Validation of an immunoassay for canine thyroid-stimulating hormone and changes in serum concentration following induction of hypothyroidism in dogs.

Objective: To validate a new immunoradiometric assay for canine thyroid-stimulating hormone (cTSH) and to document changes in serum cTSH concentration during induction of hypothyroidism in dogs.

Animals: Six healthy adult male Beagles.

Procedure: Sensitivity, specificity, precision, and accuracy of the cTSH assay were evaluated in vitro.

Hormonal effects on kallikrein, esterase A2, and their inhibitors in rat urine.

The effects of various hormones on the urinary excretion of kallikrein and esterase A2 were studied in rats. Chronic treatment with antidiuretic hormone had no effect on the excretion of either enzyme. Deoxycorticosterone treatment or a low sodium diet stimulated urinary kallikrein excretion (as is well known), but had no effect on urinary esterase A2.

Isolation and partial characterization of rat urinary esterase A2.

An enzyme, esterase A2, which hydrolyzes tosyl-arginine methyl ester was isolated from the urine of female, inbred, Dahl-salt-resistant rats using DEAE-Sephadex ion-exchange, aprotinin-agarose affinity and molecular sieve column chromatography. The purest preparation obtained showed four closely migrating bands on polyacrylamide gel electrophoresis. All four bands of the esterase A2 preparation had enzyme activity since all were stainable on zymograms using N-acetyl-L-methionine alpha-naphthyl ester as substrate.

Alteration in immune complex glomerulonephritis by arachidonic acid.

We employed a model of immune complex glomerulonephritis produced in mice by the daily injection of apoferritin to study the effect of treatment with arachidonic acid (AA). Apoferritin injections produced demonstrable glomerular damage by light microscopy associated with deposition of immunoglobulin along peripheral capillary loops. Treatment with AA 100 micrograms daily resulted in significantly less glomerular damage and a shift inthe location of immune complex deposition to the mesangium.

Anomalous response of urinary kallikrein to deoxycorticosterone in Dahl salt-sensitive rats.

Previous evidence shows that salt-sensitive (S) rats have a net increase in plasma mineralocorticoid activity due to 18-hydroxy-11-deoxycorticosterone and decreased urinary kallikrein excretion compared to salt-resistant (R) rats. Since mineralocorticoids stimulate urinary kallikrein excretion, these results are inconsistent. This inconsistency was explained by the fact that, while R rats responded normally to treatment with deoxycorticosterone (DOC) by an increase in urinary kallikrein excretion, S rats showed no change in urinary kallikrein even when treated with 10 mg of DOC/day for 24 days.

Developmental patterns of blood pressure and urinary protein, kallikrein, and prostaglandin E2 in Dahl salt-hypertension-susceptible rats.

S and R female rats were raised on a 1% NaCl diet, and excretion rates of urinary protein, kallikrein esterase activity, and PGE2 were measured (1) at 1 1/2 months of age, when both S and R rats were normotensive, (2) at 3 months of age, when S rats were mildly hypertensive and R controls remained normotensive, and (3) at 6 months of age, when S rats were markedly hypertensive relative to the still normotensive R rats. Urinary protein excretion rate in S compared to R rats was slightly elevated at 1 1/2 months of age and greatly elevated at 3 and 6 months of age. Urinary kallikrein was measured by hydrolysis of TAME after separation of kallikrein from nonkallikrein TAME esterases on DEAE-Sephadex minicolumns.

Evidence for an androgen-dependent urinary arginine esterase in the rat: separation from other urinary arginine esterases including kallikrein.

DEAE-Sephadex chromatography of male rat urine resolved three peaks of arginine esterase activity using the synthetic substrate alpha-N-p-tosyl-L-arginine methyl ester . HCl (Tos-Arg-O-Me). Esterase activity in peak 1 (esterase A1 fraction) was present in sexually mature males, but it was not found in mature females, castrated mature males, or sexually immature males.

Effects of rat urinary arginine esterases on rat kidney to release renin.

Urinary kallikrein has been reported to activate human plasma inactive renin. Our previous report suggests that rat urinary kallikrein releases active renin from rat renal cortical slices. Recently, McPartland et al.

Cecal diverticulitis.

Cecal diverticula may be solitary or an extension of leftsided diverticulosis. They may be true or false. Diverticulitis in the cecal area is usually found at the time of surgery for presumed appendicitis.

Effects of dexamethasone on excretion of urinary kallikrein and urinary protein in Dahl salt-sensitive and salt-resistant rats.

The effect of glucocorticoid treatment on urinary kallikrein excretion was assessed in Dahl salt-hypertension susceptible (S) and salt-hypertension resistant (R) rats. A single dose of dexamethasone (100 micrograms) caused a marked water diuresis and a slight decrease in urinary kallikrein excretion in both S and R rats. A single dose of dexamethasone also caused the S rat to excrete massive amounts of protein into the urine, almost 3-fold higher than S rats treated with oil; the effect on R rat urinary protein was similar, but less severe.

A qualitative difference in plasma renin activity in Dahl rats susceptible or resistant to salt-induced hypertension.

Plasma renin activity (PRA) was studied in the rats bred by Dahl for susceptibility (S-strain) or resistance (R-strain) to salt (NaCl) induced hypertension. The pH curves for PRA had different shapes. The difference in shape of the pH curves was reflected in the ratio of PRA pH 8/PRA pH 6.

Total and kallikrein arginine esterase activities in the urine of salt-hypertensive susceptible and resistant rats.

Urinary enzymes that hydrolyze the artificial substrate alpha-N-p-tosyl-L-arginine methyl ester (TAME) were studied in Dahl salt-sensitive (S) and salt-resistant (R) rats. Total urinary TAME esterase activity (kallikrein and non-kallikrein) showed a marked increase with dialysis against water, but only in hypertensive S rats with proteinuria. This phenomenon suggests the presence of dialyzable TAME esterase inhibitor(s) in urine following renal damage, but these data do not define what urinary esterases might be affected.