Sjogren C

References (3)

Title : Urinary bladder and urethral responses to pelvic and hypogastric nerve stimulation and their relation to vasoactive intestinal polypeptide in the anaesthetized dog - Andersson_1990_Acta.Physiol.Scand_138_409
Author(s) : Andersson PO , Sjogren C , Uvnas B , Uvnas-Moberg K
Ref : Acta Physiologica Scandinavica , 138 :409 , 1990
Abstract : The effects on the urinary bladder and urethra of pelvic and hypogastric nerve stimulation and their relation to vasoactive intestinal polypeptides (VIP) were investigated in the anaesthetized dog. Both pelvic and hypogastric nerve stimulation elicited a twofold increase in urinary bladder blood flow and a clear-cut increase in bladder venous effluent VIP concentration. Hypogastric nerve stimulation induced an initial, partly alpha-adrenergic and partly non-adrenergic, non-cholinergic, contraction of the urinary bladder followed by a relaxation. The urethra response was a maintained alpha-adrenergic contraction. Pelvic nerve stimulation elicited a bladder contraction with an initial non-cholinergic peak, whereafter the bladder pressure was maintained at a lower level, an effect which was mainly cholinergic in origin. The urethral response was an initial non-adrenergic, non-cholinergic contraction followed by a maintained cholinergic contractile response. Afferent pelvic nerve stimulation led to an efferent activity that seemed to be a combination of activity in pelvic and hypogastric pathways to the urinary bladder and the urethra. VIP (10 nmol) injected i.v. induced a relaxation of the urinary bladder and the urethra, together with a fall in systemic blood pressure. However, despite high plasma concentrations, no vasodilation was elicited in the urinary bladder. Thus, the main target for the VIP release during pelvic and hypogastric nerve stimulation is probably not the bladder vasculature, but instead perhaps the bladder smooth muscle proper.
ESTHER : Andersson_1990_Acta.Physiol.Scand_138_409
PubMedSearch : Andersson_1990_Acta.Physiol.Scand_138_409
PubMedID: 2327267

Title : Source of calcium for contractions induced by depolarization and muscarinic receptor stimulation in rabbit urinary bladder - Batra_1987_Acta.Physiol.Scand_130_545
Author(s) : Batra S , Sjogren C , Andersson KE , Fovaeus M
Ref : Acta Physiologica Scandinavica , 130 :545 , 1987
Abstract : Omission of calcium or the inclusion of lanthanum in the bathing medium resulted in an almost complete inhibition of contractile responses induced by either K+ depolarization or carbachol in strips of rabbit urinary bladder. D-600 inhibited K+-induced contractions significantly more than carbachol-induced responses. The influx of 45Ca into cells was stimulated both by K+ depolarization and carbachol. Over a 2-min period the increase in 45Ca influx induced by high K+ and carbachol was 98 and 65%, respectively. Both lanthanum and D-600 blocked 45Ca influx stimulated by either K+ depolarization or carbachol. The inhibition of 45Ca influx by these calcium-channel blocking agents, particularly by D-600, was dependent on the length of exposure. Application of carbachol during 45Ca efflux in pre-loaded muscle strips had no effect on the rate of 45Ca efflux. These results indicate that the contractile responses of the urinary bladder to depolarization and to carbachol are highly dependent on an extracellular source of calcium.
ESTHER : Batra_1987_Acta.Physiol.Scand_130_545
PubMedSearch : Batra_1987_Acta.Physiol.Scand_130_545
PubMedID: 3630733

Title : Effects of calcium, calcium channel blockers and Bay K 8644 on contractions induced by muscarinic receptor stimulation of isolated bladder muscle from rabbit and man - Fovaeus_1987_J.Urol_137_798
Author(s) : Fovaeus M , Andersson KE , Batra S , Morgan E , Sjogren C
Ref : J Urol , 137 :798 , 1987
Abstract : In isolated bladder smooth muscle from both rabbit and man, carbachol-induced contractions were reduced by the calcium channel blocker nifedipine, whereas the calcium channel promotor Bay K 8644 had no effect. In nominally calcium-free medium containing 10(-4) M EGTA, carbachol-induced contractions were reduced by 69% (rabbit) and 87% (man). These contractions were abolished by nifedipine, whereas Bay K 8644 significantly increased their amplitude, in rabbit preparations almost to control level. Electrical field stimulation produced contractions which could be suppressed by scopolamine by about 50% (rabbit) and more than 90% (man). These contractions were abolished by calcium-free medium (10(-4) M EGTA), suppressed by nifedipine, but significantly enhanced by Bay K 8644. The depressant effects of nifedipine, verapamil and diltiazem were reversed by Bay K 8644. The calcium channel blockers relaxed K+-induced contractions to base line, and this action was counteracted by Bay K 8644, less effectively when relaxations were induced by diltiazem. It is concluded that contractions produced by muscarinic receptor stimulation are primarily dependent on calcium bound to the outside of the membrane of the smooth muscle, and/or coming from the extracellular medium. Electrically evoked, scopolamine sensitive contractions seem to be mediated by a mechanism different from that of contractions produced by exogenously added muscarinic receptor agonist. The present data support the view that combined blockade of muscarinic receptors and calcium channels is an effective way of inhibiting bladder contractions in both rabbit and man.
ESTHER : Fovaeus_1987_J.Urol_137_798
PubMedSearch : Fovaeus_1987_J.Urol_137_798
PubMedID: 2435928