Vasopressin V1 receptors contribute to hemodynamic and sympathoinhibitory responses evoked by stimulation of adenosine A2a receptors in NTS

2006 ◽  
Vol 290 (5) ◽  
pp. H1889-H1898 ◽  
Author(s):  
Tadeusz J. Scislo ◽  
Donal S. O'Leary
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Autonomic Response ◽  
Receptor Subtypes ◽  
Response Patterns ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Receptor Stimulation ◽  
A2a Receptors ◽  
Stimulation Of

Activation of adenosine A2a receptors in the nucleus of the solitary tract (NTS) decreases mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), whereas increases in preganglionic adrenal sympathetic nerve activity (pre-ASNA) occur, a pattern similar to that observed during hypotensive hemorrhage. Central vasopressin V1 receptors may contribute to posthemorrhagic hypotension and bradycardia. Both V1 and A2a receptors are densely expressed in the NTS, and both of these receptors are involved in cardiovascular control; thus they may interact. The responses elicited by NTS A2a receptors are mediated mostly via nonglutamatergic mechanisms, possibly via release of vasopressin. Therefore, we investigated whether blockade of NTS V1 receptors alters the autonomic response patterns evoked by stimulation of NTS A2a receptors (CGS-21680, 20 pmol/50 nl) in α-chloralose-urethane anesthetized male Sprague-Dawley rats. In addition, we compared the regional sympathetic responses to microinjections of vasopressin (0.1–100 ng/50 nl) into the NTS. Blockade of V1 receptors reversed the normal decreases in MAP into increases (−95.6 ± 28.3 vs. 51.4 ± 15.7 ∫Δ%), virtually abolished the decreases in HR (−258.3 ± 54.0 vs. 18.9 ± 57.8 ∫Δbeats/min) and RSNA (−239.3 ± 47.4 vs. 15.9 ± 36.1 ∫Δ%), and did not affect the increases in pre-ASNA (279.7 ± 48.3 vs. 233.1 ± 54.1 ∫Δ%) evoked by A2a receptor stimulation. The responses partially returned toward normal values ∼90 min after the blockade. Microinjections of vasopressin into the NTS evoked dose-dependent decreases in HR and RSNA and variable MAP and pre-ASNA responses with a tendency toward increases. We conclude that the decreases in MAP, HR, and RSNA in response to NTS A2a receptor stimulation may be mediated via release of vasopressin from neural terminals in the NTS. The differential effects of NTS V1 and A2a receptors on RSNA versus pre-ASNA support the hypothesis that these receptor subtypes are differentially located/expressed on NTS neurons/neural terminals controlling different sympathetic outputs.

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.

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.

scholarly journals Activation of NTS A2a adenosine receptors differentially resets baroreflex control of renal vs. adrenal sympathetic nerve activity

2009 ◽  
Vol 296 (4) ◽  
pp. H1058-H1068 ◽  
Author(s):  
Tomoko K. Ichinose ◽  
Donal S. O'Leary ◽  
Tadeusz J. Scislo
Keyword(s):  
Receptor Antagonist ◽  
Adenosine Receptors ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Response Curves ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
A2a Adenosine Receptors ◽  
Stimulation Of

The role of nucleus of solitary tract (NTS) A2a adenosine receptors in baroreflex mechanisms is controversial. Stimulation of these receptors releases glutamate within the NTS and elicits baroreflex-like decreases in mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), whereas inhibition of these receptors attenuates HR baroreflex responses. In contrast, stimulation of NTS A2a adenosine receptors increases preganglionic adrenal sympathetic nerve activity (pre-ASNA), and the depressor and sympathoinhibitory responses are not markedly affected by sinoaortic denervation and blockade of NTS glutamatergic transmission. To elucidate the role of NTS A2a adenosine receptors in baroreflex function, we compared full baroreflex stimulus-response curves for HR, RSNA, and pre-ASNA (intravenous nitroprusside/phenylephrine) before and after bilateral NTS microinjections of selective adenosine A2a receptor agonist (CGS-21680; 2.0, 20 pmol/50 nl), selective A2a receptor antagonist (ZM-241385; 40 pmol/100 nl), and nonselective A1 + A2a receptor antagonist (8-SPT; 1 nmol/100 nl) in urethane/α-chloralose anesthetized rats. Activation of A2a receptors decreased the range, upper plateau, and gain of baroreflex-response curves for RSNA, whereas these parameters all increased for pre-ASNA, consistent with direct effects of the agonist on regional sympathetic activity. However, no resetting of baroreflex-response curves along the MAP axis occurred despite the marked decreases in baseline MAP. The antagonists had no marked effects on baseline variables or baroreflex-response functions. We conclude that the activation of NTS A2a adenosine receptors differentially alters baroreflex control of HR, RSNA, and pre-ASNA mostly via non-baroreflex mechanism(s), and these receptors have virtually no tonic action on baroreflex control of these sympathetic outputs.

INFLUENCE OF SHORT-TERM VERSUS PROLONGED CARDIOPULMONARY RECEPTOR STIMULATION ON RENAL AND ADRENAL SYMPATHETIC NERVE ACTIVITY IN RATS

2004 ◽  
Vol 22 (Suppl. 2) ◽  
pp. S68
Author(s):  
T. Ditting ◽  
K. F. Hilgers ◽  
K. E. Scrogin ◽  
P. Linz ◽  
R. Veelken ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Short Term ◽  
Nerve Activity ◽  
Receptor Stimulation

Effects of corticospinal tract stimulation on renal sympathetic nerve activity in rats with intact and chronically lesioned spinal cords

2007 ◽  
Vol 293 (1) ◽  
pp. R178-R184 ◽  
Author(s):  
Baohan Pan ◽  
Matthew R. Zahner ◽  
Ewa Kulikowicz ◽  
Lawrence P. Schramm
Keyword(s):  
Spinal Cord ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Corticospinal Tract ◽  
Sympathetic Neurons ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Sympathetic Nerve ◽  
Renal Sympathetic ◽  
Stimulation Of

Sympathetic preganglionic neurons and interneurons are closely apposed (presumably synapsed upon) by corticospinal tract (CST) axons. Sprouting of the thoracic CST rostral to lumbar spinal cord injuries (SCI) substantially increases the incidence of these appositions. To test our hypothesis that these additional synapses would increase CST control of sympathetic activity after SCI, we measured the effects of electrical stimulation of the CST on renal sympathetic nerve activity (RSNA) and arterial pressure (AP) in α-chloralose-anesthetized rats with either chronically intact or chronically lesioned spinal cords. Stimuli were delivered to the CST at intensities between 25–150 μA and frequencies between 25 and 75 Hz. Stimulation of the CST at the midcervical level decreased RSNA and AP. These decreases were not mediated by direct projections of the CST to the thoracic spinal cord because we could still elicit them by midcervical stimulation after acute lesions of the CST at caudal cervical levels. In contrast, caudal thoracic CST stimulation increased RSNA and AP. Neither the responses to cervical nor thoracic stimulation were affected by chronic lumbar SCI. These data show that the CST mediates decreases in RSNA via a cervical spinal system but excites spinal sympathetic neurons at caudal thoracic levels. Because chronic lumber spinal cord injury affected responses evoked from neither the cervical nor thoracic CST, we conclude that lesion-induced or regeneration-induced formation of new synapses between the CST and sympathetic neurons may not affect cardiovascular regulation.

A highly selective cardiorenal serotonergic 5-HT3-mediated reflex in rats

1993 ◽  
Vol 264 (6) ◽  
pp. H1871-H1877 ◽  
Author(s):  
R. Veelken ◽  
K. F. Hilgers ◽  
M. Leonard ◽  
K. Scrogin ◽  
J. Ruhe ◽  
...  
Keyword(s):  
Sympathetic Nerve ◽  
Receptor Agonist ◽  
Sympathetic Nerve Activity ◽  
Short Term ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
Prolonged Stimulation ◽  
Saline Loading ◽  
Renal Sympathetic ◽  
Stimulation Of

To elucidate whether prolonged stimulation of cardiopulmonary serotonergic (5-HT3) receptors could play a role in the control of renal sympathetic nerve activity (RSNA), we compared 15-min intravenous infusions to bolus administrations of the 5-HT3 receptor agonist phenyl biguanide (PBG) and to a 0.9% saline load (5% body wt) in rats. Short-term and prolonged stimulation of 5-HT3-sensitive cardiopulmonary reflexes caused dose-related decreases in RSNA but not in lumbar sympathetic nerve activity (LSNA); only short-term stimulation caused decreases in blood pressure (BP) and heart rate (HR). Saline loading lowered RSNA but not LSNA, BP, or HR. Baroreceptor denervation did not influence any of these responses. Scopolamine attenuated BP and HR but not RSNA responses to bolus PBG. Pretreatment with a 5-HT3 receptor antagonist inhibited responses to PBG but not to saline. Vagotomy abolished all responses to all interventions. Thus 1) the prolonged stimulation of cardiopulmonary 5-HT3 receptors caused sustained suppression of RSNA, 2) decreased BP and HR were manifest only during short-term stimulation (3 min), and 3) blockade of 5-HT3 receptors did not influence responses to cardiopulmonary mechanoreceptor stimulation.

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