PHARMACOLOGICAL EVIDENCE FOR THE EXISTENCE OF TWO COMPONENTS IN THE TWITCH RESPONSE TO FIELD STIMULATION OF DETRUSOR STRIPS FROM THE RAT URINARY BLADDER

We investigated the role of large-conductance Ca2+-activated K+ (BK) channels in β3-adrenoceptor (β3-AR)-induced relaxation in rat urinary bladder smooth muscle (UBSM). BRL 37344, a specific β3-AR agonist, inhibits spontaneous contractions of isolated UBSM strips. SR59230A, a specific β3-AR antagonist, and H89, a PKA inhibitor, reduced the inhibitory effect of BRL 37344. Iberiotoxin, a specific BK channel inhibitor, shifts the BRL 37344 concentration response curves for contraction amplitude, net muscle force, and tone to the right. Freshly dispersed UBSM cells and the perforated mode of the patch-clamp technique were used to determine further the role of β3-AR stimulation by BRL 37344 on BK channel activity. BRL 37344 increased spontaneous, transient, outward BK current (STOC) frequency by 46.0 ± 20.1%. In whole cell mode at a holding potential of Vh = 0 mV, the single BK channel amplitude was 5.17 ± 0.28 pA, whereas in the presence of BRL 37344, it was 5.55 ± 0.41 pA. The BK channel open probability was also unchanged. In the presence of ryanodine and nifedipine, the current-voltage relationship in response to depolarization steps in the presence and absence of BRL 37344 was identical. In current-clamp mode, BRL 37344 caused membrane potential hyperpolarization from −26.1 ± 2.1 mV (control) to −29.0 ± 2.2 mV. The BRL 37344-induced hyperpolarization was eliminated by application of iberiotoxin, tetraethylammonium or ryanodine. The data indicate that stimulation of β3-AR relaxes rat UBSM by increasing the BK channel STOC frequency, which causes membrane hyperpolarization and thus relaxation.

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Effects of ZD6169, a KATP channel opener, on neurally-mediated plasma extravasation in the rat urinary bladder induced by chemical or electrical stimulation of nerves

Brain Research ◽

10.1016/j.brainres.2003.10.007 ◽

2004 ◽

Vol 996 (1) ◽

pp. 41-46 ◽

Cited By ~ 8

Author(s):

Yongbei Yu ◽

Mathew O. Fraser ◽

William C. de Groat

Keyword(s):

Electrical Stimulation ◽

Urinary Bladder ◽

Katp Channel ◽

Plasma Extravasation ◽

Rat Urinary Bladder ◽

Channel Opener ◽

Katp Channel Opener ◽

Stimulation Of

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EVIDENCE OF ADENOSINE 5′-TRIPHOSPHATE RELEASE FROM NERVE AND P2X-PURINOCEPTOR MEDIATED CONTRACTION DURING ELECTRICAL STIMULATION OF RAT URINARY BLADDER SMOOTH MUSCLE

The Journal of Urology ◽

10.1016/s0022-5347(01)64196-x ◽

1997 ◽

Vol 158 (5) ◽

pp. 1973-1977 ◽

Cited By ~ 37

Author(s):

Yat-Ching Tong ◽

Ying-Cho Hung ◽

Kazumasa Shinozuka ◽

Masaru Kunitomo ◽

Juei-Tang Cheng

Keyword(s):

Smooth Muscle ◽

Electrical Stimulation ◽

Urinary Bladder ◽

Bladder Smooth Muscle ◽

Rat Urinary Bladder ◽

Urinary Bladder Smooth Muscle ◽

P2x Purinoceptor ◽

Stimulation Of

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Potentiation of nerve-induced bladder contractions after calcium channel blockade

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1985.249.4.r417 ◽

1985 ◽

Vol 249 (4) ◽

pp. R417-R423

Author(s):

F. G. Carpenter

Keyword(s):

Urinary Bladder ◽

Tetraethylammonium Chloride ◽

Rat Urinary Bladder ◽

Dependent Relation ◽

Motor Nerves ◽

Dose Dependent ◽

Ca2 Channels ◽

Stimulation Of

The potentiation of nerve-induced bladder contractions (NIC) by tetraethylammonium chloride (TEA), K+, or carbachol could result from a greater Ca2+ entry through Ca2+ channels in the muscle or from a greater release of transmitter by nerve terminals. Contractions of equal magnitude by the rat urinary bladder in vitro were initiated by carbachol, K+, or transmural stimulation of urinary bladder motor nerves at 1 Hz. Contractions elicited by K+ or carbachol were drastically reduced by verapamil (0.5 microM), but NICs were unaffected. Thus the role of Ca2+ channels in NICs seems uncertain. NICs are potentiated approximately 50% by K+ (15 mM), carbachol (0.5 microM), or 4-aminopyridine (0.2 mM) and over twofold by TEA (5 mM). Although verapamil (1–5 microM) reduced NICs in a dose-dependent relation, potentiation by each compound was the same. Thus Ca2+ channels probably play no role in potentiation. The resistance of the bladder to distention reflects its viscoelasticity and is Ca2+ sensitive. Because viscoelasticity was decreased by verapamil coincident with the reduction in NICs, both may result from lowered intracellular Ca2+ (Cai2+). However, because the potentiating compounds failed to restore bladder viscoelasticity, they probably did not elevate Cai2+. Therefore, in verapamil-treated preparations potentiation is most probably caused by an enhancement of transmitter release.

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