Urinary kallikrein response to repeated frusemide injections in rats: Effect of adrenalectomy and deoxycorticosterone acetate treatment

1986 ◽  
Vol 71 (5) ◽  
pp. 497-503 ◽  
Author(s):  
L. F. O. Obika ◽  
M. Marin-Grez
Keyword(s):  
Urine Volume ◽  
Urinary Kallikrein ◽  
Deoxycorticosterone Acetate ◽  
Intravenous Injections ◽  
Urinary Kallikrein Excretion ◽  
Mineralocorticoid Activity ◽  
Sodium And Potassium ◽  
Adrenalectomized Rats

1. The effect of repeated intravenous injections of frusemide (0.17 mg/kg) on the urinary kallikrein excretion of normal, adrenalectomized and deoxycorticosterone acetate (D0CA)-treated adrenalectomized rats was studied. 2. Adrenalectomy decreased baseline urinary kallikrein excretion, while DOCA treatment restored it to normal. 3. Frusemide injections repeatedly increased urinary kallikrein excretion in the three groups of rats studied. Compared with control and DOCA-treated animals, adrenalectomized rats were less responsive. 4. The excretion of urinary kallikrein was positively correlated with urine volume and with the excretion of sodium and potassium in all groups. The regression lines were shifted to the left in DOCA-treated adrenalectomized rats showing that mineralocorticoids enhance the effect of frusemide on urinary kallikrein excretion. The regression lines between urinary kallikrein excretion and the measured variables in adrenalectomized rats did not differ from those of control animals. 5. We conclude that the response of urinary kallikrein to frusemide is influenced by the level of mineralocorticoid activity. The effect of frusemide on urinary kallikrein excretion does not appear to be a ‘wash-out’ of the enzyme since its influence did not subside after repeated injections.

Abnormal diurnal urinary sodium and water excretion in diabetic autonomic neuropathy

1987 ◽  
Vol 73 (3) ◽  
pp. 259-265 ◽  
Author(s):  
G. M. Bell ◽  
W. Reid ◽  
D. J. Ewing ◽  
A. D. Cumming ◽  
M. L. Watson ◽  
...  
Keyword(s):  
Autonomic Neuropathy ◽  
Sodium Excretion ◽  
Urine Output ◽  
Urine Volume ◽  
Urinary Sodium ◽  
Diabetic Patients ◽  
Urinary Kallikrein ◽  
Diurnal Patterns ◽  
Urinary Kallikrein Excretion ◽  
Sodium And Potassium

1. Diurnal patterns of urine output and sodium and potassium excretion were studied in 10 diabetic patients with and 10 without autonomic neuropathy, and in 10 normal subjects. 2. The diurnal patterns of excretion in the diabetic patients with autonomic neuropathy differed significantly from the two other groups, as a smaller proportion of the 24 h output of urine, sodium and potassium was excreted during the day and a larger proportion was excreted at night. 3. Similar changes were noted in the diurnal patterns of urinary kallikrein excretion in diabetic patients with autonomic neuropathy, and urinary kallikrein output correlated significantly with urine volume but not with urinary sodium excretion. 4. The diurnal patterns of excretion of urinary prostaglandin E2 and 6-keto-PGF1α were not significantly different in diabetic patients with autonomic neuropathy. 5. Nocturia was a common complaint in this group, and the number of nocturnal voidings correlated with night urine volume. There was no evidence of premature bladder emptying. 6. The changes observed in the day/night urine output and sodium excretion could not be explained by glycosuria, insulin regimens, impaired renal function or abnormal diurnal prostaglandin excretion; their possible relevance to the diurnal changes of urinary kallikrein excretion is discussed.

Mineralocorticoid activity of 19-nor-DOC and 19-OH-DOC in adrenalectomized rat

1982 ◽  
Vol 242 (5) ◽  
pp. E305-E308
Author(s):  
R. D. Perrone ◽  
H. H. Bengele ◽  
S. L. Dale ◽  
J. C. Melby ◽  
E. A. Alexander
Keyword(s):  
Adrenal Glands ◽  
Sodium Reabsorption ◽  
Potassium Excretion ◽  
Mineralocorticoid Activity ◽  
Sodium And Potassium ◽  
Adrenalectomized Rats

Excess mineralocorticoid activity is thought to be responsible for the increased sodium reabsorption found after adrenal enucleation, but no known mineralocorticoid has been demonstrated in quantities sufficient to account for this antinatriuresis. 19-Hydroxydeoxycorticosterone (19-OH-DOC) has been synthesized by the incubated enucleate adrenal capsule and 19-nordeoxycorticosterone (19-nor-DOC), a possible metabolite, has been found in the urine of rats with regenerating adrenal glands. To evaluate the in vivo mineralocorticoid potency of these steroids, we studied glucocorticoid-replete adrenalectomized rats and measured the sodium and potassium excretion after administration of these steroids. Our results indicate that 19-nor-DOC has equipotent antinatriuretic activity compared to aldosterone but was less kaluretic. 19-OH-DOC had no significant antinatriuretic or kaluretic activity. We conclude that 19-nor-DOC is a potent mineralocorticoid and may be responsible for the enhanced sodium reabsorption found after adrenal enucleation.

Amiloride inhibits the rise of urinary kallikrein excretion induced by frusemide administration in the rat

1987 ◽  
Vol 72 (4) ◽  
pp. 449-454 ◽  
Author(s):  
L. F. O. Obika ◽  
M. MARIN-GREZ
Keyword(s):  
Continuous Infusion ◽  
Sodium Excretion ◽  
Regression Line ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Urinary Kallikrein ◽  
Sprague Dawley ◽  
Urinary Kallikrein Excretion ◽  
Urinary Potassium

1. The effect of amiloride administration on the urinary kallikrein response to the injection or continuous infusion of frusemide in normal Sprague–Dawley rats was investigated. 2. Injections of frusemide induced repeatedly an increase in urinary kallikrein excretion. This effect was suppressed by amiloride. Amiloride also blocked the response to mannitol injection. A continuous infusion of frusemide lasting 100 min also induced an increase in urinary kallikrein excretion which persisted throughout the experiment. This response was completely blocked by the injection of amiloride. 3. Urinary kallikrein excretion was directly and positively related to urine volume and urinary sodium excretion before and after amiloride injection. The regression lines had markedly decreased slopes after amiloride administration. The urinary kallikrein excretion was also positively related to the urine volume and urinary sodium excretion when frusemide was continuously infused. However, these relationships were abolished after amiloride injection. 4. In both the injection and the infusion experiments, there was a direct relationship of urinary kallikrein excretion to urinary potassium excretion. Although this relationship persisted after amiloride injection, the regression line was shifted to the left. 5. The suppression of the kallikrein stimulating effect of frusemide by the sodium channel blocker amiloride indicates that distal tubule sodium re-absorption is the triggering factor in urinary kallikrein excretion. The study suggests that the mechanism involved in the release of kallikrein by the distal tubular cells is linked to the renal mechanism affected by amiloride.

Alteration of Renal Response to Carbonic Anhydrase Inhibitor by Synthetic Adrenal Steroids

1958 ◽  
Vol 195 (1) ◽  
pp. 142-146 ◽  
Author(s):  
Joseph H. Perlmutt ◽  
Donald A. Olewine
Keyword(s):  
Carbonic Anhydrase ◽  
Urine Volume ◽  
Significant Rise ◽  
Carbonic Anhydrase Inhibitor ◽  
Adrenal Steroids ◽  
Renal Response ◽  
Significant Change ◽  
Adrenalectomized Rats ◽  
Intact Rats

The increased urinary Na+ output induced by Diamox in water-loaded adrenalectomized rats was partially antagonized by the mineralocorticoid, desoxycorticosterone glucoside (DCG), the increased K+ excretion was augmented and urine volume was not affected. Intact rats subjected to the same treatment showed only a small, but significant, rise in K+ excretion. Under the same conditions, the glucocorticoid, hydrocortisone hemisuccinate (compound FH), significantly elevated Na+, K+ and H2O excretion in adrenalectomized rats receiving Diamox; intact rats showed an increase in Na+ and H2O excretion with no significant change in K+ output. Of particular interest is the finding that 2.5 mg compound FH alone increased H2O excretion in adrenalectomized rats to a slightly greater extent than Diamox alone with considerably less Na+ loss.

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