Inter-relationship between urinary kallikrein-kinins and arginine vasopressin in man

1989 ◽  
Vol 76 (1) ◽  
pp. 13-18 ◽  
Author(s):  
K. Yamada ◽  
K. Hasunuma ◽  
T. Shiina ◽  
K. Ito ◽  
Y. Tamura ◽  
...  
Keyword(s):  
Urinary Excretion ◽  
Arginine Vasopressin ◽  
Control Period ◽  
Urine Volume ◽  
Free Water ◽  
Normal Subjects ◽  
Urine Flow ◽  
Urinary Kallikrein ◽  
Plasma Aldosterone Concentration ◽  
Water Loading

1. Physiological saline solution was infused in nine normal subjects and six patients with central diabetes insipidus (DI). At 120 min after the start of infusion, arginine vasopressin (AVP) was injected intramuscularly. Urine was collected in 30 min fractions before and after AVP administration. 2. The urinary excretions of kallikrein-like activity (KAL-A) (S-2266 hydrolysis activity) and immunoreactive kinins (i-kinins) were significantly lower in patients with DI than in normal subjects before AVP administration, while there were no differences in plasma renin activity, plasma aldosterone concentration, creatinine clearance and blood pressure between the two groups, except for a marked water diuresis in patients with DI. The urinary excretion of KAL-A and i-kinins correlated positively with the urinary excretion of AVP. 3. AVP administration increased both plasma AVP and urinary excretion of AVP to similar levels in both groups. As a result, urine volume decreased to a greater degree in patients with DI than in normal subjects. In contrast, the urinary excretions of KAL-A and i-kinins were increased by AVP administration, with a greater response in normal subjects than in the patients with DI. 4. After overnight fasting, acute water loading was carried out orally for 15 min in six normal subjects. At 30 min plasma AVP was suppressed by water loading to almost the basal level found in patients with DI. Urinary excretions of KAL-A and i-kinins in the first 30 min fraction after loading were also suppressed to the basal level in patients with DI. Later, the urinary excretion of KAL-A increased together with the increase in urine flow. Urine volume and free water clearance markedly increased except in the first 30 min fraction, compared with the control period. 5. Thus it is suggested that AVP is one of the factors regulating the renal kallikrein-kinin system in man, although it seems likely that urine flow is still a major factor in urinary kallikrein-kinin excretion.

Cardiovascular, renal, and endocrine responses in male quadriplegics during head-out water immersion

1990 ◽  
Vol 258 (6) ◽  
pp. R1424-R1430 ◽  
Author(s):  
F. Tajima ◽  
S. Sagawa ◽  
J. Iwamoto ◽  
K. Miki ◽  
B. J. Freund ◽  
...  
Keyword(s):  
Water Immersion ◽  
Urine Volume ◽  
Systolic Pressure ◽  
Free Water ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Urine Flow ◽  
Cervical Cord ◽  
Free Water Clearance ◽  
Normal Men

The present study was undertaken to determine the relative influence of the action of the central nervous system on the mechanism of water-immersion-induced diuresis by comparing physiological responses of quadriplegic (QP) and normal subjects. After overnight fasting seven male QP subjects with complete cervical cord transections (C5-C8) and six normal men were tested before, during, and after 3 h of head-out immersion (HOI) in thermoneutral water (34.5-35.0 degrees C). The reversible increase in urine flow and the total urine volume (309 +/- 53 ml in 3 h) in QP subjects were comparable with that of the normal subjects (318 +/- 96 ml in 3 h). While osmolal excretion was increased in QP subjects, its magnitude was less when compared with that of normal subjects. Instead, the increased urine flow in QP subjects was characterized by increased glomerular filtration rate (GFR) and free water clearance, in contrast to a predominantly osmotic diuresis with no changes in GFR in the normal subjects. The HOI elevated (P less than 0.05) systolic pressure only in QP subjects, whereas the increase in cardiac output was the same in both groups. While plasma renin activity and aldosterone responses to HOI in QP subjects were comparable with those of normal individuals, plasma atrial natriuretic factor (ANF) in QP subjects was twofold higher (P less than 0.05) during HOI, and the approximately threefold increase in ANF (P less than 0.05) in QP subjects due to HOI was the same as that of normal subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

URINARY EXCRETION OF SODIUM AND POTASSIUM IN RELATION TO PLASMA ALDOSTERONE CONCENTRATION

1972 ◽  
Vol 53 (3) ◽  
pp. 425-431 ◽  
Author(s):  
A. R. ADAMSON ◽  
S. W. JAMIESON
Keyword(s):  
Urinary Excretion ◽  
Low Dose ◽  
Urine Volume ◽  
Normal Subjects ◽  
Plasma Aldosterone ◽  
Urinary Sodium ◽  
Potassium Excretion ◽  
Plasma Aldosterone Concentration ◽  
Dose Infusion ◽  
Sodium And Potassium

SUMMARY The effect of a low dose infusion of aldosterone (7·0–8·4 ng/kg/min) on urinary sodium and potassium excretion was assessed in six normal subjects. Plasma aldosterone levels during these infusions (mean 38, range 23–62 ng/100 ml) compared favourably with levels obtained during Na+ deprivation (mean 38, range 30–46 ng/100 ml). In four paired experiments, aldosterone infused in this dose for 2 h produced a significant reduction in Na+ excretion (P < 0·01) and urine volume (P < 0·05) in the 4th hour after the start of the infusion compared with the control infusions. There was no significant change in K+ excretion. Prolonging the aldosterone infusion reduced Na+ excretion. A 10 h infusion of aldosterone (7·7 ng/kg/min) in one subject reduced Na+excretion to 6 μequiv./min. These results are compared to the levels of Na+ excretion obtained in dietary Na+ deprivation.

scholarly journals Intermittent negative pressure ventilation may increase urine flow in normal subjects

1994 ◽  
Vol 112 (2) ◽  
pp. 551-554 ◽  
Author(s):  
Ricardo Marques Dias ◽  
Carlos Stabile ◽  
Pedro Dotto ◽  
José Roberto Jardim
Keyword(s):  
Flow Rate ◽  
Negative Pressure ◽  
Venous Blood ◽  
Urine Volume ◽  
Free Water ◽  
Normal Subjects ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Negative Pressure Ventilation ◽  
Two Phases

In order to analyze the effect of intermittent negative pressure ventilation (NPV) on renal function, we studied 20 healthy male volunteers (mean age 29±4.1 years). NPV was performed with an "Emerson Chest Respirator Pump", adjusted to a breathing frequency of 10 respirations per minute, with inspiratory time/total respiratory time ratio of 0.4 and negative pressure of 25 cmH2O. The experimental protocol was carried out in two phases of two hours each - spontaneous breathing and NPV breathing. At the end of each phase, urine volume of the whole period was collected as well as venous blood sample for biochemical determinations. During NPV there was significant increase (P<0.05) in urine flow rate (1.43±0.81 to 2.76±1.95 ml/min) as well as in natriuresis (258±201 to 389±175 mcEq/min), kaliuresis (61±45 to 98±49 mcEq/min), fractional sodium excretion (1.38±0.88 to 1.96±0.98%), osmolar clearance (3.13±1.82 to 4.32±1.24 ml/min) and pH (7.37± 0.04 to 7.41±0.07) with unchanged creatinine and free water clearances. We concluded that NPV increases urine flow rate, kaliuresis and natriuresis but the data we have do not allow us to explain the mechanisms underlying such a phenomenon.

Active and Inactive Urinary Kallikrein in Man: Effects of Diuresis and Antidiuresis

1990 ◽  
Vol 79 (2) ◽  
pp. 117-121 ◽  
Author(s):  
Derek G. Waller ◽  
Satvinder S. Bhatia ◽  
Sara K. Campbell ◽  
Janet D. M. Albano ◽  
J. Gavin B. Millar
Keyword(s):  
Flow Rate ◽  
Arginine Vasopressin ◽  
Urine Flow ◽  
Urine Flow Rate ◽  
Urinary Kallikrein ◽  
Flow Rates ◽  
Water Load ◽  
Water Loading ◽  
Regression Relationship ◽  
Antidiuretic Action

1. The urinary excretion of active and inactive kallikrein was studied in volunteers during diuresis induced by water loading or oral frusemide and during antidiuresis induced by desamino-d-arginine-vasopressin. 2. During acute oral water loading, excretion of active kallikrein was unchanged, despite high urine flow rates and low urine osmolalities being achieved. Excretion of inactive kallikrein correlated with the urine flow rate. 3. After desamino-d-arginine-vasopressin in eight water-loaded and six normally hydrated subjects, excretion of inactive kallikrein also correlated with the urine flow rate. There were no significant changes in the excretion of active kallikrein. 4. After frusemide there was a small transient increase in excretion of active kallikrein 1–2 h after dosing which coincided with the maximum diuresis and natriuresis. Excretion of inactive kallikrein again correlated with urine flow rate but the regression relationship between the two variables was different for water-load-induced and frusemide-induced diuresis. 5. These studies do not support a role for urinary kallikrein in the modulation of the antidiuretic action of vasopressin, but suggest that it may contribute to the natriuretic action of frusemide.

Adrenocortical hormone secretory response to chronic NH4Cl-induced metabolic acidosis

1987 ◽  
Vol 252 (4) ◽  
pp. E454-E460 ◽  
Author(s):  
M. Schambelan ◽  
A. Sebastian ◽  
B. A. Katuna ◽  
E. Arteaga
Keyword(s):  
Metabolic Acidosis ◽  
Urinary Excretion ◽  
Potassium Concentration ◽  
Control Period ◽  
Plasma Potassium ◽  
Plasma Aldosterone ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Hydrogen Ion Concentration ◽  
Adrenocortical Hormone

We examined the effect of chronic metabolic acidosis on adrenocortical hormone production by administering NH4Cl for 5 days to four normal subjects. Plasma aldosterone concentration, aldosterone secretion, and urinary excretion of aldosterone-18-glucuronide increased significantly, whereas there were no significant changes in the plasma concentrations of cortisol, corticosterone, or deoxycorticosterone, or in the urinary excretion of 17-hydroxycorticoids. By day 2, plasma renin activity (PRA) and concentration (PRC) were not significantly different from control, and the slope of the regression line relating plasma aldosterone concentration to PRA was significantly greater than the slope in the control period, i.e., the sensitivity of aldosterone secretion to renin stimulation was increased. By day 5, however, PRA and PRC were increased above control. Plasma potassium concentration did not change significantly. Thus chronic NH4Cl-induced acidosis induces a sustained stimulation of aldosterone secretion in the absence of a change in adrenocorticotropin-dependent adrenocortical hormone secretion. Factors other than an increase in renin secretion and plasma potassium concentration may be involved in at least the early phase of aldosterone stimulation, suggesting that plasma hydrogen ion concentration might be a separate regulator of aldosterone secretion.

Effects of thyroid hormones on urinary and renal kallikreins

1992 ◽  
Vol 263 (3) ◽  
pp. E430-E434
Author(s):  
S. Avigdor ◽  
F. Alhenc-Gelas ◽  
J. Bouhnik
Keyword(s):  
Thyroid Hormones ◽  
Urinary Excretion ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Single Measurement ◽  
Kidney Weight ◽  
Plasma Aldosterone Concentration ◽  
Renal Kallikrein ◽  
Enzyme Changes ◽  
Intact Rats

The effects of thyroid hormones on the urinary excretion of kallikrein and on renal kallikrein were studied in rats. Total and active urinary kallikrein was decreased after thyroidectomy, but renal kallikrein content remained unchanged. Diuresis increased, and kidney weight and plasma aldosterone concentration decreased. Treatment with 3,5,3'-triiodo-L-thyronine restored the urinary kallikrein in thyroidectomized rats to normal and increased it in intact rats. It also produced increases in kidney weight and plasma aldosterone and a decrease in diuresis. The effect of thyroid hormones on the urinary kallikrein response to mineralocorticoids was also tested. Deoxycorticosterone acetate increased urinary kallikrein more in normal than in thyroidectomized rats. These results suggest that thyroidectomy decreases renal kallikrein synthesis and lowers the turnover rate of the enzyme, changes not detectable by a single measurement of the renal kallikrein content but reflected by an alteration in the urinary excretion of the enzyme. Thyroid hormones participate in the control of urinary kallikrein. This effect, however, is probably indirect and may be mediated by mineralocorticoids since thyroid function affects both the plasma level of aldosterone, which is known to influence renal kallikrein, and the kallikrein response to exogenous mineralocorticoids.

Effects of water immersion on sympathoadrenal and dopa-dopamine systems in humans

1992 ◽  
Vol 262 (6) ◽  
pp. R993-R999 ◽  
Author(s):  
E. Grossman ◽  
D. S. Goldstein ◽  
A. Hoffman ◽  
I. R. Wacks ◽  
M. Epstein
Keyword(s):  
Urinary Excretion ◽  
Plasma Levels ◽  
Water Immersion ◽  
Venous Blood ◽  
Urine Volume ◽  
Normal Subjects ◽  
Urinary Sodium Excretion ◽  
Peptide System ◽  
Triphasic Pattern ◽  
Atrial Natriuretic

Water immersion to the neck increases central blood volume and evokes a marked diuresis and natriuresis. The present study examined simultaneously effects of water immersion on activities of three endogenous systems thought to participate in sodium homeostasis: the sympathetic nervous system, the atrial natriuretic peptide system, and the renal dopa-dopamine system. Hourly urine collections and antecubital venous blood samples were obtained from 10 normal subjects before, during, and after sitting in a water-immersion tank for 3 h; four control subjects were studied while seated without immersion. Urine volume was increased by more than threefold after 1 h of immersion (from 1.2 +/- 0.2 ml/min at baseline to 5.9 +/- 0.7 ml/min, P less than 0.001) and peaked during the second hour. Urinary sodium excretion increased by more than twofold (from 103 +/- 17 mu eq/min at baseline to 196 +/- 36 mu eq/min at 1 h, P less than 0.001) and peaked during the third hour. Plasma levels and urinary excretion of norepinephrine (NE) and epinephrine were suppressed consistently during immersion (P less than 0.05). There was a marked, prompt, and sustained increase in plasma levels of immunoreactive atrial natriuretic factor (irANF) from 6.9 +/- 1.9 pg/ml baseline to 17.3 +/- 4.3 pg/ml at 1 h (P less than 0.001). Urinary excretion of dopa, dopamine, and 3,4-dihydroxyphenylglycol, a neuronal metabolite of NE, changed in a triphasic pattern, with decreased excretion during the first hour of immersion (P less than 0.01), small but consistent increases during the next 2 h, and decreased excretion, to below baseline, during recovery (P less than 0.01 for dopa and dopamine).(ABSTRACT TRUNCATED AT 250 WORDS)

The Role of Intrarenal Vasoactive Substances in the Pathogenesis of Essential Hypertension

1978 ◽  
Vol 55 (s4) ◽  
pp. 363s-366s ◽  
Author(s):  
K. Abe ◽  
M. Yasujima ◽  
N. Irokawa ◽  
M. Seino ◽  
S. Chiba ◽  
...  
Keyword(s):  
Essential Hypertension ◽  
Urinary Excretion ◽  
Plasma Renin ◽  
Normal Subjects ◽  
Prostaglandin E ◽  
Plasma Aldosterone Concentration ◽  
Renin Angiotensin ◽  
Vasoactive Substances ◽  
Angiotensin Ii Antagonist ◽  
Renal Kallikrein

To investigate the role of renal vasoactive substances in the pathogenesis of essential hypertension, urinary prostaglandin E excretion, urinary kallikrein excretion, plasma renin activity, plasma aldosterone concentration and urinary Na excretion were measured in normal subjects and patients with essential hypertension after stimulation of the renin—angiotensin—aldosterone system by the intravenous injection of frusemide or a low Na diet; after the inhibition of renin—angiotensin—aldosterone by an angiotensin II antagonist and after the inhibition of renal prostaglandin E synthesis by indomethacin. The urinary excretions of prostaglandin E and kallikrein, plasma renin activity and plasma aldosterone concentration increased after frusemide administration. The urinary excretion of kallikrein increased after frusemide or a low Na diet but decreased after the angiotensin II antagonist and indomethacin during Na depletion. Changes in urinary kallikrein excretion paralleled those in the renin—angiotensin—aldosterone system after various stimuli. The urinary excretion of prostaglandin E increased after frusemide. However, a dissociation between the urinary excretions of prostaglandin E and kallikrein was found during the low Na diet: the former decreased and the latter increased. The urinary excretion of prostaglandin E was closely related to urinary Na output after various stimuli. Basal levels of urinary prostaglandin E and kallikrein excretion were lower in essential hypertension than in normal subjects. The release of renal prostaglandin E and kallikrein after frusemide was also suppressed in essential hypertension compared with that in normal subjects. The data indicate that renal kallikrein—kinin and renin—angiotensin—aldosterone may interact in a dynamic fashion to maintain blood pressure, that renal prostaglandin E may be involved in renal Na handling and that the suppression of renal kallikrein—kinin and prostaglandin E in essential hypertension may be an etiological factor in essential hypertension.

Effect of Carbamazepine on Plasma and Urine Arginine-Vasopressin

1978 ◽  
Vol 54 (4) ◽  
pp. 419-424 ◽  
Author(s):  
T. H. Thomas ◽  
S. G. Ball ◽  
J. K. Wales ◽  
M. R. Lee
Keyword(s):  
Drug Treatment ◽  
Arginine Vasopressin ◽  
Water Deprivation ◽  
Direct Action ◽  
Control Period ◽  
Urine Osmolality ◽  
Normal Subjects ◽  
Plasma Sodium ◽  
Sodium Plasma

1. Five normal subjects were studied before and during treatment with carbamazepine. 2. Plasma sodium, plasma and urine arginine-vasopressin and urine osmolality were measured during a day of water deprivation, before and during drug treatment. 3. During treatment with carbamazepine plasma sodium increased whereas plasma and urine arginine-vasopressin and urine osmolality decreased. Plasma and urine arginine-vasopressin were significantly correlated with urine osmolality. However, carbamazepine did not affect the osmolality of urine produced by the kidney, in response to endogenous arginine-vasopressin. 4. Plasma and urine arginine-vasopressin were significantly correlated with plasma sodium on both control and drug-treatment days, but the relationships of plasma and urine arginine-vasopressin to plasma sodium were different during carbamazepine treatment, as compared with the control period. 5. It is suggested that the threshold of the hypothalamic osmoreceptors for release of arginine-vasopressin is modified by carbamazepine, and that this may be either a direct action or secondary to another action of the drug.

Vasopressin regulation of inner medullary collecting ducts and compensatory changes in mice lacking adenosine A1 receptors

2008 ◽  
Vol 294 (3) ◽  
pp. F638-F644 ◽  
Author(s):  
Timo Rieg ◽  
Kanishka Pothula ◽  
Jana Schroth ◽  
Joseph Satriano ◽  
Hartmut Osswald ◽  
...  
Keyword(s):  
Arginine Vasopressin ◽  
Free Water ◽  
Urinary Flow ◽  
Free Water Clearance ◽  
Water Excretion ◽  
Water Loading ◽  
Collecting Ducts ◽  
Camp Formation

Activation of adenosine A1 receptors (A1R) can inhibit arginine vasopressin (AVP)-induced cAMP formation in isolated cortical and medullary collecting ducts. To assess the in vivo consequences of the absence of A1R, we performed experiments in mice lacking A1R (A1R−/−). We assessed the effects of the vasopressin V2 receptor (V2R) agonist 1-desamino-8-d-arginine vasopressin (dDAVP) on cAMP formation in isolated inner medullary collecting ducts (IMCD) and on water excretion in conscious water-loaded mice. dDAVP-induced cAMP formation in isolated IMCD was significantly greater (∼2-fold) in A1R−/− compared with wild-type mice (WT) and, in contrast to WT, was not inhibited by the A1R agonist N6-cyclohexyladenosine. A1R−/− and WT had similar basal urinary excretion of vasopressin, expression of aquaporin-2 protein in renal cortex and medulla, and acute increases in urinary flow rate and electrolyte-free water clearance in response to the V2R antagonist SR121463 or acute water loading; the latter increased inner medullary A1R expression in WT. Dose dependence of dDAVP-induced antidiuresis after acute water loading was not different between the genotypes. However, A1R−/− had greater inner medullary expression of cyclooxygenase-1 under basal conditions and of the P2Y2 and EP3 receptor in response to water loading compared with WT mice. Thus vasopressin-induced cAMP formation is enhanced in isolated IMCD of mice lacking A1R, but the adenosine-A1R/V2R interaction demonstrated in vitro is likely compensated in vivo by multiple mechanisms, a number of which can be “uncovered” by water loading.

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