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Methionine and its derivatives increase bladder excitability by inhibiting stretch-dependent K(+) channels.

ABSTRACT: During the bladder filling phase, the volume of the urinary bladder increases dramatically, with only minimal increases in intravesical pressure. To accomplish this, the smooth muscle of the bladder wall must remain relaxed during bladder filling. However, the mechanisms responsible for the stabilization of bladder excitability during stretch are unclear. We hypothesized that stretch-dependent K(+) (TREK) channels in bladder smooth muscle cells may inhibit contraction in response to stretch.Bladder tissues from mouse, guinea pig and monkey were used for molecular, patch clamp, mechanical, electrical, Ca(2+) imaging and cystometric responses to methionine and its derivatives, which are putative blockers of stretch-dependent K(+) (SDK) channels.SDK channels are functionally expressed in bladder myocytes. The single channel conductance of SDK channels is 89pS in symmetrical K(+) conditions and is blocked by L-methionine. Expressed TREK-1 currents are also inhibited by L-methioninol. All three types of bladder smooth muscle cells from mouse, guinea pig and monkey expressed TREK-1 genes. L-methionine, methioninol and methionine methyl ester but not D-methionine increased contractility in concentration-dependent manner. Methioninol further increased contractility and depolarized the membrane in the presence of blockers of Ca(2+)-activated K(+) conductance. L-methionine induced Ca(2+) waves that spread long distances through the tissue under stretched conditions and were associated with strong contractions. In cystometric assays, methioninol injection increased bladder excitability mimicking overactive bladder activity.Methioninol-sensitive K(+) (SDK, TREK-1) channels appear to be important to prevent spread of excitation through the syncitium during bladder filling.

SUBMITTER: Baker SA

PROVIDER: S-EPMC2275456 | biostudies-other | 2008 Mar

REPOSITORIES: biostudies-other

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Project description:Even though the acute effects of pre-exercise static stretching and dynamic muscle activity on muscular and functional performance have been largely investigated, their effects on the corticospinal pathway are still unclear. For that reason, this study examined the acute effects of 5×20 s of static stretching, dynamic muscle activity and a control condition on spinal excitability, corticospinal excitability and plantar flexor neuromuscular properties. Fifteen volunteers were randomly tested on separate days. Transcranial magnetic stimulation was applied to investigate corticospinal excitability by recording the amplitude of the motor-evoked potential (MEP) and the duration of the cortical silent period (cSP). Peripheral nerve stimulation was applied to investigate (i) spinal excitability using the Hoffmann reflex (Hmax), and (ii) neuromuscular properties using the amplitude of the maximal M-wave (Mmax) and corresponding peak twitch torque. These measurements were performed with a background 30% of maximal voluntary isometric contraction. Finally, the maximal voluntary isometric contraction torque and the corresponding electromyography (EMG) from soleus, gastrocnemius medialis and gastrocnemius lateralis were recorded. These parameters were measured immediately before and 10 s after each conditioning activity of plantar flexors. Corticospinal excitability (MEP/Mmax) was significantly enhanced after static stretching in soleus (P = 0.001; ES = 0.54) and gastrocnemius lateralis (P<0.001; ES = 0.64), and after dynamic muscle activity in gastrocnemius lateralis (P = 0.003; ES = 0.53) only. On the other hand, spinal excitability (Hmax/Mmax), cSP duration, muscle activation (EMG/Mmax) as well as maximal voluntary and evoked torque remained unaltered after all pre-exercise interventions. These findings indicate the presence of facilitation of the corticospinal pathway without change in muscle function after both static stretching (particularly) and dynamic muscle activity.

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Methionine and its derivatives increase bladder excitability by inhibiting stretch-dependent K(+) channels.

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