scholarly journals Rostral ventral medulla 5-HT1A receptors selectively inhibit the somatosympathetic reflex

2001 ◽  
Vol 280 (5) ◽  
pp. R1261-R1268 ◽  
Author(s):  
Takashi Miyawaki ◽  
Ann K. Goodchild ◽  
Paul M. Pilowsky

The role of the 5-hydroxytryptamine (5-HT1A) receptors in the rostral ventrolateral medulla (RVLM) on somatosympathetic, baroreceptor, and chemoreceptor reflexes was examined in anesthetized rats. Microinjection of the selective 5-HT1A agonist 8-hydroxy-di- n-propylamino tetralin (8-OH-DPAT) decreased arterial blood pressure and splanchnic sympathetic nerve activity (SNA). Electrical stimulation of the hindlimb evoked early and late excitatory sympathetic responses. Bilateral microinjection in the RVLM of 8-OH-DPAT markedly attenuated both the early and late responses. This potent inhibition of the somatosympathetic reflex persisted even after SNA and arterial blood pressure returned to preinjection levels. Preinjection of the selective 5-HT1A antagonist NAN-190 in the RVLM blocked the sympathoinhibitory effect of 8-OH-DPAT and attenuated the inhibitory effect on the somatosympathetic reflex. 8-OH-DPAT injected in the RVLM did not affect baroreceptor or chemoreceptor reflexes. Our findings suggest that activation of 5-HT1A receptors in the RVLM exerts a potent, selective inhibition on the somatosympathetic reflex.

2009 ◽  
Vol 81 (3) ◽  
pp. 589-603 ◽  
Author(s):  
Sergio L. Cravo ◽  
Ruy R. Campos ◽  
Eduardo Colombari ◽  
Mônica A. Sato ◽  
Cássia M. Bergamaschi ◽  
...  

Several forms of experimental evidence gathered in the last 37 years have unequivocally established that the medulla oblongata harbors the main neural circuits responsible for generating the vasomotor tone and regulating arterial blood pressure. Our current understanding of this circuitry derives mainly from the studies of Pedro Guertzenstein, a former student who became Professor of Physiology at UNIFESP later, and his colleagues. In this review, we have summarized the main findings as well as our collaboration to a further understanding of the ventrolateral medulla and the control of arterial blood pressure under normal and pathological conditions.


2009 ◽  
Vol 297 (4) ◽  
pp. H1478-H1486 ◽  
Author(s):  
Zhi-Ling Guo ◽  
Stephanie C. Tjen-A-Looi ◽  
Liang-Wu Fu ◽  
John C. Longhurst

Our previous studies have shown that nitric oxide (NO) synthase (NOS)-containing neurons in the rostral ventrolateral medulla (rVLM) are activated during cardiac sympathoexcitatory reflexes (Refs. 12 and 13 ). However, the precise function of NO in the rVLM in regulation of these reflexes has not been defined. Three isoforms of NOS, including neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS), are located in the rVLM. We explored the role of NO, derived from different NOS isoforms in the rVLM, in processing cardiac-sympathetic reflexes using whole animal reflex and electrophysiological approaches. We found that, in anesthetized cats, increased mean arterial blood pressure and renal sympathetic nerve activity elicited by epicardial application of bradykinin (BK; 1–10 μg/ml, 50 μl) were significantly attenuated following unilateral rVLM microinjection of the nonselective NOS inhibitor, Nω-nitro-l-arginine methyl ester (50 nmol/50 nl), or a specific nNOS inhibitor, 7-nitroindazole (7-NI; 5–10 pmol/50 nl; both P < 0.05). In contrast, the responses of mean arterial blood pressure and renal sympathetic nerve activity to cardiac BK stimulation were unchanged by unilateral rVLM microinjection of Nω-nitro-d-arginine methyl ester (inactive isomer of Nω-nitro-l-arginine methyl ester, 50 nmol/50 nl), 3–6% methanol (7-NI vehicle), N6-(1-iminoethyl)-l-lysine (250 pmol/50 nl; iNOS inhibitor), or N5-(1-iminoethyl)-l-ornithine (250 nmol/50 nl; eNOS inhibitor). Furthermore, in separate cats, we noted that iontophoresis of 7-NI (0.1 mM) reduced the increased discharge of cardiovascular sympathoexcitatory rVLM neurons in response to cardiac stimulation with BK ( P < 0.05). These neurons were characterized by their responses to inputs from baroreceptors, and their cardiac rhythmicity was determined through frequency and time domain analyses, correlating their discharge to arterial blood pressure and cardiac sympathetic efferent nerve activity. These data suggest that NO, specifically nNOS, mediates sympathetic cardiac-cardiovascular responses through its action in the rVLM.


1986 ◽  
Vol 250 (6) ◽  
pp. R1065-R1073 ◽  
Author(s):  
R. B. McCall

The purpose of the present investigation was to determine if gamma-aminobutyric acid (GABA) mediates the baroreceptor-induced inhibition of sympathetic nerve discharge (SND) in dialurethan-anesthetized cats. The GABA antagonists picrotoxin and bicuculline produced marked elevations in arterial blood pressure and inferior cardiac SND. The inhibition of SND observed during pressor responses was occasionally slightly depressed after picrotoxin or bicuculline. Midcollicullar transection blocked or reversed the increase in blood pressure and SND produced by GABA antagonists. Under these conditions, baroreceptor inhibition of SND was not affected by picrotoxin. Microinjections of picrotoxin into the rostral ventrolateral medulla produced increases in arterial blood pressure and SND but failed to affect baroreceptor-induced sympathoinhibition. GABA antagonists given intravenously also failed to affect the baroreceptor-induced inhibition of sympathetically related neurons recorded in the rostral ventrolateral medulla. However, intravenous picrotoxin did antagonize the inhibitory affect of microiontophoretically applied GABA on these neurons. These data provide no evidence to support the contention that GABA mediates the baroreceptor-induced inhibition of SND. The role of GABA in regulating SND is discussed.


2020 ◽  
Vol 129 (6) ◽  
pp. 1310-1323
Author(s):  
Jennifer L. Magnusson ◽  
Craig A. Emter ◽  
Kevin J. Cummings

The role of serotonin in arterial blood pressure (ABP) regulation across states of vigilance is unknown. We hypothesized that adult rats devoid of CNS serotonin (TPH2−/−) have low ABP in wakefulness and NREM sleep, when serotonin neurons are active. However, TPH2−/− rats experience higher ABP than TPH2+/+ rats in wakefulness and REM only, a phenotype present only in older males and not females. CNS serotonin may be critical for preventing high ABP in males with aging.


1990 ◽  
Vol 64 (4) ◽  
pp. 1115-1124 ◽  
Author(s):  
A. Randich ◽  
K. Ren ◽  
G. F. Gebhart

1. Supraspinal substrates mediating vagal afferent stimulation (VAS)-induced inhibition of the nociceptive tail-flick reflex were examined by the use of the soma-selective neurotoxin ibotenic acid and the nonselective local anesthetic lidocaine. Fifty rats were studied in the lightly anesthetized state maintained with pentobarbital sodium. 2. The threshold intensity of VAS required to inhibit the tail-flick reflex to a cut-off latency of 10 s was established in all rats. Ibotenic acid (5 or 10 micrograms, 0.5 microliter) or lidocaine (4%, 0.5 microliter) was then microinjected into various regions of the brain stem followed by reestablishment of the intensity of VAS required to produce inhibition of the tail-flick reflex. 3. Microinjections of ibotenic acid into the ipsilateral nucleus tractus solitarius (NTS), medial rostroventral medulla (principally the nucleus raphe magnus; NRM), or bilaterally into the dorsolateral pons (principally the locus coeruleus/subcoeruleus; LC/SC), significantly increased the threshold intensity of VAS required to inhibit the tail-flick reflex. Microinjections of ibotenic acid into either the rostral or caudal ventrolateral medulla (RVLM or CVLM, respectively) ipsilateral to the vagus nerve stimulated or ipsilateral LC/SC did not significantly affect the inhibition produced by VAS. Arterial blood pressure decreases produced by VAS were significantly attenuated or eliminated after microinjections of ibotenic acid into the NTS, RVLM, CVLM, or NRM. Lidocaine microinjected into the ipsilateral CVLM also significantly increased the intensity of VAS required to inhibit the tail-flick reflex. 4. These outcomes obtained with behavioral measures are consistent with the outcomes of the preceding study using electrophysiological measures in establishing that cells in the NTS, LC/SC, and NRM regions and fibers of passage in the CVLM are important in mediating the inhibitory effects of VAS. The present studies confirm previous reports of the importance of the RVLM and CVLM in VAS-produced depressor responses but also demonstrate that the NRM is critical for this cardiovascular response.


2013 ◽  
Vol 304 (5) ◽  
pp. H759-H766 ◽  
Author(s):  
Seth T. Fairfax ◽  
Jaume Padilla ◽  
Lauro C. Vianna ◽  
Michael J. Davis ◽  
Paul J. Fadel

Previous studies in humans attempting to assess sympathetic vascular transduction have related large reflex-mediated increases in muscle sympathetic nerve activity (MSNA) to associated changes in limb vascular resistance. However, such procedures do not provide insight into the ability of MSNA to dynamically control vascular tone on a beat-by-beat basis. Thus we examined the influence of spontaneous MSNA bursts on leg vascular conductance (LVC) and how variations in MSNA burst pattern (single vs. multiple bursts) and burst size may affect the magnitude of the LVC response. In 11 young men, arterial blood pressure, common femoral artery blood flow, and MSNA were continuously recorded during 20 min of supine rest. Signal averaging was used to characterize percent changes in LVC for 15 cardiac cycles following heartbeats associated with and without MSNA bursts. LVC significantly decreased following MSNA bursts, reaching a nadir during the 6th cardiac cycle (single bursts, −2.9 ± 1.1%; and multiple bursts, −11.0 ± 1.4%; both, P < 0.001). Individual MSNA burst amplitudes and the total amplitude of consecutive bursts were related to the magnitude of peak decreases in LVC. In contrast, cardiac cycles without MSNA bursts were associated with a significant increase in LVC (+3.1 ± 0.5%; P < 0.001). Total vascular conductance decreased in parallel with LVC also reaching a nadir around the peak rise in arterial blood pressure following an MSNA burst. Collectively, these data are the first to assess beat-by-beat sympathetic vascular transduction in resting humans, demonstrating robust and dynamic decreases in LVC following MSNA bursts, an effect that was absent for cardiac cycles without MSNA bursts.


2017 ◽  
Vol 2 (1) ◽  
pp. 14-17
Author(s):  
Sachin Vaishnav ◽  
Anita Shetty ◽  
Manjula Sarkar

ABSTRACT The stress response to an intense painful surgical stimulus is characterized by activation of the sympathetic nervous system and an increased secretion of the stress hormones. The ability of the alpha agonist dexmedetomidine (DEX) to decrease heart rate (HR) and arterial blood pressure in perioperative period was tested. One hundred and thirty two patients undergoing craniotomy for supratentorial tumor were randomly distributed to receive either saline (B group) or DEX (A group). The placebo group received saline, whereas the treatment group (A group) received a single bolus dose of DEX (1μg/kg) intravenously over 10 minutes before induction of anesthesia. Hemodynamic parameters, such as HR and arterial blood pressure were measured. Both the groups were comparable with respect to age, sex, American Society for Anesthesiologist grade, and duration of surgery. The arterial blood pressure and HR were found to be lower in the DEX group when compared with the placebo group. How to cite this article Vaishnav S, Shetty A, Sarkar M. Prospective Randomized Controlled Study to assess the Role of Dexmedetomidine on Perioperative Hemodynamics in Patients with Supratentorial Tumor undergoing Surgery. Res Inno in Anesth 2017;2(1):14-17.


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