Smooth muscle intracellular pH: measurement, regulation, and function

1988 ◽  
Vol 254 (2) ◽  
pp. C213-C225 ◽  
Author(s):  
S. Wray
Keyword(s):  
Smooth Muscle ◽  
Intracellular Ph ◽  
Smooth Muscles ◽  
Muscle Membrane ◽  
Resonance Spectroscopy ◽  
Striated Muscles ◽  
Needed Information ◽  
Smooth Muscle Membrane ◽  
Muscle Types ◽  
And Function

Smooth muscle performs many functions that are essential for the normal working of the human body. Changes in pH are thought to affect many aspects of smooth muscle. Despite this, until recently little was known about either intracellular pH (pHi) values or pHi regulation in smooth muscle. Recent work measuring pHi with either microelectrodes or nuclear magnetic resonance spectroscopy is now providing some of this much needed information for smooth muscles. From these studies, it can be concluded tentatively that pHi is the same in different smooth muscles, approximately 7.06 (37 degrees C). This value is very close to those obtained in cardiac and skeletal muscle. It is clear that H+ is not in equilibrium across the smooth muscle membrane; i.e., pHi is regulated. Preliminary results in smooth muscle suggest that certain aspects of this regulation are different from that described for other muscle types. Changes in pHi have been found to produce marked effects on contraction in smooth muscle. Of particular interest is the fact that, unlike striated muscles, some smooth muscles can product more force during an intracellular acidification.

Endothelium-dependent hyperpolarization elicited by adenine compounds in rabbit carotid artery

1991 ◽  
Vol 260 (4) ◽  
pp. H1037-H1042 ◽  
Author(s):  
G. Chen ◽  
H. Suzuki
Keyword(s):  
Smooth Muscle ◽  
Carotid Artery ◽  
Direct Action ◽  
Smooth Muscles ◽  
Muscle Membrane ◽  
Dependent Manner ◽  
Rabbit Carotid Artery ◽  
Mechanical Removal ◽  
Smooth Muscle Membrane ◽  
Adventitial Cells

Electrical responses of the membrane of intimal and adventitial smooth muscle cells of the rabbit carotid artery to ATP, ADP, AMP, and adenosine were recorded. In intimal cells, these compounds hyperpolarized the membrane. Mechanical removal of the endothelium altered the responses to ATP and ADP to one of a transient depolarization, with no alteration of the response to AMP and adenosine. In the adventitial cells, ATP and ADP produced a transient depolarization, whereas AMP and adenosine produced a sustained hyperpolarization, irrespective of the presence or absence of the endothelium. In tissues with an intact endothelium, 5'-adenylylimidodiphosphate tetralithium salt and alpha,beta-methylene ATP (mATP) transiently depolarized the membrane in these smooth muscles. In case of stabilization with mATP, only hyperpolarization was generated by ATP, in an endothelium-dependent manner. Our interpretation of these observations is that 1) ATP and ADP depolarize smooth muscle membrane by a direct action and hyperpolarize the membrane indirectly through the release of endothelium-derived hyperpolarizing factor, 2) AMP and adenosine hyperpolarize the membrane, independently of the endothelium, and 3) ATP receptors present on the endothelial cell membrane differ from those on smooth muscle membrane.

Hyperpolarization of arterial smooth muscle induced by endothelial humoral substances

1991 ◽  
Vol 260 (6) ◽  
pp. H1888-H1892 ◽  
Author(s):  
G. Chen ◽  
Y. Yamamoto ◽  
K. Miwa ◽  
H. Suzuki
Keyword(s):  
Smooth Muscle ◽  
Coronary Artery ◽  
Carotid Artery ◽  
Smooth Muscles ◽  
Electrical Signal ◽  
Muscle Membrane ◽  
Coronary Smooth Muscle ◽  
K Channels ◽  
Smooth Muscle Membrane ◽  
Pig Coronary Artery

A sandwich preparation was obtained by placing a segment of the endothelium-free guinea pig coronary artery over the intact carotid artery with the objective being to determine whether the endothelium-dependent hyperpolarization by acetylcholine chloride (ACh) is mediated by a humoral factor. ACh hyperpolarized the sandwiched coronary smooth muscle membrane, the amplitude being larger than that of the carotid artery and smaller than that of the intact coronary artery. When spontaneously active smooth muscles (stomach antrum or portal vein) were used as the donor tissue, no electrical signal was transducted to the overlying coronary smooth muscles. In the sandwiched coronary artery, the ACh-induced hyperpolarization was not inhibited by ouabain, indomethacin, or nitroarginine. Pinacidil hyperpolarized the coronary smooth muscle membrane; the responses were inhibited by glybenclamide but not by tetraethylammonium chloride (TEA). The ACh-induced hyperpolarization was inhibited by TEA but not by glybenclamide. These results suggest that the ACh-induced hyperpolarization is mediated by an endothelium-derived humoral substance (endothelium-derived hyperpolarizing factor). Possible contribution of Ca-dependent K channels, but not ATP-sensitive K channels, to the endothelium-derived hyperpolarizing factor-induced hyperpolarization was considered.

Are gap junctions necessary for cell-to-cell coupling of smooth muscle?: an update

1992 ◽  
Vol 70 (4) ◽  
pp. 481-490 ◽  
Author(s):  
R. E. Garfield ◽  
G. Thilander ◽  
M. G. Blennerhassett ◽  
N. Sakai
Keyword(s):  
Smooth Muscle ◽  
Gap Junctions ◽  
Current Knowledge ◽  
Smooth Muscles ◽  
Cell Communication ◽  
Circular Muscle ◽  
Cell Coupling ◽  
And Function ◽  
Longitudinal Layer ◽  
Cell Cell

Earlier, it was questioned whether gap junctions (GJs) were necessary for cell–cell communication in smooth muscle, and GJs were not seen in some smooth muscles. We reexamined this question in the myometrium and in intestinal smooth muscle, in light of current knowledge of the presence and function of GJs. In the uterus, numerous studies show that an increase in GJ number is associated with the onset of delivery and is required for effective parturition. In all cases, this increase in GJ number and the changes in uterine contractility were correlated with increased electrical and metabolic coupling. Evidence for the much smaller, but detectable, degree of electrical coupling in the preterm uterus is explained by the small (but again detectable) number of GJs present. In the intestine, GJs are readily detected in the circular muscle layer but have not been described in the adjacent longitudinal layer. While our immunohistochemical studies failed to detect GJs in the longitudinal layer, this may not be adequate to prove their absence. Therefore, current knowledge of GJ number and function is adequate to explain cell–cell coupling in the uterus. Although it remains uncertain whether GJs are absent from the longitudinal muscle of the intestine, there is no definitive evidence that cell–cell coupling can occur by means other than GJs.Key words: gap junctions, myometrium, connexins, smooth muscle, cell communication.

Effects of bethanechol and the octapeptide of cholecystokinin on colonic smooth muscle in the cat

1987 ◽  
Vol 252 (5) ◽  
pp. G654-G661
Author(s):  
W. J. Snape ◽  
S. T. Tan ◽  
H. W. Kao
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Slow Wave ◽  
Spike Activity ◽  
Membrane Resistance ◽  
Wave Pattern ◽  
Isometric Tension ◽  
Muscle Membrane ◽  
Maximum Effect ◽  
Smooth Muscle Membrane

The aim of this study is to compare the action of the cholinergic agonist, bethanechol, with the action of the octapeptide of cholecystokinin (CCK-OP) on feline circular colonic smooth muscle membrane potential and isometric tension, using the double sucrose gap. Depolarization of the membrane greater than 10 mV by K+ or bethanechol increased tension and spontaneous spike activity. CCK-OP (10(-9) M) depolarized the membrane (6.1 +/- 1.3 mV) without an increase in tension or spike activity. Depolarization of the membrane by increasing [K+]o was associated with a decrease in the membrane resistance. The slow-wave duration (2.3 +/- 0.2 s) was unchanged by administration of K+ or bethanechol but was prolonged after increasing concentrations of CCK-OP. The maximum effect occurred at a 10(-10) M concentration of CCK-OP (4.5 +/- 0.4 s, P less than 0.01). At higher concentrations of CCK-OP (greater than 10(-10) M), the slow-wave pattern became disorganized. Addition of increasing concentrations of [K+]o or bethanechol, but not CCK-OP, stimulated a concentration-dependent increase in the maximum rate of rise (dV/dtmax) of an evoked spike potential. These studies suggest 1) bethanechol decreased the membrane potential without altering the slow-wave activity, whereas CCK-OP has a minimal effect on the membrane potential but distorted the slow-wave shape; 2) an increased amplitude of the spike and dV/dtmax of the spike were associated with an increase in phasic contractions after bethanechol or increased [K+]o; 3) the lack of an increase in the spike amplitude and the dV/dtmax to CCK-OP was associated with no increase in phasic contraction.

Sarcoplasmic Reticulum Function in Smooth Muscle

2010 ◽  
Vol 90 (1) ◽  
pp. 113-178 ◽  
Author(s):  
Susan Wray ◽  
Theodor Burdyga
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Physiological Activity ◽  
Smooth Muscles ◽  
Outward Current ◽  
Integrated Approach ◽  
Transient Outward Current ◽  
Coupling Mechanism ◽  
Striated Muscles ◽  
Development And Aging

The sarcoplasmic reticulum (SR) of smooth muscles presents many intriguing facets and questions concerning its roles, especially as these change with development, disease, and modulation of physiological activity. The SR's function was originally perceived to be synthetic and then that of a Ca store for the contractile proteins, acting as a Ca amplification mechanism as it does in striated muscles. Gradually, as investigators have struggled to find a convincing role for Ca-induced Ca release in many smooth muscles, a role in controlling excitability has emerged. This is the Ca spark/spontaneous transient outward current coupling mechanism which reduces excitability and limits contraction. Release of SR Ca occurs in response to inositol 1,4,5-trisphosphate, Ca, and nicotinic acid adenine dinucleotide phosphate, and depletion of SR Ca can initiate Ca entry, the mechanism of which is being investigated but seems to involve Stim and Orai as found in nonexcitable cells. The contribution of the elemental Ca signals from the SR, sparks and puffs, to global Ca signals, i.e., Ca waves and oscillations, is becoming clearer but is far from established. The dynamics of SR Ca release and uptake mechanisms are reviewed along with the control of luminal Ca. We review the growing list of the SR's functions that still includes Ca storage, contraction, and relaxation but has been expanded to encompass Ca homeostasis, generating local and global Ca signals, and contributing to cellular microdomains and signaling in other organelles, including mitochondria, lysosomes, and the nucleus. For an integrated approach, a review of aspects of the SR in health and disease and during development and aging are also included. While the sheer versatility of smooth muscle makes it foolish to have a “one model fits all” approach to this subject, we have tried to synthesize conclusions wherever possible.

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