Potassium Depolarization and Raised Calcium Induces α-Synuclein Aggregates

The effects of the organic calcium channel blocker nitrendipine was tested on electrically evoked twitches and on potassium depolarization-induced contractures of rat lumbricalis muscles. Nitrendipine (10−7 to 5 × 10−5 M) blocked only the potassium contractures. It was concluded that blocking calcium uptake through the slow voltage-senstitive calcium channels during potassium depolarization blocks the mechanical response of the muscle. Thus extracellular calcium ions are required for the excitation–contraction (E–C) coupling during depolarization contractures. On the other hand, electrically evoked twitches were not affected by nitrendipine; therefore, extracellular calcium ions entering via the slow voltage-sensitive channels are not required for E–C coupling during the twitch.

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Ionomycin stimulates secretion of catecholamines from cat adrenal gland and spleen

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1982.242.3.e137 ◽

1982 ◽

Vol 242 (3) ◽

pp. E137-E145 ◽

Cited By ~ 1

Author(s):

M. H. Carvalho ◽

J. C. Prat ◽

A. G. Garcia ◽

S. M. Kirpekar

Keyword(s):

Chromaffin Cells ◽

Adrenal Glands ◽

Secretory Response ◽

Adrenergic Nerve ◽

Nerve Terminals ◽

Potassium Depolarization ◽

Calcium Dependent ◽

Dopamine Beta Hydroxylase ◽

Adequate Stimulus ◽

Adrenergic Nerve Terminals

Ionomycin, a polyether antibiotic, stimulated the secretion of catecholamines and dopamine beta-hydroxylase from perfused adrenal glands and [3H]norepinephrine ([3H]NE) from spleens of the cat. Release was calcium dependent, and strontium or barium did not substitute for calcium. Ionomycin failed to release [3H]NE from reserpinized spleens. High magnesium did not interfere in the ionomycin response, but lanthanum and manganese blocked it. Ionomycin response that was pH dependent was not affected by potassium depolarization. The secretory response to ionomycin was enhanced when both glycolysis and oxidative metabolism were inhibited. It is concluded that ionomycin introduces calcium into the chromaffin cells and adrenergic nerve terminals to cause the secretory response and that a rise in intracellular calcium may be an adequate stimulus for secretion.

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Calcium diffusion in uterine smooth muscle sheets.

The Journal of General Physiology ◽

10.1085/jgp.80.2.257 ◽

1982 ◽

Vol 80 (2) ◽

pp. 257-277 ◽

Cited By ~ 5

Author(s):

S Kato ◽

T Ogasawara ◽

T Osa

Keyword(s):

Potassium Depolarization ◽

High Potassium ◽

Tension Development ◽

Uterine Smooth Muscle ◽

Rate Limiting Step ◽

Ca Addition ◽

Calcium Diffusion ◽

Apparent Diffusion ◽

The Difference ◽

Rate Limiting

The potassium contracture in the longitudinal muscle of estrogen-treated rat uterus was kinetically investigated. The rates of tension development after Ca addition and relaxation after Ca removal were measured under the high-potassium depolarization. Both rates decreased with an increase in preparation thickness. The relaxation rate had only a slight dependence on temperature. On the contrary, both relaxation and contraction rates in a contraction induced by an electrical stimulation strongly depended on temperature, but not on preparation size. These results suggest that the Ca diffusion process in the extracellular space is the rate-limiting step in relaxation of Ca-dependent contracture under potassium depolarization. The diffusion model, in which the effect of the unstirred layer was considered, could quantitatively explain the experimental results. The apparent diffusion coefficient in the muscle sheet was estimated to be approximately 3 x 10(-7) cm2/s. The difference from that in aqueous solution is discussed.

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Tachycardia heart failure alters rabbit aortic smooth muscle responsiveness to angiotensin II

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.266.3.h1228 ◽

1994 ◽

Vol 266 (3) ◽

pp. H1228-H1232

Author(s):

E. Porsa ◽

G. L. Freeman ◽

J. T. Herlihy

Keyword(s):

Heart Failure ◽

Smooth Muscle ◽

Angiotensin Ii ◽

Calcium Chloride ◽

Maximal Response ◽

Vasoactive Agents ◽

Potassium Depolarization ◽

Smooth Muscle Tissue ◽

Aortic Smooth Muscle ◽

And Control

The effects of heart failure on the responsiveness of aortic smooth muscle tissue to various vasoactive agents were examined. Heart failure was induced in rabbits by sustained rapid ventricular pacing (400 beats/min) for 6-7 wk. After the rabbits were killed, strips of thoracic aorta were prepared and mounted in tissue baths. Responsiveness of these aortic strips to potassium depolarization and cumulative additions of vasoactive agents was determined. Aortic strips from control and tachycardia heart failure (THF) rabbits developed similar maximum forces to stimulation by potassium depolarization (0.77 +/- 0.08 vs. 0.96 +/- 0.16 kg/cm2), calcium chloride (0.71 +/- 0.09 vs. 0.88 +/- 0.06 kg/cm2), and phenylephrine (0.90 +/- 0.08 vs. 1.14 +/- 0.09 kg/cm2). The maximum relaxation to isoproterenol was also unaffected by THF (0.08 +/- 0.02 vs. 0.07 +/- 0.01 kg/cm2). In contrast, the maximum response of aortic strips from THF rabbits to angiotensin II was significantly lower than control (0.37 +/- 0.07 vs. 0.069 +/- 0.09 kg/cm2). With regard to aortic smooth muscle sensitivity, no differences in the concentrations at which 50% of the maximal response is achieved (EC50) were observed between THF and control strips for calcium chloride (0.10 +/- 0.01 vs. 0.16 +/- 0.04 mM), isoproterenol (51.5 +/- 13.5 vs. 51.0 +/- 5.4 nM), and phenylephrine (65.2 +/- 12.3 vs. 92.5 +/- 18.0 nM). However, THF was associated with a significant increase in the EC50 value for angiotensin II response (2.03 +/- 0.25 vs. 0.58 +/- 0.05 nM). These results demonstrate that THF is associated with a specific and significant reduction in the sensitivity and maximal responsiveness of aortic smooth muscle to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)

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