Intracellular pH response to hypercapnia in neurons from chemosensitive areas of the medulla

1997 ◽  
Vol 273 (1) ◽  
pp. R433-R441 ◽  
Author(s):  
N. A. Ritucci ◽  
J. B. Dean ◽  
R. W. Putnam
Keyword(s):  
Intracellular Ph ◽  
Medulla Oblongata ◽  
Imaging System ◽  
Brain Slices ◽  
Ventrolateral Medulla ◽  
Disulfonic Acid ◽  
Hypoglossal Nucleus ◽  
Hypercapnic Acidosis ◽  
Sprague Dawley ◽  
Chemosensitive Areas

We investigated whether neurons in two chemosensitive areas of the medulla oblongata [nucleus of the solitary tract (NTS) and ventrolateral medulla (VLM)] respond to hypercapnia differently than neurons in two nonchemosensitive areas of the medulla oblongata [inferior olive (IO) and hypoglossal nucleus (Hyp)]. Medullary brain slices from preweanling Sprague-Dawley rats were loaded with 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein, and intracellular pH (pHi) was followed in individual neurons at 37 degrees C with the use of a fluorescence imaging system. Most neurons from the NTS and VLM did not exhibit pHi recovery when CO2 was increased from 5 to 10% at constant extracellular HCO3- concentration [extracellular pH (pHo) decreased approximately 0.3 pH unit] (hypercapnic acidosis). However, when CO2 was increased from 5 to 10% at constant pHo (isohydric hypercapnia), pHi recovery was seen. In contrast, all neurons from the IO and Hyp exhibited pHi recovery during hypercapnic acidosis. All pHi recovery in the four areas studied was inhibited by 1 mM amiloride and unaffected by 0.5 mM 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid. These data indicate that 1) pHi regulation differs between neurons in chemosensitive (NTS and VLM) and nonchemosensitive (IO and Hyp) areas of the medulla, 2) pHi recovery is due solely to Na+/H+ exchange in all four areas, and 3) Na+/H+ exchange is more sensitive to inhibition by extracellular acidosis in NTS and VLM neurons than in IO and Hyp neurons.

Plasticity of GABAergic control of hypothalamic presympathetic neurons in hypertension

2006 ◽  
Vol 290 (3) ◽  
pp. H1110-H1119 ◽  
Author(s):  
De-Pei Li ◽  
Hui-Lin Pan
Keyword(s):  
Brain Slices ◽  
Functional Change ◽  
Ventrolateral Medulla ◽  
Sympathetic Outflow ◽  
Sprague Dawley ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Whole Cell Patch Clamp ◽  
Output Neurons ◽  
Wistar Kyoto

Increased sympathetic outflow contributes to the pathogenesis of hypertension. However, the mechanisms of increased sympathetic drive in hypertension remain unclear. We examined the tonic GABAergic inhibition in control of the excitability of paraventricular (PVN) presympathetic neurons in spontaneously hypertensive rats (SHR) and normotensive controls, including Sprague-Dawley (SD) and Wistar-Kyoto (WKY) rats. Whole cell patch-clamp recordings were performed on retrogradely labeled PVN neurons projecting to the rostral ventrolateral medulla (RVLM) in brain slices. The basal firing rate of PVN neurons was significantly decreased in 13-wk-old SD and WKY rats but increased in 13-wk-old SHR, compared with their respective 6-wk-old controls. The GABAA antagonist bicuculline consistently increased the firing of PVN neurons in normotensive controls. Surprisingly, bicuculline either decreased the firing or had no effect in 59.3% of labeled cells in 13-wk-old SHR. In contrast, the GABAB antagonist CGP-55845 had no effect on the firing of PVN neurons in normotensive controls but significantly increased the firing of 75% of cells studied in 13-wk-old SHR. Furthermore, the evoked GABAA current decreased significantly in labeled PVN neurons of 13-wk-old SHR compared with that in normotensive controls. Both the frequency and amplitude of GABAergic spontaneously inhibitory postsynaptic currents were also reduced in 13-wk-old SHR. This study demonstrates an unexpected functional change in GABAA and GABAB receptors in regulation of the firing activity of PVN-RVLM neurons in SHR. This change in GABAA receptor function and GABAergic inputs to PVN output neurons may contribute to increased sympathetic outflow in hypertension.

HYPERCAPNIC ACIDOSIS PRECONDITIONS BRAIN SLICES TO HYPOXIA

2003 ◽  
Vol 99 (Supplement) ◽  
pp. B12
Author(s):  
Ozan Akça ◽  
Ralphiel S Payne ◽  
Franz Kehl ◽  
Daniel I Sessler ◽  
Avital Schurr
Keyword(s):  
Brain Slices ◽  
Hypercapnic Acidosis

Effect of systemic acid-base disorders on ileal intracellular pH and ion transport

1986 ◽  
Vol 250 (5) ◽  
pp. G588-G593 ◽  
Author(s):  
J. D. Wagner ◽  
P. Kurtin ◽  
A. N. Charney
Keyword(s):  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Strong Correlations ◽  
Sprague Dawley ◽  
Acid Base ◽  
Ileal Mucosa ◽  
Arterial Pco2 ◽  
Co2 Partial Pressure ◽  
Arterial Ph ◽  
Acute Metabolic Acidosis

We previously reported that changes in ileal net Na absorption correlated with arterial pH, changes in net HCO3 secretion correlated with the plasma HCO3 concentration, and changes in net Cl absorption correlated with arterial CO2 partial pressure (PCO2) during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediated these effects, we measured pHi and calculated [HCO3]i in the distal ileal mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4,-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis, and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, mucosal pHi was not altered, but there were strong correlations between mucosal [HCO3]i and both arterial PCO2 (r = 0.97) and [HCO3] (r = 0.61). When we considered the rates of ileal electrolyte transport that characterized these acid-base disorders [A. N. Charney and L.P. Haskell, Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G230-G235, 1983], we found strong correlations between mucosal [HCO3]i and both net Cl absorption (r = 0.88) and net HCO3 secretion (r = 0.82). These findings suggest that the systemic acid-base disorders do not affect ileal mucosal pHi but do alter mucosal [HCO3]i as a consequence of altered arterial PCO2 and [HCO3]. The effects of these disorders on ileal net Cl absorption and HCO3 secretion may be mediated by changes in [HCO3]i. Arterial pH does not appear to alter ileal Na absorption through changes in the mucosal acid-base milieu.

scholarly journals Role of the medulla oblongata in normal and high arterial blood pressure regulation: the contribution of Escola Paulista de Medicina - UNIFESP

2009 ◽  
Vol 81 (3) ◽  
pp. 589-603 ◽  
Author(s):  
Sergio L. Cravo ◽  
Ruy R. Campos ◽  
Eduardo Colombari ◽  
Mônica A. Sato ◽  
Cássia M. Bergamaschi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Blood Pressure ◽  
Medulla Oblongata ◽  
Neural Circuits ◽  
Ventrolateral Medulla ◽  
Vasomotor Tone ◽  
Arterial Blood ◽  
Pathological Conditions ◽  
De Medicina

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.

Effect of electroacupuncture on pressor reflex during gastric distension

2002 ◽  
Vol 283 (6) ◽  
pp. R1335-R1345 ◽  
Author(s):  
Peng Li ◽  
Kasra Rowshan ◽  
Melissa Crisostomo ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Peroneal Nerve ◽  
Cardiovascular Response ◽  
Pressor Response ◽  
Gastric Wall ◽  
Ventrolateral Medulla ◽  
Gastric Distension ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Stomach Meridian ◽  
Pressor Reflex

The effect of electroacupuncture (EA) on the reflex cardiovascular response induced by mechanical distension of the stomach was studied in ventilated male Sprague-Dawley rats anesthetized by ketamine and α-chloralose. Repeated balloon inflation of the stomach to produce 20 mmHg tension on the gastric wall induced a consistent rise in mean arterial pressure, while heart rate (372 ± 22 beats/min) was unchanged. This response was reversed by transection of the splanchnic nerves. Bilateral application of EA (1–2 mA, 2 Hz) at Neiguan-Jianshi acupoints (pericardial meridian, Pe 5–6) over the median nerve for 30 min significantly decreased the pressor response from 33 ± 6 to 18 ± 4 mmHg ( n = 7, P < 0.05). This effect began after 10 min of EA and continued for 40 min after termination of EA. EA at Zusanli-Shangquxu acupoints (stomach meridian, St 36–37) over the deep peroneal nerve similarly inhibited the pressor response. The effect lasted for 10 min after EA was stopped ( n = 6, P < 0.05), while EA at Guangming-Xuanzhong acupoints (gallbladder meridian, GB 37–39) over the superficial peroneal nerve did not inhibit the pressor response. Naloxone injected intravenously ( n = 6) immediately after termination of EA or administered by microinjection into the rostral ventrolateral medulla (rVLM) 25 min after initiation of EA ( n = 6) reversed the inhibition by EA, suggesting an opiate mechanism, including the rVLM, was involved.

Contribution of α2-adrenoceptors in caudal ventrolateral medulla to cardiovascular regulation in rat

1998 ◽  
Vol 274 (4) ◽  
pp. R1119-R1124 ◽  
Author(s):  
Shogo Sesoko ◽  
Hiromi Muratani ◽  
Masanobu Yamazato ◽  
Hiroshi Teruya ◽  
Shuichi Takishita ◽  
...  
Keyword(s):  
Cardiovascular Effect ◽  
Ventrolateral Medulla ◽  
Sprague Dawley ◽  
Renal Sympathetic Nerve Activity ◽  
Caudal Ventrolateral Medulla ◽  
Adrenoceptor Antagonist ◽  
Sprague Dawley Rats ◽  
Artificial Cerebrospinal Fluid ◽  
Cardiovascular Neurons ◽  
Selective Blocker

The inhibitory action of α2-agonists on the cardiovascular neurons has been elucidated in the rostral ventrolateral medulla (RVLM) but not in the caudal ventrolateral medulla (CVLM). Our study aimed to clarify whether microinjection of clonidine into the CVLM elicits any cardiovascular effect and whether endogenous α2-adrenoceptor-mediated mechanisms contribute to the tonic activity of the CVLM neurons. In male Sprague-Dawley rats (7–9 wk old, 270–320 g) anesthetized with urethan, unilateral microinjection of 8 nmol of clonidine into the CVLM ( n = 10) increased mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) by 12.1 ± 1.8 mmHg (mean ± SE, P < 0.01) and 25.8 ± 4.8% ( P < 0.01), while heart rate (HR) remained unaltered. Unilateral microinjection of 2 nmol of SKF-86466, a selective blocker of the α2-adrenoceptors, into the CVLM ( n = 10) decreased MAP, HR, and RSNA (−11.6 ± 2.6 mmHg, −26 ± 7 beats/min, and −15.3 ± 1.7%, respectively, P < 0.01 for each). Artificial cerebrospinal fluid caused neither a cardiovascular effect nor a sympathetic response. Prior injection of SKF-86466 into the ipsilateral CVLM attenuated the effects of clonidine. Bilateral microinjection of muscimol into the RVLM abolished the effects of both clonidine and SKF-86466 injected into the CVLM. The pressor and sympathoexcitatory effects of clonidine injected into the CVLM suggest a neuroinhibitory action of the drug on the CVLM neurons. In addition,the depressor and sympathoinhibitory effects of SKF-86466 injected into the CVLM indicated that activation of α2-adrenoceptors by endogenous ligand inhibits CVLM neurons. The effects of clonidine and the α2-adrenoceptor antagonist in the CVLM require the integrity of the RVLM.

Actions of Angiotensin II in the Ventrolateral Medulla Oblongata

1991 ◽  
pp. 95-103 ◽  
Author(s):  
Andrew M. Allen ◽  
Shuichi Sasaki ◽  
Roger A. L. Dampney ◽  
Frederick A. O. Mendelsohn ◽  
William W. Blessing
Keyword(s):  
Angiotensin Ii ◽  
Medulla Oblongata ◽  
Ventrolateral Medulla

Intracellular pH transients in rat diaphragm muscle measured with DMO

1978 ◽  
Vol 235 (1) ◽  
pp. C49-C54 ◽  
Author(s):  
A. Roos ◽  
W. F. Boron
Keyword(s):  
Intracellular Ph ◽  
Weak Acid ◽  
Diaphragm Muscle ◽  
Disulfonic Acid ◽  
Free Solution ◽  
Rat Diaphragm ◽  
Control Value ◽  
Acid Load ◽  
Acid Extrusion ◽  
Acid Loading

Changes of the intracellular pH of rat diaphragm muscle were monitored at 30-min intervals with the weak acid DMO (5,5-dimethyl-2,4-oxazolidinedione). Transferring the muscle from a CO2-containing to a CO2-free solution caused intracellular pH (pHi) to rise by an average of 0.18 during the first 30 min and then to level off at a slightly lower value over the next 60-90 min. Transferring the muscle from a CO2-free to a CO2-containing solution caused pHi to fall by 0.18 during the first 30 min and then to recover by 0.05 over the next 90 min. Subsequent return to the CO2-free solution caused pHi to overshoot the control value by 0.10. Both the recovery and the overshoot can be accounted for by an acid-extruding pump. Intracellular acid loading with 118 mM DMO similarly caused pHi to fall initially, to recover slowly during the acid loading, and then to overshoot the control pHi on removal of the acid load. In the absence of HCO3-/CO2, acid extrusion was reduced by about a fifth. SITS (4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid) had no effect. The absence of either Na+ or Cl- from HCO3-/CO2- free solution reduced acid extrusion by about a half.

scholarly journals Characterization of adrenergic and purinergic contractile responses in rat mesenteric arteries and veins

SURG Journal ◽  
2008 ◽  
Vol 2 (1) ◽  
pp. 30-38
Author(s):  
Rebekah Carter ◽  
Nathan Ludwig
Keyword(s):  
Purinergic Receptors ◽  
Pyridoxal Phosphate ◽  
Sympathetic Neurons ◽  
P2y Receptors ◽  
Mesenteric Arteries ◽  
Disulfonic Acid ◽  
Computer Assisted ◽  
Sprague Dawley ◽  
Contractile Responses ◽  
Arteries And Veins

Norepinephrine (NE) and adenosine 5’-triphosphate (ATP) are neurotransmitters released from sympathetic neurons that act to alter net vascular tone in the mesentery via activation of adrenergic (α1 and α2) and purinergic (P2X and P2Y) receptors. This study was designed to identify adrenergic and purinergic receptors in third order mesenteric arteries and veins in male Sprague-Dawley rats. Agonists and antagonists of adrenergic and purinergic receptors were exogenously applied to vessels and contractile responses were measured using computer assisted video microscopy. NE and ATP both caused contractions of mesenteric arteries and veins. The selective α1 antagonist prazosin attenuated NE-derived constriction of the vessels. The selective α1 agonist phenylephrine was a more efficacious constrictor of both mesenteric arteries and veins than the selective α2 agonist clonidine. The P2X/P2Y1 receptor antagonist pyridoxal-phosphate-6-azophenyl-2’,4-disulfonic acid (PPADS) caused a rightward shift in the ATP dose response curve in mesenteric arteries but not veins. These data indicate that the α1 adrenergic receptors are the primary adrenoreceptors mediating contraction to NE in mesenteric vessels. Additionally, these data suggest that the P2X/P2Y1 receptors mediate substantial contractile responses to ATP in mesenteric arteries but not veins.

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