Monkey cerebral arterial relaxation caused by hypercapnic acidosis and hypertonic bicarbonate

1993 ◽  
Vol 265 (3) ◽  
pp. H929-H933 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
M. Enokibori ◽  
T. Okamura
Keyword(s):  
Japanese Monkey ◽  
Cerebral Arteries ◽  
High Pco2 ◽  
Hypercapnic Acidosis ◽  
Experimental Conditions ◽  
Na Pump ◽  
Vasoactive Substances ◽  
Arterial Relaxation ◽  
Electrogenic Na Pump ◽  
Bicarbonate Solutions

In helical strips of Japanese monkey cerebral arteries contracted with vasoconstrictors, applications of high CO2 (15% compared with 5% CO2 in control media) and hypertonic NaHCO3 (50 mM) produced relaxations. Similar relaxations were also obtained in human cerebral arterial strips. Hypercapnia increased PCO2 and resulted in acidosis in the bathing media, and the addition of NaHCO3 restored the pH to normal with high PCO2 and increased the osmotic pressure. The relaxant responses were not influenced by endothelium denudation and treatment with indomethacin. The hypercapnia-induced relaxation was suppressed by ouabain but was unaffected by amiloride. On the other hand, hypertonic bicarbonate-induced relaxations were inhibited by ouabain as well as by amiloride. Removal of Na+ from the bathing media abolished the hypercapnia-induced relaxation but did not alter the hyperosmolar relaxation. In contrast to hypertonic NaHCO3, isotonic bicarbonate solutions contracted the arterial strips by neutralizing the pH under hypercapnia. It may be concluded that relaxations elicited by hypercapnic acidosis are associated with a fall of extracellular pH and an activation of the electrogenic Na+ pump, and those caused by hyperosmolarity are due to stimulation of the Na(+)-H+ exchange and the Na+ pump. Endothelium-derived vasoactive substances and cyclooxygenase products do not appear to be involved in these relaxations of monkey cerebral arteries under the experimental conditions used.

Mechanisms underlying response to hypercapnia and bicarbonate of isolated dog cerebral arteries

1989 ◽  
Vol 257 (1) ◽  
pp. H141-H146 ◽  
Author(s):  
N. Toda ◽  
Y. Hatano ◽  
K. Mori
Keyword(s):  
Superoxide Dismutase ◽  
Cerebral Arteries ◽  
Extracellular Ph ◽  
Na Pump ◽  
Prostaglandin F2 Alpha ◽  
Electrogenic Na Pump ◽  
Cerebral Vasodilatation ◽  
High Level ◽  
Arterial Tone ◽  
Hcl Solution

In helical strips of dog cerebral arteries contracted with K+ or prostaglandin F2 alpha, the increase in CO2 from 5 to 15% in the gas aerating the bathing media produced a persistent relaxation in association with a rise of PCO2 and a fall of pH and PO2. Elevation of the NaHCO3 concentration from 25 to 75 mM in the bathing media under hypercapnia almost reversed the arterial tone when the osmolarity was balanced; the pH was completely reversed, whereas PCO2 was maintained at the high level. When 50 mM NaHCO3 were applied to the hypercapnic media without having the osmolarity balanced, the arteries relaxed further. Infusions of the HCl solution lowered the pH and relaxed the arterial strips; however, such a relaxation was significantly less than that caused by hypercapnia-induced acidosis. Relaxant responses to hypercapnia were attenuated by treatment with ouabain but were not influenced by amiloride and superoxide dismutase or by removal of endothelium. Relaxations due to hypertonic NaHCO3 were abolished or reversed to contractions by ouabain and were reduced by treatment with amiloride. It may be concluded that the hypercapnia-induced cerebroarterial relaxation is associated mainly with a fall of extracellular pH and is mediated partly by an activation of the electrogenic Na+ pump. Cerebral vasodilatation by increased osmolarity with NaHCO3 appears to result from stimulated Na+-H+ exchange and activated Na+ pump.

Mechanism underlying mannitol-induced relaxation in isolated monkey cerebral arteries

1992 ◽  
Vol 262 (3) ◽  
pp. H897-H902 ◽  
Author(s):  
N. Toda ◽  
K. Ayajiki ◽  
H. Toda ◽  
Y. Hatano ◽  
T. Okamura
Keyword(s):  
Superoxide Dismutase ◽  
Hydroxyl Radicals ◽  
Choline Chloride ◽  
Cerebral Arteries ◽  
Combined Treatment ◽  
The Other ◽  
Na Pump ◽  
Prostaglandin F2 Alpha ◽  
Arterial Contraction ◽  
Electrogenic Na Pump

The addition of mannitol (25, 50, and 100 mM) increased osmotic pressures of the bathing media from 293 to 317, 340 and 383 mosmol, respectively, and elicited a dose-related relaxation in monkey cerebral artery strips precontracted with K+ or prostaglandin F2 alpha. This relaxation was attenuated by ouabain, amiloride, catalase and oxyhemoglobin but was not influenced by superoxide dismutase and indomethacin. Combined treatment of the strips exposed to ouabain and amiloride with catalase produced an additional inhibition. H2O2 produced a contraction, which was abolished by catalase. Replacement of entire NaCl with choline chloride markedly suppressed the mannitol-induced relaxation. Relaxations caused by the addition of hypertonic NaHCO3 (25 and 50 mM) were also attenuated by ouabain and amiloride but were unaffected by catalase and oxyhemoglobin. It may be concluded that the mannitol-induced cerebroarterial relaxation is associated with an activation of the electrogenic Na+ pump and the Na(+)-H+ exchange and probably with scavenging of hydroxyl radicals responsible for the arterial contraction. On the other hand, hypertonic NaHCO3 relaxes monkey cerebral arteries, possibly due to an activation of the Na+ pump and the Na(+)-H+ exchange.

Characteristics of active Na transport in intact cardiac cells

1979 ◽  
Vol 236 (2) ◽  
pp. H189-H199 ◽  
Author(s):  
H. G. Glitsch
Keyword(s):  
Heart Muscle ◽  
Muscle Cells ◽  
Cardiac Cells ◽  
Na Transport ◽  
Concentration Gradients ◽  
Experimental Conditions ◽  
Na Pump ◽  
Na Efflux ◽  
Heart Muscle Cells ◽  
K Concentration

An active Na transport maintains the Na and K concentration gradients across the cell membrane of many cells and restores them following excitation. Heart muscle cells display frequent electrical discharges and thus the cardiac Na pump is of fundamental functional significance. Some methods for studying active Na transport are described. The active Na efflux from heart muscle cells is activated by an increase in the intracellular Na and the extracellular K concentration. The linkage between active Na efflux and active K influx varies widely according to the experimental conditions. The cardiac Na pump is electrogenic and can contribute directly to the membrane potential of the cells. The effects of active Na transport on contraction and intercellular coupling in myocardium are discussed.

scholarly journals Reversible Cerebrovascular Syndrome

2017 ◽  
pp. 63
Author(s):  
Mohammad Saadatnia
Keyword(s):  
Hemorrhagic Stroke ◽  
Cerebral Arteries ◽  
Age Groups ◽  
Pressure Control ◽  
Channel Blockers ◽  
Main Symptom ◽  
Vasoactive Substances ◽  
Short Course ◽  
Fourth Decade ◽  
Peripartum Period

Reversible cerebrovascular syndrome (RCVS) is clinico-radiological syndrome defined as severe recurrent thunderclap headache with or without seizures or neurologic deficits and constriction of cerebral arteries which resolves spontaneously within 1-3 months. RCVS affects patients in various racial and ethnic groups and in all age groups, although most commonly in the fourth decade of life.  Headache is the main symptom. Headache is usually “thunderclap variety”, peaks within one minute and very intense. Many conditions and exposures have been linked to RCVS, including vasoactive drugs, metabolic disorder, vasculitis and the peripartum period. Associated strokes and cerebral hemorrhages are not uncommon. As complications we can see Localized cortical SAH (20-25%), Ischemic or hemorrhagic stroke (5-10%), posterior reversible encephalopathic syndrome ( PRES). Permanent sequelae of RCVS is usually benign entity. Prognosis is highly dependent on the occurrence of stroke (6-9%), otherwise, by definition, most resolve completely without any sequelae. Treatment is Symptomatic (pain, seizures, blood pressure control), trigger avoidance should be done (either activity or vasoactive substances), calcium channel blockers, IV magnesium and Short-course of steroids may be effective.  

scholarly journals Ocean acidification and high irradiance stimulate the photo-physiological fitness, growth and carbon production of the Antarctic cryptophyte <i>Geminigera cryophila</i>

2019 ◽  
Vol 16 (15) ◽  
pp. 2997-3008 ◽  
Author(s):  
Scarlett Trimborn ◽  
Silke Thoms ◽  
Pascal Karitter ◽  
Kai Bischof
Keyword(s):  
Ocean Acidification ◽  
Coastal Waters ◽  
High Irradiance ◽  
High Pco2 ◽  
Experimental Conditions ◽  
Phytoplankton Assemblages ◽  
Beneficial Effects ◽  
Carbon Production ◽  
Geminigera Cryophila ◽  
The Antarctic

Abstract. Ecophysiological studies on Antarctic cryptophytes to assess whether climatic changes such as ocean acidification and enhanced stratification affect their growth in Antarctic coastal waters in the future are lacking so far. This is the first study that investigates the combined effects of the increasing availability of pCO2 (400 and 1000 µatm) and irradiance (20, 200 and 500 µmol photons m−2 s−1) on growth, elemental composition and photophysiology of the Antarctic cryptophyte Geminigera cryophila. Under ambient pCO2, this species was characterized by a pronounced sensitivity to increasing irradiance with complete growth inhibition at the highest light intensity. Interestingly, when grown under high pCO2 this negative light effect vanished, and it reached the highest rates of growth and particulate organic carbon production at the highest irradiance compared to the other tested experimental conditions. Our results for G. cryophila reveal beneficial effects of ocean acidification in conjunction with enhanced irradiance on growth and photosynthesis. Hence, cryptophytes such as G. cryophila may be potential winners of climate change, potentially thriving better in more stratified and acidic coastal waters and contributing in higher abundance to future phytoplankton assemblages of coastal Antarctic waters.

scholarly journals Regulation of Ca2+sensitization by PKC and rho proteins in ovine cerebral arteries: effects of artery size and age

1998 ◽  
Vol 275 (3) ◽  
pp. H930-H939 ◽  
Author(s):  
Sergey E. Akopov ◽  
Lubo Zhang ◽  
William J. Pearce
Keyword(s):  
G Protein ◽  
Cerebral Arteries ◽  
Rho Kinase ◽  
Cerebrovascular Reactivity ◽  
Rho Proteins ◽  
Experimental Conditions ◽  
Fetal Sheep ◽  
Middle Cerebral Arteries ◽  
Near Term ◽  
Nonpregnant Adult

G protein-regulated Ca2+ sensitivity of vascular contractile proteins plays an important role in cerebrovascular reactivity. The present study examines the intracellular mechanisms that govern G protein-regulated Ca2+ sensitivity in cerebral arteries of different size and age. We studied β-escin-permeabilized segments of common carotid, basilar, and middle cerebral arteries from nonpregnant adult and near-term fetal sheep. Activation of protein kinase C (PKC) by (−)-indolactam V or a phorbol ester produced receptor-independent increases in Ca2+ sensitivity. Such increases were more marked in immature arteries and were inversely correlated with artery size in both mature and immature arteries. However, inhibitors of PKC did not significantly affect increases in Ca2+ sensitivity in responses to either serotonin (5-hydroxytryptamine, 5-HT) or guanosine 5′- O-(3-thiotriphosphate) (GTPγS). Alternatively, deactivation of rho p21, a small G protein associated with Rho kinase, by exotoxin C3 fully prevented increases in Ca2+ sensitivity in responses to 5-HT or GTPγS in both adult and fetal arteries of all types. Neither inhibitors of PKC nor exotoxin C3 altered baseline Ca2+ sensitivity. We conclude that patterns of receptor- and/or G protein-mediated modulation of Ca2+ sensitivity are dependent on an intracellular pathway that involves activation of small G proteins and Rho kinase. In contrast, PKC has little, if any, role in agonist-induced Ca2+ sensitization under the present experimental conditions.

Effects of maturation on adrenergic neurotransmission in ovine cerebral arteries

1999 ◽  
Vol 277 (4) ◽  
pp. R931-R937 ◽  
Author(s):  
William J. Pearce ◽  
Sue P. Duckles ◽  
John Buchholz
Keyword(s):  
Cerebral Arteries ◽  
Age Groups ◽  
Peptidergic Neurons ◽  
Synaptic Density ◽  
Vasoactive Substances ◽  
Age Related ◽  
Middle Cerebral Arteries ◽  
Adrenergic Neurotransmission ◽  
Fractional Release ◽  
Two Age Groups

The present studies examine the hypothesis that multiple adrenergic neuroeffector mechanisms are not fully developed in fetal, compared with adult, ovine middle cerebral arteries. In arteries denuded of endothelium and pretreated with 1 μM atropine to block involvement of muscarinic receptors, 10 μM capsaicin to deplete sensory peptidergic neurons, and 10 μM nitro-l-arginine methyl ester (l-NAME) to block possible influences from nitric oxidergic innervation, transmural stimulation at 16 Hz increased contractile tensions to 9.5 ± 3.7% ( n = 6) of the potassium maximum in adult arteries. Corresponding values in fetal arteries, however, were significantly less and averaged only 1.1 ± 0.6% ( n =10). However, postsynaptic sensitivity to norepinephrine (NE) was similar in the two age groups; NE pD2 values (−log EC50) averaged 6.11 ± 0.12 ( n = 6) and 6.33 ± 0.09 M ( n = 9) in fetal and adult arteries, respectively. Similarly, NE content measured via HPLC was also similar in the two age groups and averaged 32.4 ± 5.0 ( n = 17) and 32.5 ± 3.9 ng/ng wet wt ( n = 13) in fetal and adult middle cerebral arteries, respectively. In contrast, stimulation-induced NE release was greater in fetal than in adult arteries, whether calculated as total mass released [883 ± 184 ( n = 17) vs. 416 ± 106 pg NE/mg wet wt ( n = 13)] or as fractional release [51.1 ± 5.3 ( n = 17) vs. 22.8 ± 3.8 pg/pg NE content per pulse × 10−6]. Measured as an index of synaptic density, neuronal cocaine-sensitive NE uptake was similar in fetal and adult arteries [1.55 ± 0.40 ( n = 10) and 1.84 ± 0.51 pmol/mg wet wt ( n = 7), respectively]. Overall, age-related differences in postsynaptic sensitivity to NE, NE release, and NE uptake capacity cannot explain the corresponding age-related differences in response to stimulation. The data thus suggest that total synaptic volume and cleft width, in particular, are probably greater and/or that adrenergic corelease of vasoactive substances other than NE is altered in fetal compared with adult middle cerebral arteries.

Mechanisms of ouabain-induced arterial muscle contraction

1980 ◽  
Vol 239 (2) ◽  
pp. H199-H205 ◽  
Author(s):  
N. Toda
Keyword(s):  
Muscle Contraction ◽  
Contractile Response ◽  
Cerebral Arteries ◽  
Peripheral Arteries ◽  
Femoral Arteries ◽  
Low Concentrations ◽  
Electrogenic Na Pump ◽  
High Concentrations ◽  
Free Media ◽  
Alpha Antagonist

Ouabain caused dose-related contractions in helically cut strips of cerebral, mesenteric, renal, and femoral arteries isolated from dogs and monkeys; the contractions were elicited at lower concentrations in cerebral than in the peripheral arteries. Contractions induced by ouabain were abolished by exposure of cerebral arteries to Ca2+-free media. Contractions induced by Ca2+ in Ca2+-free media were potentiated by ouabain. Substitution of LiCl for NaCl and reduction of [K+]0 suppressed the contractile response of cerebral arteries to ouabain. Pretreatment of dogs with reserpine abolished the response of peripheral arteries to ouabain but not the cerebroarterial response. Phentolamine also abolished the response of peripheral arteries. Once oubain-induced contractions were stabilized, the alpha-antagonist caused a marked relaxation in peripheral but not in cerebral arteries. Ouabain-induced contractions appear to be mediated by an increase in the Ca2+ influx that results mainly from an inhibition of the electrogenic Na+ pump in low concentrations (cerebral arteries) and from a release of norepinephrine from nerves in high concentrations (mesenteric, renal, and femoral arteries).

scholarly journals Effects of hypercapnia and hypocapnia on [Ca2+]i mobilization in human pulmonary artery endothelial cells

2001 ◽  
Vol 90 (6) ◽  
pp. 2094-2100 ◽  
Author(s):  
Kazumi Nishio ◽  
Yukio Suzuki ◽  
Kei Takeshita ◽  
Takuya Aoki ◽  
Hiroyasu Kudo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Pulmonary Artery ◽  
Vascular Tone ◽  
Extracellular Ph ◽  
Hypercapnic Acidosis ◽  
Extracellular Medium ◽  
Vasoactive Substances ◽  
Intracellular Ca ◽  
Human Pulmonary Artery ◽  
Hypocapnic Alkalosis

The hydrogen ion is an important factor in the alteration of vascular tone in pulmonary circulation. Endothelial cells modulate vascular tone by producing vasoactive substances such as prostacyclin (PGI2) through a process depending on intracellular Ca2+ concentration ([Ca2+]i). We studied the influence of CO2-related pH changes on [Ca2+]iand PGI2 production in human pulmonary artery endothelial cells (HPAECs). Hypercapnic acidosis appreciably increased [Ca2+]i from 112 ± 24 to 157 ± 38 nmol/l. Intracellular acidification at a normal extracellular pH increased [Ca2+]i comparable to that observed during hypercapnic acidosis. The hypercapnia-induced increase in [Ca2+]i was unchanged by the removal of Ca2+ from the extracellular medium or by the depletion of thapsigargin-sensitive intracellular Ca2+ stores. Hypercapnic acidosis may thus release Ca2+ from pH-sensitive but thapsigargin-insensitive intracellular Ca2+ stores. Hypocapnic alkalosis caused a fivefold increase in [Ca2+]i compared with hypercapnic acidosis. Intracellular alkalinization at a normal extracellular pH did not affect [Ca2+]i. The hypocapnia-evoked increase in [Ca2+]i was decreased from 242 ± 56 to 50 ± 32 nmol/l by the removal of extracellular Ca2+. The main mechanism affecting the hypocapnia-dependent [Ca2+]i increase was thought to be the augmented influx of extracellular Ca2+ mediated by extracellular alkalosis. Hypercapnic acidosis caused little change in PGI2 production, but hypocapnic alkalosis increased it markedly. In conclusion, both hypercapnic acidosis and hypocapnic alkalosis increase [Ca2+]i in HPAECs, but the mechanisms and pathophysiological significance of these increases may differ qualitatively.

Isoflavones and gastrointestinal infection: Two potential triggers for reversible cerebral vasoconstriction syndrome

Cephalalgia ◽  
2017 ◽  
Vol 38 (5) ◽  
pp. 984-987 ◽  
Author(s):  
Björn Machner ◽  
Tobias Boppel ◽  
Thomas Münte
Keyword(s):  
Differential Diagnosis ◽  
Post Partum ◽  
Cerebral Arteries ◽  
Thunderclap Headache ◽  
Reversible Cerebral Vasoconstriction Syndrome ◽  
Gastrointestinal Infection ◽  
Cerebral Vasoconstriction ◽  
Vasoactive Substances ◽  
Important Differential Diagnosis ◽  
Estrogenic Potential

Background Reversible cerebral vasoconstriction syndrome (RCVS) is an important differential diagnosis of singular or recurrent thunderclap headache. Prognosis is generally good, however complications of the transient segmental vasospasms of cerebral arteries such as stroke, subarachnoidal hemorrhage and brain edema may worsen the clinical outcome. Although the exact pathomechanism is still unclear, various vasoactive substances and conditions (e.g. post partum) have been identified as triggering RCVS. Cases We report on the clinical course and management of two cases of typical RCVS that were associated with two different precipitants previously not described: A gastrointestinal infection and isoflavones, which are phytoestrogens used for menopausal vasomotor symptoms. Discussion In the case of gastrointestinal infection, either systemic inflammatory processes might lead to disturbances of vascular tone, or the repetitive vomiting that resembles Valsalva manoeuvers known to trigger RCVS. In the case of isoflavone intake, it may be their estrogenic potential that induces dysregulation of cerebral arteries, a mechanism known from other states of hormonal change such as post-partum angiopathy. However, the association of both precipitating factors with RCVS in our two cases is not a proof for a causal relationship, and there may have been additional potential triggers for RCVS. Conclusion In patients with (gastrointestinal) infection and concomitant thunderclap headache, RCVS should be considered as an important differential diagnosis due to its major complications. Since RCVS may be triggered by various vasoactive substances, taking the medical history should always include over-the-counter drugs and dietary supplements (such as the isoflavones) beside the regular medication.

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