Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0403608 (ureter)
 9,655 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The local motor response to bradykinin and the bacterial chemotactic peptide, formyl-methionyl-leucyl-phenylalanine (FMLP) was investigated in the guinea-pig isolated renal pelvis and ureter in relation to possible activation of capsaicin-sensitive primary afferent nerves and release of sensory neuropeptides. Both bradykinin (1 nM-10 microM) and FMLP (10 nM-10 microM) produced a concentration-dependent positive inotropic effect in the isolated renal pelvis which was unaffected by in vitro capsaicin desensitization. The response to bradykinin was antagonized by HOE 140, a bradykinin receptor antagonist, while it was unaffected by MEN 10,376, a tachykinin receptor antagonist, hCGRP(8-37) a calcitonin gene-related peptide (CGRP) receptor antagonist and N-t-BOC-Phe-DLeu-Phe-DLeu-Phe (BPLPLP), an FMLP antagonist. The response to FMLP was blocked by BPLPLP while it was unaffected by HOE 140, MEN 10,376 or hCGRP(8-37). Indomethacin (10 microM) enhanced the response to both bradykinin and FMLP. Bradykinin transiently activated rhythmic contractions in the isolated ureter. The response to bradykinin was blocked by HOE 140 and was unaffected by in vitro capsaicin desensitization, indomethacin, MEN 10,376 or BPLPLP. FMLP had no motor effect on the resting ureter but when rhythmic background contractions were evoked by the addition of 100 nM endothelin 1, it produced a transient suppression of ureteral motility. This inhibitory effect was unchanged by in vitro capsaicin desensitization or HOE 140 while it was abolished by indomethacin or BPLPLP pretreatment. Both bradykinin and FMLP evoked the release of CGRP-like immunoreactivity in the renal pelvis. The effect of bradykinin but not that of FMLP was abolished by indomethacin. By contrast neither bradykinin nor FMLP did evoke a significant CGRP-LI release in the ureter. It is concluded that bradykinin and FMLP affect pyeloureteral motility through specific and independent pathways. The local motor responses produced by these chemical stimulants are independent from the release of sensory neuropeptides from capsaicin-sensitive primary afferent neurons. Direct neurochemical evidence was obtained for activation of capsaicin-sensitive primary afferents in the renal pelvis: such a mechanism could be involved in the genesis of ureteral pain whenever bradykinin or FMLP come into contact with sensory nerves in the pyeloureteral wall.
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PMID:Local motor responses to bradykinin and bacterial chemotactic peptide formyl-methionyl-leucyl-phenylalanine (FMLP) in the guinea-pig isolated renal pelvis and ureter. 133 50

Bradykinin (BK) causes vasodilation and increases free water and sodium excretion in the kidney and stimulates smooth muscle contraction in the ureter and bladder. Several proposed sites of action for BK include the renal medullary collecting duct, renal blood vessels and the ureter and bladder smooth muscle. This study employs 3H-BK autoradiography to localize the sites of BK action. 3H-BK binding sites in the kidney are localized in the medullary interstitium where BK may produce prostaglandins which mediate its blood flow, natriuretic and diuretic effects. 3H-BK binding sites in the ureter and bladder are localized in the lamina propria below the basal epithelial layer and absent over the muscle layers suggesting an indirect action on urinary tract smooth muscle.
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PMID:3H-bradykinin binding site localization in guinea pig urinary system. 288 Apr 81

The mechanism of the increased prostaglandin production and induction of sensitivity to bradykinin by the cortex of the hydronephrotic rabbit kidney was investigated using tissue culture techniques. Cortical interstitial cells from normal, unilaterally hydronephrotic and contralateral kidneys were grown in tissue culture. Cells derived from hydronephrotic kidneys, but not normal or contralateral, increased PGE2 production when incubated with bradykinin. Of the two cell types, fibroblasts and macrophages, grown from hydronephrotic explants, neither increased prostaglandin production when grown alone in tissue culture. Recombining the two cell types restored bradykinin responsiveness. Bradykinin responsiveness could be induced in either normal or contralateral cell cultures when macrophages from the hydronephrotic kidney were added to cultures of cells from normal or contralateral cortex. The data indicate unique characteristics of hydronephrotic macrophages are involved in the induction of bradykinin responsiveness in the cortex of the ureter-ligated kidney.
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PMID:Cortical interstitial cell interactions induce sensitivity of hydronephrotic kidney to bradykinin. 316 39

Bradykinin, a known smooth-muscle stimulant, affects ureteral perlstalsis in the dog; the changes were judged by cinefluorography, peristaltic pressures, and ureteral perfusions. No effect on urine flow was detected. Experiments with rats also demonstrated the effect of the drug on the ureter.
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PMID:Bradykinin: effect on ureteral peristalsis. 590 65

Bradykinin (BK)-like activity, which was detected by BK-enzyme-immunoassay, was purified from 80 ml of ureter urine of Sprague-Dawley rats by Sephadex G 25 chromatography, FPLC, and reversed phase HPLC. The purified kinin fraction showed the same retention time as authentic BK on HPLC and produced contraction of isolated rat uterus, the contraction being suppressed by a B2-antagonist Hoe140. There was no other kinin detected on the HPLC at the corresponding retention time to kallidin, arginyl-BK or T-kinin. The peptide showed an amino acid sequence identical to that of BK by amino acid sequence analysis.
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PMID:Identification of rat urinary kinin as bradykinin. 764 25