Subregions of rostral ventral medulla control arterial pressure and regional hemodynamics

1989 ◽  
Vol 257 (3) ◽  
pp. R635-R640 ◽  
Author(s):  
B. F. Cox ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Tidal Volume ◽  
Vascular Resistance ◽  
Neural Control ◽  
Cardiovascular Response ◽  
Cardiovascular Effects ◽  
Ventrolateral Medulla ◽  
Ventral Medulla ◽  
Ventromedial Medulla ◽  
Regional Hemodynamics

The cardiovascular effects of inactivating rostral ventromedial medulla (RVMM) under conditions of normal (2.5 ml) and reduced (1.5 ml) tidal volume were studied in urethan-anesthetized rats. Bilateral microinjection of lidocaine (200 nl, 4%) reduced mean arterial pressure (MAP), renal, mesenteric, and particularly hindquarter vascular resistance. These effects were not significantly altered by reducing tidal volume. Electrical stimulation of RVMM increased MAP and regional vascular resistances, again with the hindquarter change most prominent. The integrated cardiovascular response to stimulating rostral ventrolateral medulla (RVLM) appears to require integrity of RVMM; however, the converse is not true. Overall, these studies indicate that 1) the potential for RVMM to maintain neurogenic control of arterial pressure is as great as RVLM; 2) RVMM is capable of playing a proportionally greater role in the controlling hindquarter vascular resistance; 3) the integrity of RVMM appears to be important for responses elicited from RVLM; and 4) unlike RVLM, neural control of arterial pressure is sustained by RVMM under conditions of reduced tidal volume. We conclude that RVLM and RVMM are functionally and anatomically distinct subregions of rostral ventral medulla with equivalent capacity to maintain vasomotor tone.

Mechanisms of pressor response produced by stimulation of nucleus ambiguus

1990 ◽  
Vol 259 (5) ◽  
pp. R955-R962
Author(s):  
B. H. Machado ◽  
M. J. Brody
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Nucleus Ambiguus ◽  
Ventrolateral Medulla ◽  
Pressor Responses ◽  
Regional Vascular Resistance ◽  
Parasympathetic Control ◽  
Renal Vascular ◽  
Stimulation Of

We showed previously that activation of nucleus ambiguus (NA) induced bradycardia and increased arterial pressure. In this study, we compared responses produced by electrical and chemical (glutamate) stimulation of NA and adjacent rostral ventrolateral medulla (RVLM). Equivalent pressor responses were elicited from both areas. However: 1) The response from RVLM was elicited at a lower frequency. 2) Regional vascular resistance changes were different, i.e., electrical stimulation of NA increased vascular resistance in hindquarters much more than the renal and mesenteric beds. In contrast, electrical and chemical stimulation of RVLM produced a more prominent effect on the renal vascular bed. 3) Bradycardia was elicited from NA at lower current intensity. 4) Glutamate produced bradycardia only when injected into NA. Studies in rats with sinoaortic deafferentation showed that bradycardic response to activation of NA was only partly reflex in origin. We conclude that 1) NA and RVLM control sympathetic outflow to regional vascular beds differentially and 2) the NA region involves parasympathetic control of heart rate and sympathetic control of arterial pressure.

scholarly journals Hemodynamic response pattern predicts susceptibility to stress-induced elevation in arterial pressure in the rat

2001 ◽  
Vol 281 (1) ◽  
pp. R31-R37 ◽  
Author(s):  
Jay R. Muller ◽  
Khoi M. Le ◽  
William R. Haines ◽  
Qi Gan ◽  
Mark M. Knuepfer
Keyword(s):  
Cardiac Output ◽  
Conditioned Stimulus ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Acute Stress ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Response Patterns ◽  
Air Jet ◽  
Poststress Period

Cocaine or air jet stress evokes pressor responses due to either a large increase in systemic vascular resistance (vascular responders) or small increases in both cardiac output and vascular resistance (mixed responders) in conscious rats. Repeated cocaine administration results in elevated arterial pressure in vascular responders but not in mixed responders. The present study examined the hypothesis that the pattern of cardiovascular responses to an unconditioned stimulus (UCS; air jet) is related to responses to a conditioned stimulus (CS; tone followed by brief foot shock) in individual rats. Our data demonstrate that presentation of the UCS produced variable cardiac output responses that correlated with responses to the CS ( n = 60). We also determined whether individual cardiovascular response patterns to acute stress correlated with predisposition to a sustained stress-induced elevation in arterial pressure. Rats were exposed to three different stressors presented one per day successively for 4 wk and during a poststress period of 3 wk while arterial pressure was recorded periodically. Mean arterial pressure was elevated in all rats during chronic stress but, during the poststress period, remained at significantly higher levels in vascular responders but not mixed responders. Therefore, we conclude that acute behavioral stress to a conditioned stimulus elicits variable hemodynamic responses that predict the predisposition to a sustained stress-induced elevation in arterial pressure.

A source of adenosine involved in cardiovascular responses to defense area stimulation

1997 ◽  
Vol 272 (1) ◽  
pp. R195-R200 ◽  
Author(s):  
J. H. St Lambert ◽  
T. Thomas ◽  
G. Burnstock ◽  
K. M. Spyer
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Arterial Pressure ◽  
Cardiovascular Response ◽  
Muscle Blood Flow ◽  
Cardiovascular Responses ◽  
Ventrolateral Medulla ◽  
Atp Metabolism ◽  
Alpha Beta ◽  
Alpha Chloralose

We have investigated the source of central adenosine important in modulating the cardiovascular response to hypothalamic defense area (HDA) stimulation in alpha-chloralose-anesthetized rats. Microinjections of an ecto-5'-nucleotidase inhibitor, alpha,beta-methylene ADP (alpha,beta-meADP), were made into caudal nucleus of the solitary tract (cNTS) and rostral ventrolateral medulla (RVLM), and its effects on HDA-evoked responses were observed. Stimulation of HDA evoked an increase in arterial pressure and a secondary rise in arterial pressure after stimulation ceased. There was also an increase in heart rate and hindlimb blood flow. alpha,beta-meADP had no effect on resting levels of arterial pressure, heart rate, and hindlimb blood flow when injected into the cNTS or RVLM. alpha,beta-meADP also had no effect on the HDA-evoked tachycardia and increase in muscle blood flow. However, alpha,beta-meADP reduced the primary increase in arterial pressure evoked by HDA stimulation when microinjected into the cNTS. In contrast, alpha,beta-meADP reduced the secondary increase in arterial pressure when microinjected into the RVLM. From these results, we suggest that at least part of the adenosine released centrally during HDA stimulation is derived extracellularly from ATP metabolism.

Role of pressor mechanisms from the NTS and CVLM in control of arterial pressure

2005 ◽  
Vol 289 (5) ◽  
pp. R1416-R1425 ◽  
Author(s):  
Thiago Santos Moreira ◽  
Monica Akemi Sato ◽  
Ana Carolina Thomaz Takakura ◽  
José Vanderlei Menani ◽  
Eduardo Colombari
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Kynurenic Acid ◽  
Ventrolateral Medulla ◽  
Solitary Tract ◽  
Baseline Levels ◽  
Renal Vascular

In the present study, we investigated the effects of inhibition of the caudal ventrolateral medulla (CVLM) with the GABAA agonist muscimol combined with the blockade of glutamatergic mechanism in the nucleus of the solitary tract (NTS) with kynurenic acid (kyn) on mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances. In male Holtzman rats anesthetized intravenously with urethane/chloralose, bilateral injections of muscimol (120 pmol) into the CVLM or bilateral injections of kyn (2.7 nmol) into the NTS alone increased MAP to 186 ± 11 and to 142 ± 6 mmHg, respectively, vs. control: 105 ± 4 mmHg; HR to 407 ± 15 and to 412 ± 18 beats per minute (bpm), respectively, vs. control: 352 ± 12 bpm; and renal, mesenteric and hindquarter vascular resistances. However, in rats with the CVLM bilaterally blocked by muscimol, additional injections of kyn into the NTS reduced MAP to 88 ± 5 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Moreover, in rats with the glutamatergic mechanisms of the NTS blocked by bilateral injections of kyn, additional injections of muscimol into the CVLM also reduced MAP to 92 ± 2 mmHg and mesenteric and hindquarter vascular resistances below control baseline levels. Simultaneous blockade of NTS and CVLM did not modify the increase in HR but also abolished the increase in renal vascular resistance produced by each treatment alone. The results suggest that important pressor mechanisms arise from the NTS and CVLM to control vascular resistance and arterial pressure under the conditions of the present study.

Descending pathways mediating cardiovascular response from dorsomedial hypothalamic nucleus

2001 ◽  
Vol 280 (6) ◽  
pp. H2891-H2901 ◽  
Author(s):  
M. A. P. Fontes ◽  
T. Tagawa ◽  
J. W. Polson ◽  
S.-J. Cavanagh ◽  
R. A. L. Dampney
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve Activity ◽  
Nucleus Tractus Solitarius ◽  
Cardiovascular Response ◽  
Ventrolateral Medulla ◽  
Hypothalamic Nucleus ◽  
Descending Pathways ◽  
Renal Sympathetic Nerve Activity ◽  
Dorsomedial Hypothalamic Nucleus ◽  
Renal Sympathetic

Physiological and anatomic methods were used to determine whether neurons in the rostral ventrolateral medulla (RVLM), nucleus tractus solitarius (NTS), or hypothalamic paraventricular nucleus (PVN) mediate the cardiovascular response evoked from the dorsomedial hypothalamic nucleus (DMH), which is believed to play a key role in mediating responses to stress. In urethane-anesthetized rats, activation of neurons in the DMH by microinjection of bicuculline resulted in a large increase in arterial pressure, heart rate, and renal sympathetic nerve activity. The pressor and sympathoexcitatory responses, but not the tachycardic response, were greatly reduced after bilateral muscimol injections into the RVLM even when baseline arterial pressure was maintained at a constant level. These responses were not reduced by muscimol injections into the PVN or NTS. Retrograde tracing experiments identified many neurons in the DMH that projected directly to the RVLM. The results indicate that the vasomotor and cardiac components of the response evoked from the DMH are mediated by pathways that are dependent and independent, respectively, of neurons in the RVLM.

Galanin microinjection into rostral ventrolateral medulla of the rat is hypotensive and attenuates sympathetic chemoreflex

2009 ◽  
Vol 296 (4) ◽  
pp. R1019-R1026 ◽  
Author(s):  
Stephen B. G. Abbott ◽  
Paul M. Pilowsky
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Response ◽  
Cardiovascular Responses ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Somatosympathetic Reflex

Galanin is present in neurons in the brain that are important in the control of arterial pressure, and intracisternal administration of galanin evokes hypotension, but the site of action is unknown. In urethane-anesthetized, vagotomized mechanically ventilated Sprague-Dawley rats ( n = 34), we investigated the effects of microinjecting galanin (1 mM, 50 nl, 50 pmol) into the rostral ventrolateral medulla on resting splanchnic sympathetic nerve activity, arterial pressure, heart rate, and phrenic nerve activity. Second, we determined the effect of microinjecting galanin into the rostral ventrolateral medulla on the cardiovascular response to stimulation of central and peripheral chemoreceptors, arterial baroreceptors, and the somatosympathetic reflex. Galanin caused a prolonged reduction in resting splanchnic sympathetic nerve activity (−37.0 ± 7.2% of baseline), mean arterial pressure (−17.0 ± 3.5 mmHg), and heart rate (−25.0 ± 9.1 beats/min). Galanin increased the sympathoinhibitory response to aortic depressor nerve stimulation by 51.8%, had no effect on the somatosympathetic reflex, and markedly attenuated the effect of hypercapnia and hypoxia on arterial pressure (by 65% and 92.4% of control, respectively). These results suggest a role for galanin neurotransmission in the integration of the cardiovascular responses to hypoxia, hypercapnia, and the sympathetic baroreflex in the rostral ventrolateral medulla. The data suggest that galanin may be an important peptide in the homeostatic regulation of chemosensory reflexes.

Mechanisms of respiration-induced changes in vasomotor control exerted by rostral ventrolateral medulla

1989 ◽  
Vol 257 (3) ◽  
pp. R626-R634 ◽  
Author(s):  
B. F. Cox ◽  
M. J. Brody
Keyword(s):  
Tidal Volume ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Base Line ◽  
Renal Sympathetic Nerve Activity ◽  
Depressor Response ◽  
Regional Hemodynamics ◽  
Vascular Beds ◽  
Induced Changes ◽  
Sympathetic Vasomotor Tone

Efferent and afferent mechanisms involved in the differential depressor response to inactivating rostral ventrolateral medulla (RVLM) under conditions of normal (2.5 ml) and reduced (1.5 ml) tidal volume were examined in urethan-anesthetized rats. Under conditions of reduced tidal volume, bilateral microinjection of lidocaine (200 nl, 4%) into RVLM produced an attenuated fall in both mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) despite the fact that base-line levels of both are unchanged. The specificity of the differential response was tested by examination of regional hemodynamics. Microinjecting lidocaine into RVLM produced an attenuated fall in renal, mesenteric, and hindquarter vascular resistances in parallel with the attenuated fall in MAP produced by reducing tidal volume. Microelectrode stimulation of RVLM produced an increase in resistance in all three vascular beds. Of the neural sensory systems examined, both vagal and chest wall afferents appear to be involved in mediating the differential depressor response. These results demonstrate the importance of afferent sensory input to the medulla in determining sites of generation and maintenance of sympathetic vasomotor tone.

scholarly journals Effects of vagotomy on cardiovascular response to periodic apneas in sedated pigs

1999 ◽  
Vol 86 (6) ◽  
pp. 1890-1896 ◽  
Author(s):  
D. Slamowitz ◽  
L. Chen ◽  
S. M. Scharf
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Mechanical Effects

There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; +19 ± 25%, P < 0.05), systemic vascular resistance (SVR; +33 ± 16%, P < 0.0005), and heart rate (HR; +5 ± 6%, P < 0.05) and decreased cardiac output (CO) and stroke volume (SV; −16 ± 10% P < 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater (∼14%, P < 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes.

Coronary vasoconstrictor pathway from anterior hypothalamus includes neurons in RVLM

1993 ◽  
Vol 265 (6) ◽  
pp. R1311-R1317 ◽  
Author(s):  
A. R. Goodson ◽  
T. S. LaMaster ◽  
D. D. Gutterman
Keyword(s):  
Electrical Stimulation ◽  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Chemical Activation ◽  
Ventrolateral Medulla ◽  
Coronary Vascular Resistance ◽  
Gamma Aminobutyric Acid ◽  
Coronary Vasoconstriction ◽  
Coronary Vasoconstrictor

We have previously identified discrete brain sites [anterior (AHA) and lateral hypothalamus, periaqueductal gray, pontine parabrachial nucleus, lateral reticular formation, and rostral ventrolateral medulla (RVLM)] in the cat, in which electrical or chemical activation produces coronary vasoconstriction. This study examines whether the most rostral (AHA) and caudal (RVLM) of these sites are connected as part of a common pathway mediating coronary vasoconstriction. In chloralose-anesthetized cats, electrical stimulation in the AHA produced maximum increases in arterial pressure (41 +/- 10%) and coronary vascular resistance (28 +/- 9%). Microinjection of lidocaine into the RVLM attenuated the increases in arterial pressure (10 +/- 3%) and coronary vascular resistance (5 +/- 1%) in response to electrical stimulation in the AHA (P < 0.05 vs. before lidocaine). Lidocaine nonspecifically inhibits neural elements in the region. gamma-Aminobutyric acid in the RVLM, which selectively inhibits cell bodies and not fibers passing through the RVLM, attenuated the increase in coronary vascular resistance (38 +/- 8 to 14 +/- 3%; P < 0.05) but not the increase in arterial pressure (87 +/- 12 to 92 +/- 16%) in response to electrical stimulation in the AHA. These data indicate that coronary vasoconstriction in response to electrical stimulation in the AHA requires cell bodies in the RVLM; however, the associated pressor response is mediated by fibers passing through the RVLM. We conclude that a polysynaptic descending pathway that mediates sympathetic coronary vasoconstriction descends from the AHA through a synaptic connection in the RVLM.

c-fos antisense in rostral ventral medulla reduces arterial blood pressure

1994 ◽  
Vol 266 (4) ◽  
pp. R1418-R1422 ◽  
Author(s):  
S. Suzuki ◽  
P. Pilowsky ◽  
J. Minson ◽  
L. Arnolda ◽  
I. J. Llewellyn-Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Arterial Blood Pressure ◽  
Antisense Oligonucleotide ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Arterial Blood ◽  
Ventral Medulla ◽  
Wistar Kyoto

The effect of blocking the expression of c-fos in the rostral ventral medulla (RVM) on the control of arterial blood pressure was determined. In six male Wistar-Kyoto rats (WKY), unilateral injection of an antisense oligonucleotide to c-fos mRNA suppressed the expression of Fos-like immunoreactivity in neurons in the RVM in response to inhibition of depressor neurons in the caudal ventrolateral medulla (CVLM). Under pentobarbital anesthesia the mean arterial pressure of rats injected with antisense oligonucleotide (n = 10) bilaterally into RVM was significantly reduced after 6 h compared with sense-treated controls (n = 9) (76.5 +/- 3.7 vs. 92.4 +/- 3.5 mmHg; P < 0.05). Furthermore, the pressor response to bilateral injection of muscimol into CVLM was significantly smaller in rats injected with antisense oligonucleotide 6 h earlier (n = 6) compared with sense-treated controls (n = 6) (changes in mean arterial pressure, +40.3 +/- 3.6 vs. +68.7 +/- 4.8 mmHg, P < 0.005). These studies demonstrate that expression of c-fos in the RVM can be blocked in vivo by treatment with an antisense oligonucleotide, and that basal and stimulated expression of the c-fos gene is important in the central control of arterial blood pressure.

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