressure and reflex reductions in LSNA. The inhibition of LSNA was mediated through the arterial baroreceptors in both species because it was abolished by sinoaortic denervation. In rats, the possibility that a high level of endogenous vasopressin may have prevented the demonstration of a facilitated baroreflex with the infusion of exogenous vasopressin is unlikely since vasopressin also did not facilitate the reflex in Brattleboro rats, which lack circulating vasopressin. Further, Sprague-Dawley rats were responsive to exogenous vasopressin since infusion of increasing doses of vasopressin caused significant increases in urinary osmolality as well as progressive increments in arterial pressure. The results indicate that intravenous vasopressin given for a period of 6 min facilitates the reflex inhibition of LSNA mediated through arterial baroreceptors in rabbits, but not in rats. Vasopressin given for a period of up to 45 min to rats also fails to facilitate baroreflexes, emphasizing the difference from rabbits. In rabbits, this facilitation appears to involve a central mechanism.

Splanchnic sympathetic nerve activity and circulating catecholamines in the hyperthermic rat

1991 ◽  
Vol 70 (4) ◽  
pp. 1821-1826 ◽  
Author(s):  
C. V. Gisolfi ◽  
R. D. Matthes ◽  
K. C. Kregel ◽  
R. Oppliger
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Heat Exposure ◽  
Splanchnic Nerve ◽  
Plasma Catecholamine ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Sprague Dawley Rats ◽  
Greater Splanchnic Nerve ◽  
Alpha Chloralose

The mechanisms responsible for the initial rise in splanchnic vascular resistance with environmental heating are controversial, and those responsible for the subsequent fall in splanchnic resistance in the severely hyperthermic animal are unknown. Thus we examined the effect of environmental heating on plasma catecholamine concentration, splanchnic sympathetic nerve activity (SNA), and select blood chemistries. In one study, 25 male Sprague-Dawley rats (270-300 g) were assigned to one of five groups on the basis of their core temperature (Tc, 37, 39, 41, 43, or 44 degrees C) at death. Heart rate (HR), mean arterial pressure (MAP), and Tc were monitored during heat stress under alpha-chloralose anesthesia (12.5 mg.ml-1.h-1). At each predetermined Tc, an aortic blood sample was drawn and analyzed for mean plasma concentration of norepinephrine (NE), epinephrine (E), Na+, K+, and lactate. From 41 to 43 degrees C, NE and E rose significantly, and the animals became hyperkalemic and lactacidemic. In a separate study, we quantitated SNA from the greater splanchnic nerve during heat exposure of artificially respired animals anesthetized with pentobarbital sodium (50 mg/kg). MAP, splanchnic SNA, and Tc were recorded. Tc was elevated from 37.0 +/- 0.12 to 41.3 +/- 0.18 degrees C in 70 min by increase of ambient temperature to 38 degrees C in an environmental chamber. Splanchnic SNA was 54 +/- 8 spikes/s at a Tc of 37 degrees C and increased significantly as Tc exceeded 39 degrees C (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

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