Ca2+-dependent facilitated shortening in isotonic contraction of trachealis muscle

1989 ◽  
Vol 66 (2) ◽  
pp. 632-637 ◽  
Author(s):  
R. W. Mitchell ◽  
S. M. Koenig ◽  
E. Kelly ◽  
N. L. Stephens ◽  
A. R. Leff
Keyword(s):  
Adrenergic Receptor ◽  
Isometric Force ◽  
Receptor Activation ◽  
Isometric Tension ◽  
Force Generation ◽  
Response Curves ◽  
Beta Adrenoceptor ◽  
Alpha Adrenergic Receptor ◽  
Isotonic Shortening

We compared isotonic shortening with isometric force generation as a function of external Ca2+ in 166 tracheal smooth muscle (TSM) strips from 27 mongrel dogs in vitro. Concentration-response curves were generated with muscarinic stimulation (acetylcholine, ACh), alpha-adrenergic receptor activation (norepinephrine after beta-adrenoceptor blockade, NE), serotonin (5-HT), and KCl-substituted Krebs-Henseleit solution. The concentrations of 5-HT causing half-maximal shortening (ECS50, 1.54 +/- 0.14 X 10(-7) M) and half-maximal active isometric tension (ECT50, 1.72 +/- 0.30 X 10(-7) M) were similar (P = NS). Likewise, ECS50 (21.9 +/- 0.7 mM) and ECT50, (22.0 +/- 0.9 mM) were similar for KCl. In contrast, facilitated isotonic shortening (i.e., greater isotonic shortening for comparable degrees of force generation) was elicited with ACh and NE for all levels of force generation between 15 and 85% of maximum and for all concentrations of ACh from 3 X 10(-8) to 3 X 10(-5) M (P less than 0.05 for all points). Facilitated isotonic shortening also was elicited for all concentrations of NE from 10(-8) to 10(-6) M (P less than 0.05 for all points). Removal of Ca2+ from the perfusate substantially reduced the potency of ACh (P less than 0.001) and abolished differences between ECS50 (2.23 +/- 0.28 X 10(-5) M) and ECT50 (2.50 +/- 0.46 X 10(-5) M, P = NS). We demonstrate that for comparable degrees of force generation, muscarinic and alpha-adrenergic receptor activation cause greater isotonic shortening than KCl or 5-HT and that this facilitated shortening is associated with the concentration of external Ca2+.

Muscarinic and alpha-adrenergic stimulation of Na and Ca uptake by dispersed lacrimal cells

1980 ◽  
Vol 239 (2) ◽  
pp. G99-G105 ◽  
Author(s):  
R. J. Parod ◽  
B. A. Leslie ◽  
J. W. Putney
Keyword(s):  
Lacrimal Gland ◽  
Adrenergic Receptor ◽  
Receptor Activation ◽  
Adrenergic Stimulation ◽  
Alpha Adrenergic Receptor ◽  
Ca Uptake ◽  
Isotope Technique ◽  
Ca Ions ◽  
Double Isotope

Rat lacrimal gland acinar cells were isolated and observed to be physiologically stable for several hours of incubation in vitro. With a double-isotope technique, it was found that carbachol and epinephrine stimulated the uptake of 22Na and 45Ca by lacrimal cells. These respnses were maximal at agonist concentrations of 10(-5) M and were blocked by atropine and phentolamine, respectively. It is concluded that muscarinic and alpha-adrenergic receptor activation increase the membrane permeability of the lacrimal gland acinar cell to Na and Ca, ions that may be important in the secretion of water by the lacrimal gland.

Stimulus-response relationships for isotonic shortening and isometric tension generation in rabbit trachealis

1994 ◽  
Vol 77 (4) ◽  
pp. 1638-1643 ◽  
Author(s):  
A. Opazo-Saez ◽  
P. D. Pare
Keyword(s):  
Smooth Muscle ◽  
Isometric Force ◽  
Electrical Field Stimulation ◽  
Isometric Tension ◽  
Maximal Response ◽  
Field Stimulation ◽  
Electrical Field ◽  
Increased Sensitivity ◽  
Isotonic Shortening

Nonspecific bronchial hyperresponsiveness in asthma is characterized by increased maximal airway narrowing (reactivity) and increased sensitivity of the airways. A decreased load on airway smooth muscle (ASM) has been suggested as a mechanism of increased reactivity. We hypothesized that decreased ASM load can also cause a leftward shift in the dose-response curve and explain increased sensitivity. We tested this hypothesis using rabbit tracheal smooth muscle strips in vitro by measuring isotonic shortening and isometric force during electrical field stimulation (1–100 Hz) at the length at which maximal active tension developed (Lmax), 90% Lmax, and 110% Lmax The frequency-response relationships expressed as frequency vs. percent maximal shortening or tension were not different at Lmax or 110% Lmax, but at 90% Lmax the frequency vs. shortening relationship was significantly shifted leftward relative to the frequency vs. tension relationship (P < 0.05). The electrical field stimulation frequencies that produced 50% maximal response for isometric tension and for isotonic shortening, respectively, were 6.7 +/- 1.9 and 3.9 +/- 0.7 Hz at 90% Lmax, 9.2 +/- 2.1 and 7.5 +/- 1.9 Hz at 100% Lmax, and 2.8 +/- 1.0 and 1.2 +/- 0.5 Hz at 110% Lmax. We conclude that, at lengths below Lmax, isotonic shortening is facilitated compared with isometric tension and therefore decreased ASM load in vivo may result in increased sensitivity.

Levobupivacaine-induced contraction of isolated rat aorta is calcium dependent

2011 ◽  
Vol 89 (7) ◽  
pp. 467-476 ◽  
Author(s):  
Ji Seok Baik ◽  
Ju-Tae Sohn ◽  
Seong-Ho Ok ◽  
Jae-Gak Kim ◽  
Hui-Jin Sung ◽  
...  
Keyword(s):  
Methylene Blue ◽  
Smooth Muscle ◽  
Calcium Influx ◽  
Rat Aorta ◽  
Isometric Tension ◽  
Guanosine Monophosphate ◽  
Response Curves ◽  
Calcium Dependent ◽  
Isolated Rat

Levobupivacaine is a long-acting local anesthetic that intrinsically produces vasoconstriction in isolated vessels. The goals of this study were to investigate the calcium-dependent mechanism underlying levobupivacaine-induced contraction of isolated rat aorta in vitro and to elucidate the pathway responsible for the endothelium-dependent attenuation of levobupivacaine-induced contraction. Isolated rat aortic rings were suspended to record isometric tension. Cumulative levobupivacaine concentration–response curves were generated in either the presence or absence of the antagonists verapamil, nifedipine, SKF-96365, 2-aminoethoxydiphenylborate, Gd3+, NW-nitro-l-arginine methyl ester (L-NAME), 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), and methylene blue, either alone or in combination. Verapamil, nifedipine, SKF-96365, 2-aminoethoxydiphenylborate, low calcium concentrations, and calcium-free Krebs solution attenuated levobupivacaine-induced contraction. Gd3+ had no effect on levobupivacaine-induced contraction. Levobupivacaine increased intracellular calcium levels in vascular smooth muscle cells. L-NAME, ODQ, and methylene blue increased levobupivacaine-induced contraction in endothelium-intact aorta. SKF-96365 attenuated calcium-induced contraction in a previously calcium-free isotonic depolarizing solution containing 100 mmol/L KCl. Levobupivacaine-induced contraction of rat aortic smooth muscle is mediated primarily by calcium influx from the extracellular space mainly via voltage-operated calcium channels and, in part, by inositol 1,4,5-trisphosphate receptor-mediated release of calcium from the sarcoplasmic reticulum. The nitric oxide – cyclic guanosine monophosphate pathway is involved in the endothelium-dependent attenuation of levobupivacaine-induced contraction.

Adrenergic activation of glycogen phosphorylase in primary culture diabetic cardiomyocytes

1992 ◽  
Vol 262 (3) ◽  
pp. H649-H653 ◽  
Author(s):  
J. A. Buczek-Thomas ◽  
S. R. Jaspers ◽  
T. B. Miller
Keyword(s):  
Hypersensitive Response ◽  
Adrenergic Receptor ◽  
Glycogen Phosphorylase ◽  
Receptor Activation ◽  
Receptor Stimulation ◽  
Beta Adrenergic ◽  
Rat Cardiomyocytes ◽  
Adult Rat ◽  
Adrenergic Activation

The basis of catecholamine-induced activation of glycogen phosphorylase was investigated in adult rat cardiomyocytes isolated from normal and alloxan-diabetic animals. Cells derived from diabetic animals exhibited a hypersensitive response to epinephrine stimulation that was apparent 3 h after cell isolation and was further enhanced on maintenance of the myocytes in culture for 24 h. Normal cells initially lacked the hypersensitive response to epinephrine stimulation, although on maintenance of these cells in culture for 24 h, the hypersensitive response was acquired in vitro. To assess alpha- and beta-adrenergic mediation of the response, normal and diabetic cardiomyocytes were incubated with propranolol, a beta-blocker, before direct alpha 1-receptor stimulation with phenylephrine. Both normal and diabetic myocytes failed to undergo activation of phosphorylase in 3- or 24-h cell cultures. In addition, the effects of epinephrine on phosphorylase activation were completely inhibited by propranolol, whereas prazosin, an alpha-blocker, was unsuccessful. The present data suggest that the hypersensitive response of glycogen phosphorylase in normal and diabetic cardiomyocytes is solely mediated through beta-adrenergic receptor activation.

In vivo and in vitro correlation of trachealis muscle contraction in dogs

1992 ◽  
Vol 73 (4) ◽  
pp. 1486-1493 ◽  
Author(s):  
M. Okazawa ◽  
K. Ishida ◽  
J. Road ◽  
R. R. Schellenberg ◽  
P. D. Pare
Keyword(s):  
Isometric Force ◽  
Optimal Length ◽  
Linear Elastic ◽  
Elastic Load ◽  
Muscle Shortening ◽  
Anesthetized Dogs ◽  
Trachealis Muscle ◽  
Isotonic Shortening

Maximal trachealis muscle shortening in vivo was compared with that in vitro in seven anesthetized dogs. In addition, the effect of graded elastic loads on the muscle was evaluated in vitro. In vivo trachealis muscle shortening, as measured using sonomicrometry, revealed maximal active shortening to be 28.8 +/- 11.7% (SD) of initial length. Trachealis muscle preparations from the same animals were studied in vitro to evaluate isometric force generation, isotonic shortening, and the effect of applying linear elastic loads to the trachealis muscle during contraction from optimal length. Maximal isotonic shortening was 66.8 +/- 8.4% of optimal length in vitro. Increasing elastic loads decreased active shortening and velocity of shortening in vitro in a hyperbolic manner. The elastic load required to decrease in vitro shortening to the extent of the shortening observed in vivo was similar to the estimated load provided by the tracheal cartilage. We conclude that decreased active shortening in vivo is primarily due to the elastic afterload provided by cartilage.

Dogfish pressor response to potassium blocked by magnesium and phentolamine

1982 ◽  
Vol 242 (3) ◽  
pp. R185-R188
Author(s):  
R. G. Carroll ◽  
D. F. Opdyke ◽  
N. E. Keller
Keyword(s):  
Adrenergic Receptor ◽  
Pressor Response ◽  
In Vitro Experiments ◽  
Spontaneous Release ◽  
Alpha Adrenergic Receptor ◽  
Receptor Sites ◽  
Catecholamine Levels ◽  
Chromaffin Tissue

In vivo infusion of MgCl2 blocks the dogfish pressor response to K+. This action of Mg2+ was contrasted to phentolamine in in vivo and in vitro experiments. Mg2+ blocks the spontaneous release of catecholamines from dogfish chromaffin tissue but does not alter the norepinephrine-induced contraction of the isolated dogfish artery. In vivo infusion of Mg2+ causes a significant decrease in resting catecholamine levels and diminishes the catecholamine release caused by K+ challenge. Both Mg2+ and phentolamine block the pressor action of K+, Mg2+ by preventing the K+-induced release of catecholamines and phentolamine by preventing the circulating catecholamines from interacting with alpha-adrenergic receptor sites.

Cardiovascular and renin responses to desmopressin in humans: role of prostacyclin and beta-adrenergic systems

1991 ◽  
Vol 260 (4) ◽  
pp. H1031-H1036 ◽  
Author(s):  
K. Hasunuma ◽  
K. Yamada ◽  
Y. Tamura ◽  
S. Yoshida
Keyword(s):  
Blood Pressure ◽  
Pulse Rate ◽  
Plasma Renin ◽  
Cardiovascular Responses ◽  
Normal Subjects ◽  
Receptor Activation ◽  
Renin Release ◽  
Beta Adrenoceptor ◽  
V2 Receptor

To investigate the involvement of prostacyclin and the sympathetic nervous system in cardiovascular responses to 1-desamino-8-D-arginine vasopressin (DDAVP), a selective V2-receptor agonist, in normal subjects, DDAVP (0.4 micrograms/kg) was infused with or without indomethacin, a cyclooxygenase inhibitor, or propranolol, a beta-adrenoceptor antagonist. A decrease in blood pressure and increases in pulse rate and plasma renin activity (PRA) were observed by DDAVP infusion. Indomethacin did not influence the DDAVP-induced changes in blood pressure and pulse rate but suppressed the increases in PRA and urinary 6-ketoprostaglandin F1 alpha excretion after DDAVP infusion. Even with propranolol administration, DDAVP produced a similar decrease in blood pressure with a reduction of the increased pulse rate. The DDAVP-induced increase in PRA was not affected either. Indomethacin or propranolol alone did not affect the basal levels of the parameters. DDAVP stimulated the in vitro renin release from rabbit renal cortical slices. The stimulation was inhibited by indomethacin or d(CH2)5[D-Ile2,Ile4]AVP, a selective V2-receptor antagonist. These findings suggest that DDAVP primarily elicits vasodilation, probably through the prostacyclin-independent endothelium-derived relaxation and DDAVP also causes an increase in renin release, which would be partly attributed to the increased synthesis of prostacyclin due to vasculoendothelial V2-like receptor activation but not mainly due to an increase in sympathetic nerve activity.

Absence of myofibrillar creatine kinase and diaphragm isometric function during repetitive activation

1998 ◽  
Vol 84 (4) ◽  
pp. 1166-1173 ◽  
Author(s):  
John J. Labella ◽  
Monica J. Daood ◽  
A. P. Koretsky ◽  
Brian B. Roman ◽  
Gary C. Sieck ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Creatine Kinase ◽  
Muscle Function ◽  
Isometric Force ◽  
Force Generation ◽  
Fatigue Properties ◽  
Specific Force ◽  
Null Mutant ◽  
Isometric Muscle

Creatine kinase (CK) provides ATP buffering in skeletal muscle and is expressed as 1) cytosolic myofibrillar CK (M-CK) and 2) sarcomeric mitochondrial CK (ScCKmit) isoforms that differ in their subcellular localization. We compared the isometric contractile and fatigue properties of 1) control CK-sufficient (Ctl), 2) M-CK-deficient (M-CK[−/−]), and 3) combined M-CK/ScCKmit-deficient null mutant (CK[−/−]) diaphragm (Dia) to determine the effect of the absence of M-CK activity on Dia performance in vitro. Baseline contractile properties were comparable across groups except for specific force, which was ∼16% lower in CK[−/−] Dia compared with M-CK[−/−] and Ctl Dia. During repetitive activation (40 Hz, [Formula: see text] duty cycle), force declined in all three groups. This decline was significantly greater in CK[−/−] Dia compared with Ctl and M-CK[−/−] Dia. The pattern of force decline did not differ between M-CK[−/−] and Ctl Dia. We conclude that Dia isometric muscle function is not absolutely dependent on the presence of M-CK, whereas the complete absence of CK acutely impairs isometric force generation during repetitive activation.

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