Potentiation of nerve-induced bladder contractions after calcium channel blockade
| Autor: | F. G. Carpenter |
|---|---|
| Rok vydání: | 1985 |
| Předmět: |
Male
medicine.medical_specialty Carbachol Physiology Urinary Bladder chemistry.chemical_element Stimulation Calcium Ion Channels chemistry.chemical_compound Physiology (medical) Internal medicine medicine Animals Urinary bladder Chemistry Tetraethylammonium Long-term potentiation Muscle Smooth Tetraethylammonium chloride Tetraethylammonium Compounds Elasticity Stimulation Chemical Rats Endocrinology medicine.anatomical_structure Verapamil Anesthesia Potassium medicine.symptom medicine.drug Muscle contraction Muscle Contraction |
| Zdroj: | The American journal of physiology. 249(4 Pt 2) |
| ISSN: | 0002-9513 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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