Intracellular Mg2+ movement during muscarinic stimulation. Mg2+ uptake by the intracellular Ca2+ store in rat sublingual mucous acini.

Pages C658-C665: G. R. Wade and S. M. Sims. “Muscarinic stimulation of tracheal smooth muscle cells activates large-conductance Ca2+-dependent K+ channel.” Page C662, Fig. 6: the second half of the trace in A was inadvertently duplicated from B. The revised Fig. 6 below shows the correct channel traces. We wish to emphasize that the scientific point of the figure, the reversible antagonism of the cholinergic response by atropine, as well as the quantification in D, remains sound. The data were filtered at 400 Hz and sampled off-line from digital videotape at 2 kHz. (See PDF)

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Muscarinic stimulation of prostacyclin synthesis by the rat penis

European Journal of Pharmacology ◽

10.1016/0014-2999(86)90688-6 ◽

1986 ◽

Vol 123 (1) ◽

pp. 67-71 ◽

Cited By ~ 22

Author(s):

Jamie Y. Jeremy ◽

Dimitri P. Mikhailidis ◽

Paresh Dandona

Keyword(s):

Muscarinic Stimulation ◽

Prostacyclin Synthesis ◽

Stimulation Of

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Effects of drugs on responses to nicotinic and muscarinic stimulation in isolated bovine adrenal medullary cells

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)53847-1 ◽

1982 ◽

Vol 32 ◽

pp. 74

Author(s):

Minoru Isosaki ◽

Joe Watanabe ◽

Hitoshi Houchi ◽

Kyoji Morita ◽

Motoo Oka

Keyword(s):

Adrenal Medullary Cells ◽

Muscarinic Stimulation ◽

Medullary Cells

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Altered nicotinic sensitivity of AV node in surgically denervated canine hearts

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1983.245.1.h27 ◽

1983 ◽

Vol 245 (1) ◽

pp. H27-H32

Author(s):

D. V. Priola ◽

M. B. Curtis ◽

C. Anagnostelis ◽

E. Martinez

Keyword(s):

Fold Increase ◽

Conduction Time ◽

Mediating Effects ◽

Extrinsic Denervation ◽

Av Node ◽

Intraventricular Conduction ◽

Denervation Supersensitivity ◽

Muscarinic Stimulation ◽

Intrinsic Cardiac Nerves ◽

Cardiac Nerves

The responses of normal and cardiac-denervated (DNV) dogs to acetylcholine (ACh) and nicotine (NIC) were examined to determine if the intrinsic cardiac nerves (ICN) that modulate electrical conduction display denervation supersensitivity. Control (n = 18) and DNV (n = 18) animals were placed on cardiopulmonary bypass. Recording of intra-atrial (P-A), intraventricular (H-V), and atrioventricular (AV) nodal (A-H) conduction times were made from the region of the His bundle. ACh (0.1-10 micrograms) was used to produce muscarinic stimulation, whereas NIC (0.1-400 micrograms) was employed to stimulate the ICN. All drugs were administered intracoronary. No supersensitivity to either ACh or NIC was seen in the data from the P-A or H-V intervals of the His electrogram in the DNV animals. However, this group displayed approximately a 10-fold increase in the negative dromotropic effect of NIC on the AV node compared with control. No significant change in muscarinic sensitivity of the AV node was observed in the DNV animals. We conclude that 1) no denervation supersensitivity of the ICN mediating effects on intra-atrial and intraventricular conduction occurs; 2) the AV node itself does not show muscarinic supersensitivity following extrinsic denervation; 3) the ICN do display denervation supersensitivity as shown by a 10-fold increase in the effects of NIC on AV nodal conduction time.

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Tachykinins activate nonselective cation currents in canine colonic myocytes

AJP Cell Physiology ◽

10.1152/ajpcell.1995.269.6.c1394 ◽

1995 ◽

Vol 269 (6) ◽

pp. C1394-C1401 ◽

Cited By ~ 43

Author(s):

H. K. Lee ◽

C. W. Shuttleworth ◽

K. M. Sanders

Keyword(s):

Cell Voltage ◽

Muscle Cells ◽

Neurokinin A ◽

Current Clamp ◽

M Current ◽

Cationic Current ◽

Primary Mechanism ◽

Cation Conductance ◽

Muscarinic Stimulation ◽

Intact Muscle

The mechanism of tachykinin-induced excitation was studied in isolated colonic muscle cells and intact muscle strips. In whole cell voltage-clamp studies performed at 33 degrees C, neurokinin A (NKA) and substance P (SP) reduced L-type Ca2+ current. NKA and SP activated a cationic current that reversed near 0 mV. This current (INKA or ISP, respectively) had properties similar to the acetylcholine (ACh)-activated nonselective cation conductance (IACh), activated by muscarinic stimulation in other gastrointestinal smooth muscle cells. INKA and ISP were decreased when external Na+ was reduced. In contrast to IACh, INKA and ISP were not facilitated by increases in internal Ca2+, but little or no current was activated by these peptides when extracellular Ca2+ was low. INKA (10(-7) M) and ISP (10(-5) M) were blocked by Cd2+ (5 x 10(-4) M), quinine (10(-3) M), and the tachykinin-receptor antagonist [D-Pro2,D-Trp7,9]SP (10(-5) M). Current clamp recordings and intracellular recordings of intact tissues showed that NKA and SP depolarized the cell membrane, which is consistent with the activation of a nonselective cation conductance. These data suggest that a primary mechanism of the tachykinins is to activate a nonselective cation conductance that leads to depolarization. The increase in Ca2+ entry due to tachykinin stimulation appears to be secondary to the activation of the nonselective cation conductance.

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