Interrelationship Between Urinary Kallikrein and Arginine-Vasopressin in Man

Yamada, Katsushi; Hasunuma, K; Shiina, Tatsuo; Ito, K.; Yoshida, Sho; Tamura, Tetsuro

doi:10.1007/978-1-4615-9543-4_97

Cited by 3 publications

(3 citation statements)

References 11 publications

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“…Plasma AVP was determined by the method previously described (Yamada et al, 1989b). AVP in EDTA-treated plasma was measured by radioimmunoassay (RIA).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of elevated arginine vasopressin secretion in response to osmotic stimulation and acute haemorrhage by U‐62066E, a κ‐opioid receptor agonist

Yamada

Yoshida

1990

British J Pharmacology

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1 The effect of kappa (K) opioid receptor activation on the increase in arginine vasopressin (AVP) secretion evoked by two acute and quite different stimuli (ie., haemorrhage and osmotic stimulus due to hypertonic saline infusion) were evaluated in conscious Long-Evans rats, by use of U-62066E, a highly selective K-opioid receptor agonist, and MR2266, an opioid receptor antagonist with some selectivity for K-receptors. 2 An acute haemorrhage, which reduced the mean blood pressure by approximately 50%, resulted in a large increase in the plasma AVP (pAVP) levels of control rats. However, the administration of U-62066E (0.2mgkg-' or 2.0mgkg-1) reduced the increase due to haemorrhage in a dose-dependent manner. In contrast, concomitant administration of 2.Omgkg-1 of MR2266 with U-62066E significantly attenuated the inhibition of pAVP levels produced by U-62066E 2.0 mg kg '. 3 Hypertonic saline infusion (5% hypertonic saline solution at a rate of 0.24 ml kg'-min 1 for 10 min) caused the elevation of plasma osmolality (pOsm) from 294.0 + 1.6 mosmol kg'-to 304.4 + 1.9 mosmol kg-1, simultaneously resulting in a significant increase in pAVP levels from 2.34 + 0.28 pgml-1 to 4.54 + 0.51 pgml-'. However, the administration of U-62066E (0.05 mg kg'-or 0.2mgkg-1) reduced the osmotically induced increase in pAVP in a dose-dependent manner although pOsm showed the same degree of increase as in controls. In contrast, concomitant administration of 0.2mgkg-1 of MR2266 with U-62066E significantly attenuated the inhibition of pAVP levels produced by U-62066E 0.2mgkg-, whereas pOsm showed the same degree of increase as in controls. No significant changes in the mean blood pressure of the respective groups were observed during this experiment. 4 It is suggested that the K-Opioid receptor activation reduces the increase in AVP secretion evoked by these two different stimuli and that the inhibitory involvement occurs in the neural lobe in the process of AVP secretion.

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“…Plasma AVP was determined by the method previously described (Yamada et al, 1989b). AVP in EDTA-treated plasma was measured by radioimmunoassay (RIA).…”

Section: Methodsmentioning

confidence: 99%

Inhibition of elevated arginine vasopressin secretion in response to osmotic stimulation and acute haemorrhage by U‐62066E, a κ‐opioid receptor agonist

Yamada

Yoshida

1990

British J Pharmacology

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“…Plasma AVP was measured by the method reported previously (9). After plasma pH was adjusted to 3.5, AVP was extracted by adsorption to a column of octadecylsilyl silica (Sep-Pak C18 cartridges) prewashed with methanol (8 mL) and then with water (12 mL); the column was then washed with 4% acetic acid (10 mL) and eluted with 2.0 mL MeOH.…”

Section: Hormone Measurementsmentioning

confidence: 99%

Effect of Administration of Corticotropin-Releasing Hormone and Glucocorticoid on Arginine VasopressinResponse to Osmotic Stimulus in Normal Subjects and Patients with Hypocorticotropinism without Overt Diabetes Insipidus

Yamada

Tamura

Yoshida

1989

The Journal of Clinical Endocrinology & Metabolism

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We examined the effect of CRH administration on the response of plasma arginine vasopressin (AVP) induced by an osmotic stimulus in six normal subjects and five patients with hypocorticotropinism without overt diabetes insipidus (four patients with Sheehan's syndrome and one with idiopathic pituitary dwarfism with ACTH deficiency). Hypertonic saline infusion (855 mmol/L saline solutions at a rate of 205 mumol/kg.min for 10 min) increased plasma AVP 5.7-fold (P less than 0.01) in normal subjects and 2.4-fold (P less than 0.05) in the patients. CRH administration significantly augmented the plasma AVP response to the osmotic stimulus in the normal subjects, but not in the patients with hypocorticotropinism. CRH administration alone did not influence plasma AVP. These findings suggest that a central CRH-related mechanism(s) was at least partly involved in the augmentation of AVP release. Based on the relatively low plasma AVP response to the osmotic stimulus in patients and their lower plasma AVP levels and higher plasma osmolality under basal conditions, we suggest that patients with hypocorticotropinism have partial diabetes insipidus, in which impairment of central CRH action might be, at least in part, involved. The response of plasma AVP to the osmotic stimulus was attenuated significantly when the patients were given cortisol. Since basal PRA, plasma aldosterone, plasma osmolality, hematocrit, body weight, mean blood pressure, and heart rate were similar with and without cortisol administration, this effect of cortisol may have been due to central suppression of the AVP response to the osmotic stimulus.

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“…Renal TK is localized at the connecting tubule cells and secreted into the urine and vascular compartment [12]. Several hormonal and neuronal factors [13][14][15][16] as well as K + are considered as secretagogues of renal TK, however, precise mechanisms for increases in renal TK secretion by those secretagogues remain to be clear. There are several reports which suggest heterogeneities in urinary KK excretion in association with K + intake.…”

Section: Introductionmentioning

confidence: 99%

Intracellular Ca2+ contributes to K+-induced increase in renal kallikrein secretion

Fujita

Ogino

Daigo

et al. 2006

International Immunopharmacology

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Interrelationship Between Urinary Kallikrein and Arginine-Vasopressin in Man

Cited by 3 publications

References 11 publications

Inhibition of elevated arginine vasopressin secretion in response to osmotic stimulation and acute haemorrhage by U‐62066E, a κ‐opioid receptor agonist

Inhibition of elevated arginine vasopressin secretion in response to osmotic stimulation and acute haemorrhage by U‐62066E, a κ‐opioid receptor agonist

Effect of Administration of Corticotropin-Releasing Hormone and Glucocorticoid on Arginine VasopressinResponse to Osmotic Stimulus in Normal Subjects and Patients with Hypocorticotropinism without Overt Diabetes Insipidus

Intracellular Ca2+ contributes to K+-induced increase in renal kallikrein secretion

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