Developmental regulation of nerve and receptor mediated contractions of mammalian urinary bladder smooth muscle.
The development of nerve-induced activation, receptor properties and cellular signalling was examined by comparing the urinary bladder of new-born (0-2 days) and adult mice. Tissue strips were isolated and the effects of different neuromuscular agents on force were investigated during electrical field stimulation. The nerve-induced contractions of the urinary bladders from new-born mice were less influenced by desensitisation with alpha, beta-methylene ATP and more sensitive to scopolamine compared with those of the adult bladder. There were no differences in alpha, beta-methylene ATP or ATP responsiveness between adult and new-born tissue, showing that the lower purinergic component of the nerve-induced responses in the new-born mice was due to properties of the transmitter release rather than to a change in receptor function. Dose-response curves for carbachol revealed a lower peak response in new-born bladders compared with adults. The phasic component of the cholinergic contractions was pronounced and initiated at low carbachol concentrations in the new-born tissue. The carbachol contractions of both new-born and adult urinary bladder tissue were inhibited by the Rho kinase inhibitor Y27632 and by the protein kinase G activator 8-Br-cGMP. However, the sustained phase of carbachol contraction was significantly less sensitive to Y27632 and 8-Br-cGMP in new-born tissue. These results suggest that the receptor mediated calcium sensitisation mechanism is less prominent in new-born compared with adult mice and that the contractions of new-born bladders are less influenced by the nitric oxide (NO)-cGMP inhibitory pathway.
Ekman
Mari
M
Department of Physiological Sciences, Lund University, Lund, Sweden.
Andersson
Karl-Erik
KE
Arner
Anders
A
D000255:Adenosine Triphosphate / Q000031:analogs & derivatives / Q000494:pharmacology; D000367:Age Factors; D000577:Amides / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D002799:Cholinergic Fibers / Q000502:physiology*; D006152:Cyclic GMP / Q000031:analogs & derivatives / Q000494:pharmacology; D017869:Cyclic GMP-Dependent Protein Kinases / Q000037:antagonists & inhibitors; D004305:Dose-Response Relationship, Drug; D004558:Electric Stimulation; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D018727:Muscarinic Antagonists / Q000494:pharmacology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology*; D009125:Muscle Relaxants, Central / Q000494:pharmacology; D009130:Muscle, Smooth / Q000187:drug effects / Q000294:innervation / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D011725:Pyridines / Q000494:pharmacology; D011976:Receptors, Muscarinic / Q000502:physiology*; D012601:Scopolamine / Q000494:pharmacology; D013779:Tetrodotoxin / Q000494:pharmacology; D001743:Urinary Bladder / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D014665:Vasodilator Agents / Q000494:pharmacology
D000577:Amides; D018679:Cholinergic Agonists; D018727:Muscarinic Antagonists; D009125:Muscle Relaxants, Central; D011725:Pyridines; D011976:Receptors, Muscarinic; D014665:Vasodilator Agents; C108830:Y 27632; C016276:8-bromocyclic GMP; D013779:Tetrodotoxin; D000255:Adenosine Triphosphate; D002217:Carbachol; D012601:Scopolamine; D017869:Cyclic GMP-Dependent Protein Kinases; D006152:Cyclic GMP; D009543:Nifedipine; C002630:alpha,beta-methyleneadenosine 5'-triphosphate