scholarly journals Lowering of the extracellular Na+ concentration enhances high-K+-induced formation of inositol phosphates in the guinea-pig ileum

1988 ◽  
Vol 252 (3) ◽  
pp. 883-888 ◽  
Author(s):  
T Sasaguri ◽  
S P Watson
Keyword(s):  
Guinea Pig ◽  
Inositol Phosphates ◽  
Induced Response ◽  
Guinea Pig Ileum ◽  
Tissue Slices ◽  
Phospholipid Hydrolysis ◽  
Collagenase Treatment ◽  
High K ◽  
K Concentration ◽  
Dispersed Cells

1. Formation of inositol phosphates (InsPs) was measured in cross-chopped slices or dispersed cells, isolated by collagenase treatment, of guinea-pig ileum longitudinal smooth muscle pre-labelled with [3H]inositol. 2. Elevation of the extracellular K+ concentration by equimolar replacement of Na+ induced accumulation of InsPs in the dispersed cells and in the tissue slices. These effects were blocked by neither tetrodotoxin (1 microM) nor atropine (10 microM), and were approximately additive with carbachol-induced accumulation. 3. In the tissue slices, the response to K+ was partially inhibited by nifedipine (10 microM) and by CdCl2 (0.3 mM), but the carbachol-induced response was not altered. 4. Accumulation of InsPs induced by KCl-excess solution (high-K+ solution without Na+ replacement) was suppressed strongly by nifedipine and completely by CdCl2. The response to KCl excess was approx. 40% of that to high K+ with Na+ replacement. 5. Low-NaCl solution (replacement of NaCl with equimolar sucrose) also produced InsPs, and this was not blocked by either nifedipine (10 microM) or CdCl2 (0.3 mM). 6. The formation of InsPs by a maximally effective concentration of carbachol (1 mM) in the presence of KCl excess or low NaCl was greater than the additive effect of the two stimuli on their own. Enhancement of the carbachol-induced response by KCl excess disappeared in the presence of CdCl2 (0.3 mM). 7. These data suggest that formation of InsPs induced by high-K+ solution with equimolar replacement of Na+ consists of two components, i.e. high-K+-induced inositol-phospholipid hydrolysis by Ca2+ entry through voltage-sensitive channels, and low-Na+-induced formation of InsPs, insensitive to Ca2+ antagonists, but that both of them do not contribute significantly to the activation of phospholipase C by muscarinic stimuli.

Adenosine potentiates flow-induced dilation of coronary arterioles by activating KATP channels in endothelium

1995 ◽  
Vol 269 (2) ◽  
pp. H541-H549 ◽  
Author(s):  
L. Kuo ◽  
J. D. Chancellor
Keyword(s):  
Katp Channels ◽  
Intraluminal Pressure ◽  
Maximum Diameter ◽  
Induced Response ◽  
Endothelial Denudation ◽  
High K ◽  
Order Of Magnitude ◽  
K Concentration ◽  
The Right ◽  
Coronary Arterioles

Coronary microvascular diameter is significantly influenced by adenosine and flow. However, the interaction between these two regulatory mechanisms in the control of coronary microvascular tone remains unknown. Because adenosine can activate ATP-sensitive K+ (KATP) channels and these channels are located on the endothelium in addition to vascular smooth muscle, we hypothesized that adenosine can potentiate flow-induced vasodilation by activating endothelial KATP channels in the coronary microcirculation. To test this hypothesis, experiments were performed in porcine subepicardial coronary arterioles (50-150 microns) using isolated, cannulated vessel techniques to allow intraluminal pressure and flow to be independently controlled. All vessels developed active tone, approximately 67-73% of maximum diameter, at 60 cmH2O intraluminal pressure and showed graded dilation to stepwise increases in flow. The magnitude of flow-induced dilation was potentiated by a threshold dose of adenosine (10(-10) M) but not by nitroprusside (10(-10) M). Luminal application of a high K+ concentration ([K+]) (40 mM) completely blocked flow-induced arteriolar dilation. In addition, luminal glibenclamide (10(-6) M) abolished the adenosine-potentiated component of flow-induced response. Indomethacin (10(-5) M) did not alter the dose-dependent dilation to adenosine. However, endothelial denudation, NG-monomethyl-L-arginine (10(-5) M), and luminal administration of a high [K+] or glibenclamide each produced identical inhibition of adenosine-induced vasodilation by shifting the 50% effective dose to the right by an order of magnitude. In contrast, vasodilation in response to nitroprusside was not altered by these pharmacological interventions.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals The Effect of High K+ Concentration in Perilymph upon the First Order Neuron of the Guinea Pig

1986 ◽  
Vol 1986 (Supplement8) ◽  
pp. 73-79
Author(s):  
Tetsuaki Kawase ◽  
Jun Kusakari ◽  
Tomonori Takasaka
Keyword(s):  
Guinea Pig ◽  
First Order ◽  
High K ◽  
Order Neuron ◽  
K Concentration

scholarly journals Relationship between stimulated phosphatidic acid production and inositol lipid hydrolysis in intestinal longitudinal smooth muscle from guinea pig

1987 ◽  
Vol 244 (3) ◽  
pp. 763-768 ◽  
Author(s):  
R S E Mallows ◽  
T B Bolton
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Substance P ◽  
Guinea Pig ◽  
Phosphatidic Acid ◽  
Inositol Phosphates ◽  
Muscle Layer ◽  
Phospholipid Hydrolysis ◽  
Longitudinal Smooth Muscle ◽  
Inositol Phospholipid

Accumulation of [32P]phosphatidic acid (PA) and total [3H]inositol phosphates (IPs) was measured in the longitudinal smooth-muscle layer from guinea-pig small intestine. Stimulation with carbachol, histamine and substance P produced increases in accumulation of both [3H]IPs and [32P]PA over the same concentration range. The increase in [32P]PA accumulation in response to carbachol (1 microM-0.1 mM) was inhibited in the presence of atropine (0.5 microM). Buffering the external free [Ca2+] to 10 nM did not prevent the carbachol-stimulated increase in [32P]PA accumulation. Carbachol and Ca2+ appear to act synergistically to increase accumulation of [32P]PA. In contrast, although incubation with noradrenaline also increased accumulation of [3H]IPs, no increase in accumulation of [32P]PA could be detected. These results suggest that an increase in formation of IPs is not necessarily accompanied by an increase in PA formation, and imply the existence of receptor-modulated pathways regulating PA concentrations other than by phospholipase-C-catalysed inositol phospholipid hydrolysis.

scholarly journals Muscarinic-receptor stimulation enhances polyphosphoinositide breakdown in guinea-pig ileum smooth muscle

1984 ◽  
Vol 223 (2) ◽  
pp. 527-531 ◽  
Author(s):  
M C Sekar ◽  
B D Roufogalis
Keyword(s):  
Guinea Pig ◽  
Muscarinic Receptor ◽  
Longitudinal Muscle ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Exchange Chromatography ◽  
Guinea Pig Ileum ◽  
Receptor Stimulation ◽  
Inositol 1 ◽  
Stimulation Of

Muscarinic-receptor stimulation by 0.1 mM-carbachol in longitudinal muscle of the guinea-pig ileum increases the incorporation of [3H]inositol into inositol-containing phospholipid. This effect was blocked by 16 microM-atropine. After 60 min incubation, carbachol increased the accumulation of total inositol phosphates 20-fold in the presence of 10 mM-Li+. Less than 20% of the total inositol phosphate corresponded to inositol 1-phosphate by ion-exchange chromatography, whereas of the remainder about two-thirds corresponded to inositol bisphosphate and one third to inositol trisphosphate. It is concluded that stimulation of muscarinic receptors in guinea-pig ileum enhances breakdown of polyphosphoinositides, suggesting that this may be a primary event associated with Ca2+ mobilization in the guinea-pig ileum.

A Na(+)-sensitive cation channel modulated by angiotensin II in cultured intestinal myocytes

1994 ◽  
Vol 266 (6) ◽  
pp. C1538-C1543 ◽  
Author(s):  
V. L. Nouailhetas ◽  
J. Aboulafia ◽  
E. Frediani-Neto ◽  
A. T. Ferreira ◽  
A. C. Paiva
Keyword(s):  
Angiotensin Ii ◽  
Guinea Pig ◽  
Cultured Cells ◽  
Single Channel ◽  
Cation Channel ◽  
Guinea Pig Ileum ◽  
Open Probability ◽  
High K ◽  
Voltage Dependent ◽  
Single Channel Currents

Single-channel currents were recorded in excised inside-out and cell-attached patches of cultured cells from the longitudinal smooth muscle of the guinea pig ileum. In the presence of symmetrical high-K+ solutions, we identified a voltage-dependent 12-pS channel. It was reversibly blocked by addition of either Ba2+ or Cs+ at the cellular side of the patch but was insensitive to Ca2+ or ATP. This channel had poor selectivity concerning cations (PLi > PK = PNa = PCa, where P is permeability) and low permeability to anions. Isosmotic substitution of NaCl for KCl in the solution facing the cellular side enhanced the channel activity by increasing NPo values where N is number of channels and Po is open probability. In the cell-attached configuration, the channel was also activated by addition of angiotensin II in the bath solution. We propose that this nonselective cation channel might play a role in the control of the membrane potential during the contractile response of the guinea pig ileum to agonists by keeping the voltage-sensitive Ca2+ channels open.

The effect of several α-adrenoceptor antagonists on the response to histamine in various tissues

1980 ◽  
Vol 58 (1) ◽  
pp. 40-44 ◽  
Author(s):  
K. M. MacLeod ◽  
C. A. Krueger ◽  
D. Smith ◽  
D. M. Iwanow ◽  
D. A. Cook
Keyword(s):  
Guinea Pig ◽  
Portal Vein ◽  
Right Ventricle ◽  
Induced Response ◽  
Guinea Pig Ileum ◽  
Receptor System ◽  
Guinea Pig Heart ◽  
Rabbit Portal Vein ◽  
Histamine Response ◽  
Antagonist Effect

The effect of various α-receptor antagonists on the histamine-induced response of guinea pig ileum, guinea pig heart, and rabbit portal vein have been studied. In guinea pig ileum, an H1 receptor system, phenoxybenzamine and dibozane are effective antagonists, phentolamine is a weak antagonist, azapetine is without antagonist effect, and tolazoline is a weak agonist. In the H2 system of guinea pig right ventricle, phentolamine and azapetine are antagonists, phenoxybenzamine and dibozane are inactive, and tolazoline is an agonist. All antagonists except tolazoline block the histamine response in portal vein which is believed to be mediated by a receptor of low selectivity. Tolazoline is an agonist in portal vein.

Hair cell changes after cationic stimulation of corti's organ

1989 ◽  
Vol 47 ◽  
pp. 798-799
Author(s):  
Cesar D. Fermin ◽  
Hans-Peter Zenner
Keyword(s):  
Organ Of Corti ◽  
Cross Sectional ◽  
Surface Areas ◽  
High K ◽  
Anatomical Arrangement ◽  
Cell Cytosol ◽  
High Concentrations ◽  
K Concentration ◽  
Cell Changes

Contraction of outer and inner hair cells (OHC&IHC) in the Organ of Corti (OC) of the inner ear is necessary for sound transduction. Getting at HC in vivo preparations is difficult. Thus, isolated HCs have been used to study OHC properties. Even though viability has been shown in isolated (iOHC) preparations by good responses to current and cationic stimulation, the contribution of adjoining cells can not be explained with iOHC preparations. This study was undertaken to examine changes in the OHC after expossure of the OHC to high concentrations of potassium (K) and sodium (Na), by carefully immersing the OC in either artifical endolymph or perilymph. After K and Na exposure, OCs were fixed with 3% glutaraldehyde, post-fixed in osmium, separated into base, middle and apex and embedded in Araldite™. One μm thick sections were prepared for analysis with the light and E.M. Cross sectional areas were measured with Bioquant™ software.Potassium and sodium both cause isolated guinea pig OHC to contract. In vivo high K concentration may cause uncontrolled and sustained contractions that could contribute to Meniere's disease. The behavior of OHC in the vivo setting might be very different from that of iOHC. We show here changes of the cell cytosol and cisterns caused by K and Na to OHC in situs. The table below shows results from cross sectional area measurements of OHC from OC that were exposed to either K or Na. As one would expect, from the anatomical arrangement of the OC, OHC#l that are supported by rigid tissue would probably be displaced (move) less than those OHC located away from the pillar. Surprisingly, cells in the middle turn of the cochlea changed their surface areas more than those at either end of the cochlea. Moreover, changes in surface area do not seem to differ between K and Na treated OCs.

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