Ultrafiltration of renin in the mouse kidney studied by inhibition of tubular protein reabsorption with lysine

1988 ◽  
Vol 75 (3) ◽  
pp. 331-336 ◽  
Author(s):  
Ingrid Mazanti ◽  
Kirstine Lintrup Hermann ◽  
Arne Høj Nielsen ◽  
Knud Poulsen
Keyword(s):  
Intraperitoneal Injection ◽  
Excretion Rate ◽  
Plasma Renin ◽  
Basic Amino Acid ◽  
Tubular Reabsorption ◽  
Renal Tubules ◽  
Plasma Renin Concentration ◽  
Protein Reabsorption ◽  
Glomerular Ultrafiltration

1. In order to study the role of the kidney in the elimination of endogenous plasma renin, renin was measured in the plasma and urine of female mice. 2. The renin concentration was two orders of magnitude lower in urine than in plasma, but it increased after intraperitoneal injection of submandibular mouse renin. No correlation between the plasma renin concentration and the urinary renin concentration and renin excretion rate could be demonstrated. 3. Blockade of the tubular reabsorption of proteins by intraperitoneal injection of the basic amino acid lysine increased the urinary renin concentration, renin excretion rate and renin clearance two to three orders of magnitude, without affecting the plasma renin concentration. 4. This finding demonstrates that ultrafiltered renin is reabsorbed almost completely in the renal tubules and that the mechanism most likely is the same as for other filtered proteins. 5. The large renal renin clearance obtained after intraperitoneal lysine is in accordance with a major role of the kidneys in the elimination of renin from the circulation, by a glomerular ultrafiltration and tubular reabsorption and metabolization of renin.

The Control of Aldosterone Secretion and Its Relationship to the Diagnosis of Hyperaldosteronism

1969 ◽  
Vol 14 (12) ◽  
pp. 420-440 ◽  
Author(s):  
R. Fraser ◽  
J. J. Brown ◽  
R. Chinn ◽  
A. F. Lever ◽  
J. I. S. Robertson
Keyword(s):  
Plasma Renin ◽  
Plasma Potassium ◽  
Aldosterone Secretion ◽  
Plasma Renin Concentration ◽  
Means Of Measurement ◽  
Secondary Hyperaldosteronism

Current concepts of the control of aldosterone secretion in man have been reviewed with particular reference to the role of the kidney. On the basis of these concepts, it is concluded that hyperaldosteronism is most conveniently diagnosed by repeated estimation of plasma potassium, which is usually persistently or intermittently reduced in this disease. Occasional cases fail to show hypokalaemia. Distinction between primary and secondary hyperaldosteronism is made by means of measurement of plasma renin concentration. Subnormal values are usually obtained in the first instance and supranormal values in the second.

Differential Effect of Prostaglandin A1 in Hypertensive Patients with Low, Normal and High Renin

1974 ◽  
Vol 48 (s2) ◽  
pp. 311s-313s
Author(s):  
L. R. Krakoff ◽  
N. Vlachakis ◽  
M. Mendlowitz ◽  
J. Stricker
Keyword(s):  
Arterial Pressure ◽  
Sodium Excretion ◽  
Excretion Rate ◽  
Plasma Renin ◽  
Systemic Arterial Pressure ◽  
Urine Sodium ◽  
Electrolyte Intake ◽  
Urine Sodium Excretion ◽  
Prostaglandin A1

1. Eighteen hypertensive in-patients were studied during a period of controlled electrolyte intake and, on the basis of determinations of mid-day plasma renin activity (PRA), were classified into low, normal and high renin sub-groups. 2. The responses of systemic arterial pressure, urine sodium excretion rate and PRA to infusion of prostaglandin A1 (PGA1) at a rate of 0.4 μg min−1 kg−1 for 60 min differed among the renin sub-groups. 3. The low renin sub-group displayed the greatest fall in arterial pressure and the greatest increase in sodium excretion rate during infusion of PGA1; PRA was unaffected. The normal renin group demonstrated a lesser reduction of arterial pressure and lesser rise in sodium excretion rate during infusion of PGA1 compared with the low renin group; PRA rose significantly during infusion of PGA1. No significant change in arterial pressure occurred in the high renin group during infusion of PGA1; sodium excretion rate rose less than that observed in the other two groups. Infusion of PGA1 caused striking increases in PRA in the high renin group. 4. The changes in PRA during infusion of PGA1 may explain the differences in arterial pressure and sodium excretion rate observed in the three renin sub-groups. The results also suggest that the role of the vasodilating prostaglandins may differ in the pathogenesis of low, normal and high renin hypertension.

Role of prostaglandins in renin suppression during acute potassium loading

1985 ◽  
Vol 248 (3) ◽  
pp. F360-F365
Author(s):  
K. A. Kirchner
Keyword(s):  
Volume Expansion ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Plasma Renin ◽  
Prostaglandin I2 ◽  
Plasma Volume Expansion ◽  
Potassium Loading ◽  
Nacl Excretion ◽  
Prostaglandin System

Acute K loading suppresses plasma renin activity (PRA) and may alter prostaglandin biosynthesis. To determine whether the effect of K on PRA was modulated through changes in the prostaglandin system, dietary NaCl-restricted rats were infused with prostaglandin I2. PRA was then determined before and 90 min after a KNO3 infusion. Control rats received only the prostaglandin infusion. PRA increased in rats receiving prostaglandins alone. K loading prevented the increase in PRA. To further exclude prostaglandins in PRA suppression during K loading, the effects of K on PRA were determined during prostaglandin inhibition with meclofenamate or indomethacin. K loading also suppressed PRA during prostaglandin inhibition. In neither study could the changes in PRA be attributed to changes in mean arterial pressure, glomerular filtration rate, plasma volume expansion, or urinary NaCl excretion rate. We conclude that the effects of K on PRA are independent of the prostaglandin system.

The Renin Angiotensin System and Bipolar Disorder: A Systematic Review

2020 ◽  
Vol 27 (6) ◽  
pp. 520-528 ◽  
Author(s):  
Izabela Guimarães Barbosa ◽  
Giulia Campos Ferreira ◽  
Diomildo Ferreira Andrade Júnior ◽  
Cássio Rocha Januário ◽  
André Rolim Belisário ◽  
...  
Keyword(s):  
Systematic Review ◽  
Bipolar Disorder ◽  
Cardiovascular Diseases ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Angiotensin Receptors ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Search Terms

Bipolar Disorder (BD) is a chronic a multifactorial psychiatric illness that affects mood, cognition, and functioning. BD is associated with several psychiatric conditions as well clinical comorbidities, particularly cardiovascular diseases. The neurobiology of BD is complex and multifactorial and several systems have been implicated. Considering that the Renin Angiotensin System (RAS) plays an important role in cardiovascular diseases and that recently evidence has suggested its role in psychiatric disorders, the aim of the present study is to summarize and to discuss recent findings related to the modulation of RAS components in BD. A systematic search of the literature using the electronic databases MEDLINE and LILACS was conducted through March 2019. The search terms were: “Bipolar Disorder”; “Renin Angiotensin System”; “Angiotensin 2”; “Angiotensin receptors”; “Angiotensin 1-7”; “ACE”; “ACE2”; “Mas Receptor”. We included original studies assessing RAS in BD patients. Two hundred twenty-two citations were initially retrieved. Eleven studies were included in our systematic review. In the majority of studies (6 of 8), the ACE insertion/deletion (I/D) polymorphism did not differ between BD patients and controls. BD patients presented higher plasma renin activity in comparison with controls. The studies evaluating the RAS molecules in BD are very scarce and heterogeneous. The literature suggests a potential role of RAS in BD. Further studies are necessary to investigate this relationship.

The Estimation of Plasma Renin Concentration in the Dog

1964 ◽  
Vol 93 (1) ◽  
pp. 3C-4C ◽  
Author(s):  
J. J. Brown ◽  
D. L. Davies ◽  
A. F. Lever ◽  
J. I. S. Robertson ◽  
M. Tree
Keyword(s):  
Plasma Renin ◽  
Plasma Renin Concentration

Peripheral corticotropin-releasing factor mediates the elevation of plasma IL-6 by immobilization stress in rats

1998 ◽  
Vol 275 (5) ◽  
pp. R1461-R1467 ◽  
Author(s):  
Tetsuya Ando ◽  
Jean Rivier ◽  
Hitoshi Yanaihara ◽  
Akira Arimura
Keyword(s):  
Intravenous Injection ◽  
Intraperitoneal Injection ◽  
Immobilization Stress ◽  
Systemic Administration ◽  
Corticotropin Releasing Factor ◽  
Elevated Plasma ◽  
Adrenalectomized Rats

We previously reported the elevation of plasma interleukin (IL)-6 activity in response to immobilization stress in rats. To investigate the role of peripheral corticotropin-releasing factor (CRF) in this response, we examined the effects of CRF antagonists on immobilization-induced IL-6 response. Intravenous pretreatment with either [d-Phe12,Nle21,38,CαMeLeu37]-anti-human rat (h/r) CRF12—41(1.5 mg/kg) or cyclo(30—33)[d-Phe12, Nle21,38,Glu30,Lys33]-h/rCRF12—41(Astressin, 0.5 mg/kg) attenuated the IL-6 response to immobilization, which confirmed our previous finding that systemic administration of an antiserum against CRF blocked this response. In addition, an intraperitoneal injection of h/rCRF (100 μg/kg) or rat urocortin (10 and 100 μg/kg) increased the plasma IL-6 activity, mimicking the response to immobilization. An intravenous injection of h/rCRF (100 μg/kg) also elevated plasma IL-6 in adrenalectomized rats. These findings suggest that peripheral CRF mediates the plasma IL-6 elevation in response to immobilization.

EXTRAHEPATIC AND EXTRARENAL RENIN INACTIVATION IN THE DOG

1974 ◽  
Vol 60 (2) ◽  
pp. 217-222
Author(s):  
R. FAGARD ◽  
E. FOSSION ◽  
M. CAMPFORTS ◽  
A. AMERY
Keyword(s):  
Blood Vessels ◽  
Pulmonary Circulation ◽  
Plasma Renin ◽  
Glass Container ◽  
Plasma Renin Concentration ◽  
Vascular Beds ◽  
Extrarenal Renin

SUMMARY It was demonstrated previously that renin disappears quickly from the circulation after nephrectomy in the hepatectomized dog. In the present study the plasma renin concentration (PRC) was measured in the efferent and afferent blood vessels of several vascular beds (pulmonary circulation, splanchnic region, spleen, both inferior limbs and pelvis, head) in the anhepatic and in the anhepatic and anephric dog in order to investigate extrarenal and extrahepatic renin inactivation. However, no significant arteriovenous differences in PRC could be traced. The blood of these dogs kept in vitro at 37 °C in a glass container showed no decline in PRC within 3 h of removal. Therefore no specific extrahepatic and extrarenal renin-inactivating mechanism was found which could explain the rapid disappearance of renin from the blood in vivo in the anhepatic and anephric dog.

scholarly journals Advances in understanding the role of cardiac glycosides in control of sodium transport in renal tubules

2014 ◽  
Vol 222 (1) ◽  
pp. R11-R24 ◽  
Author(s):  
Syed Jalal Khundmiri
Keyword(s):  
Heart Failure ◽  
Intracellular Signaling ◽  
Cardiac Contractility ◽  
Myocardial Cell ◽  
Renal Tubules ◽  
Intracellular Signaling Pathway ◽  
Body Sodium ◽  
Membrane Bound ◽  
Total Body

Cardiotonic steroids have been used for the past 200 years in the treatment of congestive heart failure. As specific inhibitors of membrane-bound Na+/K+ATPase, they enhance cardiac contractility through increasing myocardial cell calcium concentration in response to the resulting increase in intracellular Na concentration. The half-minimal concentrations of cardiotonic steroids required to inhibit Na+/K+ATPase range from nanomolar to micromolar concentrations. In contrast, the circulating levels of cardiotonic steroids under physiological conditions are in the low picomolar concentration range in healthy subjects, increasing to high picomolar levels under pathophysiological conditions including chronic kidney disease and heart failure. Little is known about the physiological function of low picomolar concentrations of cardiotonic steroids. Recent studies have indicated that physiological concentrations of cardiotonic steroids acutely stimulate the activity of Na+/K+ATPase and activate an intracellular signaling pathway that regulates a variety of intracellular functions including cell growth and hypertrophy. The effects of circulating cardiotonic steroids on renal salt handling and total body sodium homeostasis are unknown. This review will focus on the role of low picomolar concentrations of cardiotonic steroids in renal Na+/K+ATPase activity, cell signaling, and blood pressure regulation.

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