Increased Urinary Kallikrein-Like Activity in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Tomita, Kimio; Shiigai, Tatsuo; Shichiri, Masayoshi; Andou, Ryoichi; Shinoda, Takeshi; Takeuchi, Jugoro

doi:10.1159/000183043

Cited by 10 publications

(3 citation statements)

References 17 publications

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“…The decrease in natriuresis observed only in our SIADH patients could result from the SPZ inhibition of the proximal secretion of such a natriuretic factor [26]. In our patients, the SPZ-induced decrease in natriuresis cannot be explained by sodium absorption at a distal site because potassium excretion does not change; neither can it be explained by an eventual increase in urinary urea concentration, which is a possible mechanism of decreased natriuresis in SIADH patients [27], Recently, it has been suggested that increased natriu resis seen in SIADH hyponatremia results from an in creased synthesis of kallikrein (and perhaps also in creased synthesis of prostaglandin) induced by hypervo lemia [28]. Now, SPZ inhibits both prostaglandin synthe sis and the kinin kallikrein system [29],…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of Hypouricemia in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux

Dumont

Waterlot

et al. 1985

Nephron

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Hypouricemia seen with hyponatremia related to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) results from an increase in uric acid renal clearance. We studied the mechanism of the increase of uric acid excretion in 6 SIADH patients through pyrazinamide (PZA), which decreases tubular secretion of uric acid, and sulfinpyrazone (SPZ) which decreases post-secretory reabsorption of uric acid. 3 g of PZA decreased the absolute uric acid excretion from 428 ± 244 to 105 ± 47 μg/min (mean ± SD, p < 0.01), and 300 mg of SPZ increased the uric acid to creatinine clearance ratio from 0.31 ± 0.05 to 0.52 ± 0.05 mg/dl glomerular filtration rate (mean ± SEM, p < 0.001), which represent an increment about half of that observed in the control group. The increase of uric acid clearance in SIADH seems to result from a decrease in the post-secretory reabsorption of uric acid. After SPZ, we saw a decrease of natriuresis from 5.6 ± 1.4 to 1.8 ± 0.3 mmol/h (p < 0.001), without any change of urinary flow or urinary potassium excretion.

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Section: Discussionmentioning

confidence: 99%

Mechanisms of Hypouricemia in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Decaux

Dumont

Waterlot

et al. 1985

Nephron

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“…This release of urinary kallikrein requires administration of ADH on water loading (Pisano and Marks, 1986), since ADH or water loading alone does not increase kallikrein excretion (Bonner et al, 1981;Zucker et al, 1983). In patients with posterior hypophysial diabetes inspidus, less kallikrein is excreted (Yamada et al, 1989), but in patients with the syndrome of inappropriate secretion of ADH, when they are allowed free access to water, urinary kallikrein excretion is increased (Tomita et al, 1983). Water-loaded rats administered ADH also increased their urinary kallikrein .…”

Section: Othersmentioning

confidence: 99%

Harmful algal blooms in Sodus Bay, Lake Ontario: A comparison of nutrients, marina presence, and cyanobacterial toxins

Perri

Sullivan

Boyer

2015

Journal of Great Lakes Research

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“…It has been reported that urinary esterase A2 has some kininogenase activity in the rat. 23 However, significant correlation (r = 0.99, p < 0.01, n = 10) was observed between activities measured by this method and the rat urinary kallikrein concentrations kindly measured by John J. Pisano (National Institutes of Health, Bethesda, Maryland) by the RIA method. 26 Blood pressure was measured by tail cuff method.…”

Section: Measurementsmentioning

confidence: 75%

Increased urinary kallikrein-like activity during ADH-induced hyponatremia in rats.

Tomita¹,

Shiigai²,

Saito³

et al. 1984

Hypertension

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SUMMARY The urinary kallikrein system was studied during hyponatremia associated with water and vasopressin administration in rats. Two groups of animals were studied. In the experimental group (n = 5), vasopressin (0.4 U/day) was injected intramuscularly for 7 days, and water (15%-20% body weight per day) was given via a stomach tube. The control group (n = 6) received only vasopressin. In the experimental group, plasma sodium concentration (PNa) decreased from 143.2 ± 0.5 to 130.8 ± 1.8 (m ± SEM) mmol/liter (5th day, p < 0.01) along with plasma osmolality. Urinary kallikrein-like activities (UkaV) increased from 99.1 ± 7.5 to 172.6 ± 23.5 /xmolmin/day (100 g body weight) (5th day, p < 0.05; 6th day, p < 0.05; and 7th day, p < 0.05) after the administration of vasopressin. Uric acid clearance (Cua) increased from 0.153 ± 0.014 to 0.275 ± 0.041 ml/min (5th day, p < 0.05; 7th day, p < 0.05). No change was observed in urinary aldosterone excretion (UAldV), creatinine clearance, or blood pressure. UkaV correlated with Cua (r = 0.81, p < 0.01) and with the degree of change of PNa (r = -0.79, p < 0.01), respectively. In the control group, no change was observed in the above parameters. A significant relationship between UkaV and fractional Na clearance (r = 0.60, p < 0.01) was observed. We conclude that the urinary kallikrein system in rats may be stimulated during hyponatremia when induced by water and vasopressin. This increased activity is probably the result of volume expansion associated with water and vasopressin and may have some relationship to fractional Na clearance in the kidney. (Hypertension 6: 511-518, 1984) KEY WORDS • antidiuretic hormone • volume expansion • vasopressin sodium clearance • kallikrein • kinin A S a possible factor in the pathogenesis of hypertension, the kallikrein-kinin system has been extensively studied after Margolius et al.1 reconfirmed the early finding by Elliot and Nuzum 2 that patients with essential hypertension excreted less kallikrein in the urine than normotensive patients. Studies of urinary kallikrein, 3 " the precise localization of renal kallikrein, 5 " 10 and kinin binding in the kidney"" 14 have been reported. However, there are several points of disagreement with regards to the mechanism or physiological role of the kallikrein system. Firstly, the kallikrein-kinin system correlates with urinary sodium excretion in some conditions, 15 but not in others. "18 Secondly, aldosterone directly stimulates kallikrein activity in kidney homogenates, although urinary kallikrein increases only after several days of deoxycorticosterone administration to dogs. in two acute experiments, 20 2I antidiuretic hormone (ADH) has been reported both to stimulate and not to stimulate urinary kallikrein. Therefore, it would be of interest to evaluate the chronic effects of ADH on the kallikrein-kinin system. Similar to the syndrome of ADH excess is the syndrome of inappropriate secretion of ADH. In this situation, urinary kallikrein-like activity increased during hyponatremia.22 " In add...

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Increased Urinary Kallikrein-Like Activity in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Cited by 10 publications

References 17 publications

Mechanisms of Hypouricemia in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Mechanisms of Hypouricemia in the Syndrome of Inappropriate Secretion of Antidiuretic Hormone

Harmful algal blooms in Sodus Bay, Lake Ontario: A comparison of nutrients, marina presence, and cyanobacterial toxins

Increased urinary kallikrein-like activity during ADH-induced hyponatremia in rats.

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