Na+/Ca2+ exchange and its role in intracellular Ca2+ regulation in guinea pig detrusor smooth muscle

2001 ◽  
Vol 280 (5) ◽  
pp. C1090-C1096 ◽  
Author(s):  
C. Wu ◽  
C. H. Fry
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Outward Current ◽  
Detrusor Smooth Muscle ◽  
Small Rise ◽  
Intracellular Ca ◽  
Net Flux ◽  
Isolated Smooth Muscle Cells

The role of Na+/Ca2+ exchange in regulating intracellular Ca2+ concentration ([Ca2+]i) in isolated smooth muscle cells from the guinea pig urinary bladder was investigated. Incremental reduction of extracellular Na+ concentration resulted in a graded rise of [Ca2+]i; 50–100 μM strophanthidin also increased [Ca2+]i. A small outward current accompanied the rise of [Ca2+]i in low-Na+ solutions (17.1 ± 1.8 pA in 29.4 mM Na+). The quantity of Ca2+ influx through the exchanger was estimated from the charge carried by the outward current and was ∼30 times that which is necessary to account for the rise of [Ca2+]i, after correction was made for intracellular Ca2+ buffering. Ca2+ influx through the exchanger was able to load intracellular Ca2+ stores. It is concluded that the level of resting [Ca2+]i is not determined by the exchanger, and under resting conditions (membrane potential −50 to −60 mV), there is little net flux through the exchanger. However, a small rise of intracellular Na+ concentration would be sufficient to generate significant net Ca2+ influx.

Desensitization of isolated smooth muscle cells from guinea pig taenia caecum to acetylcholine

1987 ◽  
Vol 65 (3) ◽  
pp. 293-297 ◽  
Author(s):  
Mitsuo Mita ◽  
Masaatsu K. Uchida
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Single Cells ◽  
Threshold Concentration ◽  
Maximal Response ◽  
Isolated Cells ◽  
Tissue Organization ◽  
Whole Muscle ◽  
Isolated Smooth Muscle Cells

The role of tissue organization of smooth muscle in short-term desensitization to acetylcholine (ACh) was examined by studying the desensitization of isolated single cells from guinea pig taenia caecum. Cells were isolated by collagenase digestion. The conditions during cell isolation were adjusted to obtain cells that showed repeated contractions. The cells contracted on treatment with 10−7–10−6 M ACh, showing an all-or-none response. Desensitized cells also showed an all-or-none response but required a higher concentration of ACh for induction of contraction; i.e., the magnitude of their maximal response was not changed appreciably but the threshold concentration of ACh for their contraction was raised. Incubation of the whole tissue with 10−4 M ACh for 10 min also caused desensitization. This desensitization was accompanied by reduction of the contractile response at intermediate concentrations. The mode of desensitization of isolated cells determined from the average response of the isolated cells was almost the same as that of whole muscle. It is concluded that the desensitization occurred in each cell irrespective of its tissue organization and that the desensitization was due to an increase of the threshold for contraction to ACh of each cell.

Electrical behavior of guinea pig tracheal smooth muscle

2000 ◽  
Vol 278 (2) ◽  
pp. L320-L328 ◽  
Author(s):  
Narelle J. Bramich
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Nerve Stimulation ◽  
Tracheal Smooth Muscle ◽  
Quiescent Cells ◽  
Voltage Dependent ◽  
Intracellular Ca ◽  
Intrinsic Nerve ◽  
Spontaneous Oscillations

Intracellular recordings were taken from the smooth muscle of the guinea pig trachea, and the effects of intrinsic nerve stimulation were examined. Approximately 50% of the cells had stable resting membrane potentials of −50 ± 1 mV. The remaining cells displayed spontaneous oscillations in membrane potential, which were abolished either by blocking voltage-dependent Ca2+channels with nifedipine or by depleting intracellular Ca2+stores with ryanodine. In quiescent cells, stimulation with a single impulse evoked an excitatory junction potential (EJP). In 30% of these cells, trains of stimuli evoked an EJP that was followed by oscillations in membrane potential. Transmural nerve stimulation caused an increase in the frequency of spontaneous oscillations. All responses were abolished by the muscarinic-receptor antagonist hyoscine (1 μM). In quiescent cells, nifedipine (1 μM) reduced EJPs by 30%, whereas ryanodine (10 μM) reduced EJPs by 93%. These results suggest that both the release of Ca2+ from intracellular stores and the influx of Ca2+ through voltage-dependent Ca2+channels are important determinants of spontaneous and nerve-evoked electrical activity of guinea pig tracheal smooth muscle.

Effect of acidosis on tension and [Ca2+]iin rat cerebral arteries: is there a role for membrane potential?

1998 ◽  
Vol 274 (2) ◽  
pp. H655-H662 ◽  
Author(s):  
Hong-Li Peng ◽  
Peter E. Jensen ◽  
Holger Nilsson ◽  
Christian Aalkjær
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Isometric Force ◽  
Cerebral Arteries ◽  
Bathing Solution ◽  
Hypercapnic Acidosis ◽  
Small Arteries ◽  
Intracellular Ca ◽  
Intracellular Microelectrodes

The cellular mechanism responsible for the reduction of tension in cerebral small arteries to acidosis is not known. In this study the role of smooth muscle intracellular Ca2+ concentration ([Ca2+]i) and membrane potential for the relaxation to acidosis was investigated in isolated rat cerebral small arteries. Isometric force was measured simultaneously with [Ca2+]i(fura 2) or with membrane potential (intracellular microelectrodes), and acidosis was induced by increasing[Formula: see text] or reducing[Formula: see text] of the bathing solution. Both hypercapnic and normocapnic acidosis were associated with a reduction of intracellular pH [measured with 2′,7′-bis-(carboxyethyl)-5 (and -6)-carboxyfluorescein], caused relaxation, and reduced [Ca2+]i. However, whereas hypercapnic acidosis caused hyperpolarization, normocapnic acidosis was associated with depolarization. It is concluded that a reduction of [Ca2+]iis in part responsible for the direct effect of the acidosis on the vascular smooth muscle both during normo- and hypercapnia. The mechanism responsible for the reduction of [Ca2+]idiffers between the hypercapnic and normocapnic acidosis, being partly explained by hyperpolarization during hypercapnic acidosis, whereas it is seen despite depolarization during normocapnic acidosis.

scholarly journals Kv2.1 channels play opposing roles in regulating membrane potential, Ca2+ channel function, and myogenic tone in arterial smooth muscle

2020 ◽  
Vol 117 (7) ◽  
pp. 3858-3866 ◽  
Author(s):  
Samantha C. O’Dwyer ◽  
Stephanie Palacio ◽  
Collin Matsumoto ◽  
Laura Guarina ◽  
Nicholas R. Klug ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Muscle Relaxation ◽  
Smooth Muscle Relaxation ◽  
Myogenic Tone ◽  
Arterial Smooth Muscle ◽  
Membrane Hyperpolarization ◽  
Intracellular Ca ◽  
Specific Regulation

The accepted role of the protein Kv2.1 in arterial smooth muscle cells is to form K+ channels in the sarcolemma. Opening of Kv2.1 channels causes membrane hyperpolarization, which decreases the activity of L-type CaV1.2 channels, lowering intracellular Ca2+ ([Ca2+]i) and causing smooth muscle relaxation. A limitation of this model is that it is based exclusively on data from male arterial myocytes. Here, we used a combination of electrophysiology as well as imaging approaches to investigate the role of Kv2.1 channels in male and female arterial myocytes. We confirmed that Kv2.1 plays a canonical conductive role but found it also has a structural role in arterial myocytes to enhance clustering of CaV1.2 channels. Less than 1% of Kv2.1 channels are conductive and induce membrane hyperpolarization. Paradoxically, by enhancing the structural clustering and probability of CaV1.2–CaV1.2 interactions within these clusters, Kv2.1 increases Ca2+ influx. These functional impacts of Kv2.1 depend on its level of expression, which varies with sex. In female myocytes, where expression of Kv2.1 protein is higher than in male myocytes, Kv2.1 has conductive and structural roles. Female myocytes have larger CaV1.2 clusters, larger [Ca2+]i, and larger myogenic tone than male myocytes. In contrast, in male myocytes, Kv2.1 channels regulate membrane potential but not CaV1.2 channel clustering. We propose a model in which Kv2.1 function varies with sex: in males, Kv2.1 channels control membrane potential but, in female myocytes, Kv2.1 plays dual electrical and CaV1.2 clustering roles. This contributes to sex-specific regulation of excitability, [Ca2+]i, and myogenic tone in arterial myocytes.

scholarly journals Role of PTHrP and Sensory Nerve Peptides in Regulating Contractility of Muscularis Mucosae and Detrusor Smooth Muscle in the Guinea Pig Bladder

2016 ◽  
Vol 196 (4) ◽  
pp. 1287-1294 ◽  
Author(s):  
Ken Lee ◽  
Retsu Mitsui ◽  
Shunichi Kajioka ◽  
Seiji Naito ◽  
Hikaru Hashitani
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Sensory Nerve ◽  
Detrusor Smooth Muscle ◽  
Muscularis Mucosae
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