Acute effects of acetylsalicylic acid on renal function in normal man

1977 ◽  
Vol 11 (2) ◽  
pp. 117-123 ◽  
Author(s):  
K. J. Berg
2014 ◽  
Vol 116 (3) ◽  
pp. 257-263 ◽  
Author(s):  
Pedro Zapater ◽  
Lucia Llanos ◽  
Claudia Barquero ◽  
Pablo Bellot ◽  
Sonia Pascual ◽  
...  

Toxicology ◽  
1984 ◽  
Vol 30 (3) ◽  
pp. 243-247 ◽  
Author(s):  
X.P. Wang ◽  
E.C. Foulkes
Keyword(s):  

1965 ◽  
Vol 209 (4) ◽  
pp. 844-848 ◽  
Author(s):  
John R. Gill ◽  
Kenneth L. Melmon ◽  
Louis Gillespie ◽  
Frederic C. Bartter

Renal function was studied in five normal subjects during the infusion of bradykinin at 0.1 and 0.4 µg/kg per min, and in four additional normal subjects during the infusion of norepinephrine at dosages beginning with 1–3 µg/ min. Bradykinin at both dosages decreased glomerular filtration rate (GFR) and tended to increase renal blood flow (ERPF). It increased sodium excretion (UNaV) at the lower dosage, but did not increase it further at the higher dosage. At all dosages, norepinephrine decreased ERPF and UNaV. The effects of bradykinin cannot be explained solely as effects of norepinephrine released by the bradykinin. During adrenergic blockade produced by guanethidine, bradykinin, 0.1 µg/kg per min, slightly decreased GFR and UNaV; at 0.4 µg/kg per min, it further decreased GFR and UNaV and tended to decrease ERPF as well. It did not lower blood pressure. The data suggest that in normal man, bradykinin increases UNaV only at low dosages. During adrenergic blockade, endogenous release of angiotensin could have prevented bradykinin from lowering blood pressure and could have caused the decreases in GFR, ERPF, and UNaV. A possible role is suggested for bradykinin in the physiologic control of renal function, and as a causative agent in producing the changes in renal function found in certain disease states characterized by excessive production of kinins.


2011 ◽  
Vol 55 (4) ◽  
pp. 249-255 ◽  
Author(s):  
Fábio M. Montenegro ◽  
Lenine G. Brandão ◽  
Gustavo F. Ferreira ◽  
Delmar M. Lourenço Jr. ◽  
Regina M. Martin ◽  
...  

OBJECTIVE: Little information is available on glomerular function changes after surgical treatment of primary hyperparathyroidism. The acute effects of some head and neck operations on renal function were studied. MATERIAL AND MATHODS: Retrospective analysis of changes in creatinine levels and estimated glomerular filtration rate (eGFR) after surgery. Preoperative values were compared with values available until 72 hours after the operation. RESULTS: In tertiary hyperparathyroidism, mean preoperative and postoperative eGFR values were 57.7 mL/min and 40.8 mL/min (p < 0.0001), respectively. A similar decrease was observed after parathyroidectomy for primary hyperparathyroidism, from 85.4 mL/min to 64.3 mL/min (p < 0.0001). After major head and neck procedures, there was a slight increase in eGFR (from 94.3 mL/min to 105.4 mL/min, p = 0.002). CONCLUSION: Parathyroidectomy may be followed by a transient decrease in eGFR that is not often observed in other head and neck operations.


1999 ◽  
Vol 17 (12) ◽  
pp. 1707-1713 ◽  
Author(s):  
Jesper Melchior Hansen ◽  
Niels Jørgen Johansen ◽  
Hanne Merete Mollerup ◽  
Niels Fogh-Andersen ◽  
Svend Strandgaard

1990 ◽  
Vol 122 (2) ◽  
pp. 206-210 ◽  
Author(s):  
Andrea Giustina ◽  
Mauro Doga ◽  
Corrado Bodini ◽  
Angela Girelli ◽  
Fabio Legati ◽  
...  

Abstract Glucocorticoids have been shown to inhibit GH secretion in normal man when administered in large amounts for several days. The aim of our study was 1. to investigate the acute effects of a single dose of glucocorticoids on GH secretion in normal man; 2. to look at the relationship between the increase in serum cortisol concentration and GH response to the stimuli. Six healthy volunteers received on three occasions in random order an iv injection of GHRH (1–29) NH2, 100 μg, alone or 60 min after oral administration of either 25 or 50 mg of cortisone acetate. Mean stimulated GH levels, GH peak and integrated GH concentration were significantly lower after GHRH plus cortisone 25 mg than after GHRH alone. Mean GH levels at 15 and 30 min after GHRH injection and the peak GH level showed a further decrease after GHRH plus cortisone 50 mg. We conclude that acute administration of pharmacological doses of glucocorticoids is able to inhibit GH response to GHRH, probably through enhancement of endogenous somatostatin release. Moreover, this pharmacological effect of glucocorticoids seems to be dose-dependent and thus directly related to serum cortisol concentrations.


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