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.

Changes in Renal and Urinary Kallikrein Activity by Mannitol-Induced Osmotic Diuresis

1981 ◽  
Vol 61 (1) ◽  
pp. 47-51 ◽  
Author(s):  
G. Bönner ◽  
M. Marin-Grez ◽  
D. Beck ◽  
M. Deeg ◽  
F. Gross
Keyword(s):  
Renal Cortex ◽  
Plasma Aldosterone ◽  
Urinary Kallikrein ◽  
Osmotic Diuresis ◽  
Plasma Aldosterone Concentration ◽  
Urinary Kallikrein Excretion ◽  
Short Period ◽  
Urinary Potassium ◽  
Renal Kallikrein ◽  
Kallikrein Activity

1. Osmotic diuresis was induced in male Sprague-Dawley rats by a 30% (w/v) mannitol solution injected three times at 15-min intervals. Kallikrein excretion increased for a short period after the first two injections, but, despite marked diuresis, the increment of kallikrein excretion after the second injection was less marked than after the first and no enhanced kallikrein excretion was observed after the third injection of mannitol. 2. Urinary kallikrein excretion correlated only with urinary potassium excretion. No correlation was found with either urine volume or urinary sodium excretion. 3. At the end of the osmotic diuresis kallikrein activity was significantly reduced both in the urine and in the renal cortex. At that time plasma aldosterone concentration was slightly greater in the mannitol-treated than that in the control group, but the difference did not reach statistical significance. 4. In this experiment no relationship was observed between the activity of the renal kallikrein-kinin system and the plasma aldosterone concentration. 5. The transient increase in urinary kallikrein excretion is interpreted as a wash-out effect of renal kallikrein, which is followed by a diminished kallikrein activity in urine and in renal cortex.

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.

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.

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.

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.

Evaluation of Biochemical Conditions Allowing Bypass of Confirmatory Testing in The Workup of Primary Aldosteronism: A Retrospective Study in a French Hypertensive Population

2019 ◽  
Vol 51 (03) ◽  
pp. 172-177 ◽  
Author(s):  
Maud Vivien ◽  
Emilie Deberles ◽  
Remy Morello ◽  
Aimi Haddouche ◽  
David Guenet ◽  
...  
Keyword(s):  
Primary Aldosteronism ◽  
Dynamic Testing ◽  
Challenge Test ◽  
Plasma Aldosterone ◽  
Aldosterone Secretion ◽  
Plasma Aldosterone Concentration ◽  
Hypertensive Patients ◽  
Hypertensive Population ◽  
Tertiary Center ◽  
Aldosterone To Renin Ratio

AbstractThe diagnostic workup for primary aldosteronism includes a screening step using the aldosterone-to-renin ratio (ARR) and a confirmatory step based on dynamic testing of aldosterone secretion autonomy. International guidelines suggest that precise clinical and biochemical conditions may allow the bypassing of the confirmatory step, however, data which validate hormone thresholds defining such conditions are lacking. At our tertiary center, we retrospectively examined a cohort of 173 hypertensive patients screened for PA by the ARR, of whom 120 had positive screening and passed a saline infusion test (SIT) or a captopril challenge test (CCT). Fifty-nine had PA, including 34 Conn adenomas and 25 with idiopathic aldosteronism (IA). Using a threshold of 160 pmol/l, post-SIT plasma aldosterone concentration (PAC) identified PA with 86.4% sensitivity, 94.7% specificity, and a negative predictive value of 92.3%. Of those subjects with a high ARR and a PAC above 550 pmol/l, 93% had a positive SIT, while 100% of subjects with a high ARR, but a PAC under 240 pmol/l had a negative SIT. Our results thus validate the biochemical conditions defined in the French and US guidelines for bypassing the confirmatory step in the workup for PA diagnosis.

Hormonal changes in normal and polycythemic high-altitude natives

1995 ◽  
Vol 79 (3) ◽  
pp. 795-800 ◽  
Author(s):  
A. M. Antezana ◽  
J. P. Richalet ◽  
I. Noriega ◽  
M. Galarza ◽  
G. Antezana
Keyword(s):  
High Altitude ◽  
Systolic Pressure ◽  
Plasma Aldosterone ◽  
Control Group ◽  
Protective Mechanism ◽  
Hormonal Changes ◽  
Plasma Aldosterone Concentration ◽  
Pulmonary Arterial ◽  
Exercise Induced ◽  
Acute And Chronic Exposure

Acute and chronic exposure to high-altitude (HA) hypoxia inhibits the renin-angiotensin-aldosterone system and may modify the release of atrial natriuretic peptide (ANP) in sea-level (SL) natives. In HA natives, the release of these hormones could be influenced by changes in blood volume or pulmonary arterial pressure. Twenty-four men residing in La Paz, Bolivia, at 3,600 m were separated into two groups: one normocythemic (HAN; with hematocrit < 57%; n = 13) and the other polycythemic (HAP; with hematocrit > 57%; n = 11). A control group of 9 SL residents was studied in normoxia (SLN) as well as after 4 days spent at 4,350 m (SLH). The groups were tested for plasma active renin (PAR), plasma aldosterone concentration, ANP, and potassium and norepineprine concentrations at rest and after a maximal exercise. Pulmonary arterial systolic pressure was assessed by a Doppler technique. It was observed that PAR and plasma aldosterone concentration at rest and after exercise were lower in the SLH than in the SLN group. PAR and norepineprine concentration were higher among highlanders than in the SLN group. Renin response to exercise was normal among the HAN group and slightly decreased among the HAP group, and an exercise-induced increase in aldosterone was attenuated in both HA groups. Aldosterone response to renin was maintained among the SLH group but was attenuated in the HA groups, possibly owing to a protective mechanism against salt and water retention. Resting and exercise ANP was lower in the HA groups than in the SLN group.

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