Substance P-Induced Changes in Kidney Function in the Conscious Rat: Relation to the Renal Prostaglandin System

1983 ◽  
Vol 6 (1) ◽  
pp. 10-18 ◽  
Author(s):  
Herbert J. Kramer ◽  
Dietrich Klingmüller ◽  
Frank A. Flachskampf ◽  
Rainer Düsing
Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1216
Author(s):  
Falk Gühne ◽  
Alexander Heinzig ◽  
Philipp Seifert ◽  
Robert Drescher ◽  
Martin Freesmeyer

Background: In addition to its SSTR-specific binding in tumors and healthy tissues, DOTATOC analogues accumulate in kidney parenchyma. Renal tracer uptake might be a surrogate of kidney function or dysfunction. This study aimed to evaluate if kidney function can be estimated from 68Ga[Ga]-DOTATOC uptake in PET/CT and its impact on the nephrotoxicity of 177Lu[Lu]-DOTATOC PRRT. Methods: Two cohorts of patients (A: 128 diagnostic patients; B: 32 PRRT patients) were evaluated retrospectively. SUV values of the kidneys, physiologically SSTR-expressing organs and in background compartments were assessed. Kidney function was calculated as eGFR by CKD-EPI creatinine equation. Pearson’s correlation coefficients and treatment-induced changes of uptake and kidney function were assessed and compared. Results: Kidney function and renal DOTATOC uptake showed a significant inverse correlation (R2 = 0.037; p = 0.029). Evaluated models of PET/CT measurements were not able to predict kidney function sufficiently. The uptake of other organs did not depend on eGFR. While the renal uptake increased after PRRT (p < 0.001), the kidney function did not change significantly (p = 0.382). Neither low pre-therapeutic eGFR nor high pre-therapeutic kidney uptake were risk factors of PRRT-induced deterioration in kidney function. Conclusion: The relevance of kidney function for renal 68Ga[Ga]-DOTATOC uptake is limited. The nephrotoxicity of 177Lu[Lu]-DOTATOC PRRT might be low and cannot be reliably predicted by pre-therapeutic measurements.


2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Christel Nielsen ◽  
Ulrika Andersson Hall ◽  
Christian Lindh ◽  
Ulf Ekström ◽  
Yiyi Xu ◽  
...  

1987 ◽  
Vol 46 (1) ◽  
pp. 75-81 ◽  
Author(s):  
Richard A. Siegel ◽  
Eva-Maria Düker ◽  
Ulrich Pahnke ◽  
Wolfgang Wuttke

1986 ◽  
Vol 251 (2) ◽  
pp. C223-C229 ◽  
Author(s):  
A. A. Gashi ◽  
D. B. Borson ◽  
W. E. Finkbeiner ◽  
J. A. Nadel ◽  
C. B. Basbaum

To determine whether serous or mucous cells in tracheal submucosal glands respond to the neuropeptides substance P (SP) and vasoactive intestinal peptide (VIP), we studied the peptide-induced changes in gland cell morphology accompanying release of 35SO4-labeled macromolecules from tracheal explants of ferrets. Explants were labeled for 1 h in medium containing 35SO4 and washed for 3.5 additional hours. Base-line secretion in the absence of drugs declined between 1.5 and 3.5 h after the pulse. Between 2.5 and 3.5 h, the average percent change in counts per minute recovered per sample period was not significantly different from zero (P greater than 0.3; n = 6). Substance P (10(-5) M) and VIP (2 X 10(-6) M) added 4 h after labeling each increased greatly the release of 35SO4-labeled macromolecules (SP, 219%; VIP, 180%) above base line. Bethanechol, a muscarinic-cholinergic agonist (10(-5) M), increased secretion by an average of 142% above base line (each effect, P less than 0.05; n = 6 each). Light and electron microscopy of the control tissues showed glands with narrow lumens and numerous secretory granules. Glands treated with SP or VIP had enlarged lumens and the serous cells were markedly degranulated. These phenomena were documented by morphometry and suggest that SP and VIP cause secretion from glands at least partially by stimulating exocytosis from serous cells.


2005 ◽  
Vol 173 (2) ◽  
pp. 615-620 ◽  
Author(s):  
KATHERINE L. MEYER-SIEGLER ◽  
PEDRO L. VERA

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