Hormone profiles for progesterone, oestradiol, prolactin, plasma renin activity, aldosterone and corticosterone during pregnancy and pseudopregnancy in two strains of rat: correlation with renal studies

1987 ◽  
Vol 113 (3) ◽  
pp. 435-444 ◽  
Author(s):  
H. O. Garland ◽  
J. C. Atherton ◽  
C. Baylis ◽  
M. R. A. Morgan ◽  
C. M. Milne
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sprague Dawley ◽  
Pregnant Rats ◽  
Corticosterone Concentration ◽  
Hormone Profile ◽  
Sd Rats ◽  
Renal Changes ◽  
Low Levels

ABSTRACT Plasma samples were obtained throughout pregnancy and pseudopregnancy from Sprague–Dawley (SD) rats and during pregnancy from rats of the Munich Wistar (MW) strain. The concentrations of progesterone, oestradiol, prolactin, plasma renin activity (PRA), aldosterone and corticosterone were measured by radioimmunoassay to establish hormonal profiles in the two strains of rat. Circulating progesterone concentrations in both strains of rat were significantly higher during pregnancy than in virgin controls, except at term in the SD group. The hormonal pattern for pseudopregnancy was similar to that of the first half of pregnancy. Oestradiol concentrations were similar to, or lower than, those in virgin controls throughout pseudopregnancy and for the first 2 weeks of pregnancy in both strains of rat. Increased concentrations of steroid were seen only in the pregnant groups towards term. In SD rats, highest prolactin concentrations were apparent during the first half of pregnancy and pseudopregnancy, and at term in the pregnant group. Pregnant MW rats showed a different profile for this hormone, with low levels throughout pregnancy except at term. In all groups PRA rose to a peak at day 9 and decreased to day 16. Pregnant SD rats also showed a significant increase at term. Aldosterone concentrations were significantly increased at several stages of pregnancy in both strains of rat, particularly during the second half of gestation. Pseudopregnant animals showed a different hormone profile, with no significant changes until day 16 when lower concentrations were recorded. There was little variation in the circulating corticosterone concentration except in pregnant rats at term when levels fell. These findings are discussed in relation to the known renal changes of pregnancy and pseudopregnancy. J. Endocr. (1987) 113, 435–444

Effect of nitric oxide synthase inhibition on cardiovascular and hormonal regulation during pregnancy in the rat

2000 ◽  
Vol 78 (5) ◽  
pp. 423-427 ◽  
Author(s):  
Yunlong Zhang ◽  
Susan Kaufman
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Plasma Renin Activity ◽  
Plasma Volume ◽  
Atrial Natriuretic Factor ◽  
Plasma Renin ◽  
Renin Activity ◽  
Pregnant Rats ◽  
Oxide Synthase ◽  
In Pregnancy

Recent studies have shown that nitric oxide (NO) biosynthesis increases in pregnancy and that inhibition of nitric oxide synthase (NOS) induces some pathological processes characteristic of preeclampsia. The current project sought to study the effect of the NOS inhibitor Nω-nitro-L-arginine methyl ester (L-NAME, 10 µg·min-1, sc for 7 days) on plasma volume, plasma atrial natriuretic factor (ANF), plasma endothelin-1 (ET), and plasma renin activity (PRA) during gestation in conscious rats. NOS inhibition caused mean arterial pressure to increase in both virgin and 21-day pregnant rats. Plasma volume fell in the pregnant rats [L-NAME, 4.5 ± 0.3 mL·100 g-1 body wt. (n = 7) vs. D-NAME, 6.8 ± 0.2 mL·100 g-1 body wt. (n = 10); P < 0.05] but not in the virgin rats [L-NAME, 4.3 ± 0.1 mL·100 g-1 body wt. (n = 6) vs. D-NAME, 4.8 ± 0.2 mL·100 g-1 body wt. (n = 8)]. There was no effect of NOS inhibition on plasma ANF levels or PRA in either the virgin or pregnant rats. However, L-NAME did decrease plasma ET levels in the pregnant rats [L-NAME, 19.6 ± 1.6 pg·mL-1 (n = 8) vs. D-NAME, 11.6 ± 2.5 pg·mL-1 (n = 9); P < 0.05]. Our results confirm that NO is involved in cardiovascular homeostasis in pregnancy; NOS inhibition selectively reduces plasma volume in pregnant rats, thus mimicking a major pathophysiological perturbation of preeclampsia. However, it does not induce the hormonal changes characteristic of preeclampsia, namely the decrease in PRA and increase in plasma ET and ANF levels. Key words: plasma volume, preeclampsia, endothelin, atrial natriuretic factor, plasma renin activity.

scholarly journals SAT-220 A Misdiagnosis Causing a Feared Complication

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Gabriela Mroueh ◽  
James K Burks
Keyword(s):  
Plasma Renin Activity ◽  
Adrenal Incidentaloma ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Abdominal Imaging ◽  
Renin Activity ◽  
Primary Hyperaldosteronism ◽  
Confirmatory Test ◽  
Low Levels ◽  
Work Up

Abstract Adrenal incidentalomas are being increasingly found with the widespread use of thoracic and abdominal imaging. Clinicians must determine the nature of the mass to decide what treatment, if any, is needed. All patients should undergo biochemical testing to rule out hypercortisolism, pheochromocytoma and if hypertension is present, primary hyperaldosteronism. These patients should ideally be evaluated by endocrinologists as misdiagnosis can lead to complications. A 60-year-old African American female with a history of hypertension and type 2 diabetes, was admitted to the internal medicine ward with intractable vomiting, abdominal pain and hypotension. Two weeks prior to admission, she had undergone a left sided adrenalectomy for a diagnosis of primary hyperaldosteronism. An adrenal adenoma was incidentally found 1 year before surgery during abdominal imaging done for diverticulitis. She was immediately referred to a surgeon for further work up and evaluation. The work up done for the adrenal incidentaloma included renin, aldosterone and plasma fractionated metanephrines. Plasma renin was low (0.2 ng/mL/hr, n: 0.5-4.0 ng/mL/hr), and Aldosterone was normal (8.1 ng/dL, n&lt;16 ng/dL) and the Aldosterone/ Renin ratio was elevated. No confirmatory test was done and no evaluation for hypercortisolism was done either. Plasma fractionated metanephrines were normal. During current hospitalization, an AM cortisol was 1.5 mcg/dL (n: 6-28 mcg/dL). An ACTH stimulation test was done which showed an inadequate response. She was subsequently started on stress dose steroids with rapid improvement in her symptoms. She was discharged with hydrocortisone and has been followed in our endocrinology clinic. She has yet to fully recover HPA axis but is currently on low dose Hydrocortisone and doing well. This patient was misdiagnosed with primary hyperaldosterenism when she most likely had subclinical hypercortisolism. Patients with primary hyperaldosteronism typically have plasma aldosterone &gt; 15 ng/dL and low levels of plasma renin, with a ratio of plasma aldosterone to plasma renin activity &gt; 20. Low levels of both plasma renin activity and aldosterone suggest nonaldosterone mineralocorticoid excess. Cushing syndrome can cause similar findings. Confirmatory tests should be done, and most patients require bilateral catheterization of the adrenal veins to measure cortisol and aldosterone levels to confirm whether the aldosterone excess is unilateral or bilateral. A 1 mg overnight dexamethasone suppression test is recommended for all adrenal incidentaloma patients to exclude asymptomatic hypercortisolism.

scholarly journals Sodium, potassium and chloride utilization by rats given various inorganic anions

1991 ◽  
Vol 66 (3) ◽  
pp. 523-532 ◽  
Author(s):  
Susan M. Kaup ◽  
Alison R. Behling ◽  
J. L. Greger
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Basal Diet ◽  
Renin Activity ◽  
Sprague Dawley ◽  
Sodium Potassium ◽  
Sprague Dawley Rats ◽  
Blood Pressures ◽  
Sodium And Potassium

The purpose of the present studies was to examine the effect of ingestion of sodium and potassium salts of various fixed anions on blood pressure, and to assess interactions among electrolytes. In the first study, Sprague-Dawley rats fed on purified diets supplemented with Na salts of chloride, sulphate, bisulphate, carbonate and bicarbonate for 7 weeks developed higher blood pressures than rats fed on the basal diet. In a second study, rats fed on Na or K salts of HSO4, HCO3 or Cl had higher blood pressures than rats fed on the basal diet. Blood pressure measurements were not correlated with plasma volume, plasma renin activity, or plasma atrial natriuretic peptide concentrations at 7 weeks. Plasma renin activity was depressed in rats fed on supplemental Na and even more in rats fed on supplemental K salts rather than the basal diet. Generally, rats fed on supplemental Na excreted Na in urine and absorbed Na in the gut more efficiently than rats fed on the basal diet or diets supplemented with K, but the anions fed also altered Na absorption and excretion. In a third study, rats fed on diets supplemented with any Cl salt, but especially KCI, absorbed K more efficiently than those fed on the basal diet. In studies 1 and 2, the efficiency of urinary excretion of K was greatest when HCO3 and CO3 salts were fed and least when HSO4 salts were fed. Despite large variations in the efficiency of absorption and excretion of Na and K, tissue levels of the electrolytes remained constant.

Failure of Loading with Sodium Bicarbonate to Protect against Acute Renal Failure Induced by Mercuric Chloride in the Rat

1977 ◽  
Vol 53 (2) ◽  
pp. 149-154 ◽  
Author(s):  
J. E. Beaumont ◽  
T. A. Kotchen ◽  
J. H. Galla ◽  
R. G. Luke
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Sodium Balance ◽  
Control Group ◽  
Sprague Dawley ◽  
Urinary Volume ◽  
Sprague Dawley Rats

1. To investigate the mechanism by which sodium loading protects against acute renal failure we compared the effects of prior chronic loading with NaCl, or with NaHCO3, on renal function after injection of HgCl2. 2. Twenty-four male Sprague-Dawley rats were divided into three groups of eight rats. One group drank isotonic NaCl solution, a second drank isotonic NaHCO3 solution and the third control group drank deionized water. Acute renal failure was induced by HgCl2 on day 9, and the rats were killed 48 h after injection. 3. Net sodium balances and plasma volumes were similar in both groups of sodium-loaded rats. After HgCl2 serum creatinine was significantly less and urinary volume was greater in NaCl-loaded than in both NaHCO3-loaded and water-drinking animals. 4. Plasma renin activity of both NaCl- and NaHCO3-loaded animals was less than that of control rats. However, renal renin content was suppressed by NaCl but not by NaHCO3 loading. 5. Loading with NaCl afforded greater protection against HgCl2-induced acute renal failure than NaHCO3. Since this difference was not related to changes in sodium balance or plasma volume before HgCl2, or plasma renin activity after HgCl2, the results support the hypothesis that intrarenal renin plays a role in the pathogenesis of HgCl2-induced acute renal failure in the rat.

Renin activity in aortic tissue of rats

1969 ◽  
Vol 47 (1) ◽  
pp. 53-56 ◽  
Author(s):  
J. Rosenthal ◽  
R. Boucher ◽  
J. M. Rojo-Ortega ◽  
J. Genest
Keyword(s):  
Plasma Renin Activity ◽  
Substrate Concentration ◽  
Plasma Renin ◽  
Bilateral Adrenalectomy ◽  
Renin Activity ◽  
Aortic Tissue ◽  
Renin Substrate ◽  
Purina Chow ◽  
Low Levels ◽  
Parallel Fashion

Plasma renin activity, aortic tissue renin, and plasma renin substrate concentrations were measured simultaneously and sequentially in groups of rats after (1) bilateral nephrectomy, (2) water deprivation, and (3) bilateral adrenalectomy. Following nephrectomy, plasma renin activity and aortic tissue renin fell in parallel fashion to undetectable or very low levels after 18 h, whereas the substrate concentration in plasma increased markedly. Rats deprived of water for 3 days, but receiving Purina Chow, showed a significant increase in plasma renin activity and in aortic tissue renin and a marked decrease in plasma substrate concentration. Bilateral adrenalectomy resulted in a. very marked augmentation of plasma renin activity and of aortic tissue renin with a concomitant suppression of plasma substrate concentration. These findings suggest that arterial tissue renin reacts to the same stimuli which modify renin activity in plasma.

Beta-adrenoceptor-stimulated renin release is blunted in old rats.

1998 ◽  
Vol 9 (7) ◽  
pp. 1318-1320
Author(s):  
C Baylis ◽  
K Engels ◽  
W H Beierwaltes
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Sprague Dawley ◽  
Angiotensin I ◽  
Beta Adrenoceptors ◽  
Beta Adrenoceptor ◽  
Sprague Dawley Rats ◽  
Old Rats

Plasma renin activity (PRA) was similar in young versus old male Sprague Dawley rats under unstressed conditions (1.3 +/- 0.2 versus 1.8 +/- 0.3 ng angiotensin I/ml per min). Airjet stress increases PRA in young but not old rats (13.9 +/- 3.8 versus 2.9 +/- 0.8 ng angiotensin I/ml per min), respectively. This response is ablated in young rats by beta-adrenoceptor blockade, suggesting that the increased PRA is mediated by beta-adrenoceptors, and this response was blunted in old rats.

Enhanced adrenal renin and aldosterone biosynthesis during sodium restriction in TGR (mREN2)27

1994 ◽  
Vol 267 (4) ◽  
pp. E515-E520 ◽  
Author(s):  
S. Rubattu ◽  
I. Enea ◽  
D. Ganten ◽  
D. Salvatore ◽  
G. Condorelli ◽  
...  
Keyword(s):  
Adrenal Cortex ◽  
Sodium Intake ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Transgenic Rat ◽  
Sodium Restriction ◽  
Sprague Dawley ◽  
Low Sodium ◽  
Sd Rats

The aim of the study was to investigate the relationships between tissue renin and the steroid production in the adrenal cortex during dietary sodium restriction in the transgenic rat (TGR) (mREN2)27. Thus the effects of a 1-wk low-sodium intake (0.04% NaCl) were studied in 5-wk-old male TGR (n = 33, systolic blood pressure = 151 +/- 3 mmHg) and in 24 age- and sex-matched outbred normotensive Sprague-Dawley (SD) rats. Measurements of plasma and tissue hormones were obtained at 0, 4, and 7 days of a low-sodium diet. Sodium restriction caused sustained increases of adrenal renin activity (from 28.5 +/- 3.5 to 87.5 +/- 4.5 ng.mg protein-1.h-1 on day 7) and of adrenal renin mRNA (+63 +/- 13 and +43 +/- 7% on days 4 and 7, respectively), whereas plasma renin activity (from 3.3 +/- 0.3 to 4.4 +/- 0.6 ng.ml-1.h-1) and renal renin activity (from 0.85 +/- 0.25 to 0.7 +/- 0.4 microgram.mg protein-1.h-1) did not change. The stimulation of the adrenal renin-angiotensin system was associated with a large increase of the aldosterone synthase cytochrome P-450 mRNA (+165 +/- 35 and +184 +/- 44%, on days 4 and 7) and of plasma aldosterone levels (from 125 +/- 32 to 338 +/- 59 pg/ml, P < 0.01). In SD rats, in spite of a more consistent increase in renal and circulating renin, mineralocorticoid production did not increase significantly. These results demonstrate that the exaggerated biosynthesis of aldosterone in TGR during sodium restriction is associated with an activation of renin in the adrenal cortex but not in the kidney.

Effect of Spironolactone on Aldosterone Regulation in Man

1980 ◽  
Vol 58 (3) ◽  
pp. 227-233 ◽  
Author(s):  
R. C. Gaillard ◽  
A. M. Riondel ◽  
P. Chabert ◽  
M. B. Vallotton
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Plasma Corticosterone ◽  
Plasma Aldosterone ◽  
Renin Activity ◽  
Minor Role ◽  
Corticosterone Concentration ◽  
Plasma Aldosterone Concentration ◽  
Normal Men

1. The action of spironolactone, a well-known antagonist of mineralocorticoids, on aldosterone regulation was investigated in normal young men to see whether it also acted as an inhibitor of biosynthesis in the adrenal gland. 2. The action of spironolactone was studied under three different conditions: (a) during 3 days of treatment with spironolactone; (b) during 1 day of combined administration with long acting adrenocorticotropic hormone (ACTH); (c) in the course of a continuous infusion of angiotensin II. 3. Spironolactone did not alter the metabolism of aldosterone or cortisol. 4. Spironolactone administration produced: (a) a marked increase in both aldosterone secretion and plasma renin activity, but no change in the plasma aldosterone/plasma renin activity ratio, the cortisol secretion rate or the plasma corticosterone concentration; (b) no blunting in the response of aldosterone to stimulation by ACTH; (c) no decrease in plasma aldosterone concentration when changes of the endogenous renin activity were prevented by an infusion of angiotensin II. 5. These results do not confirm the considerable inhibition of aldosterone excretion found by others after spironolactone administration to normal men. We observed no inhibition of aldosterone biosynthesis by spironolactone. However, a minimal, short-lived inhibition of biosynthesis cannot be excluded, but this possible action of spironolactone plays at best a minor role in the action of this drug.

scholarly journals Parathyroid hormone-related protein stimulates plasma renin activity via its anorexic effects on sodium chloride intake

2012 ◽  
Vol 303 (4) ◽  
pp. E457-E463 ◽  
Author(s):  
Douglas K. Atchison ◽  
Elizabeth Westrick ◽  
David L. Szandzik ◽  
Kevin L. Gordish ◽  
William H. Beierwaltes
Keyword(s):  
Drinking Water ◽  
Parathyroid Hormone ◽  
Sodium Chloride ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Related Protein ◽  
Sprague Dawley ◽  
Parathyroid Hormone Related Protein

Parathyroid hormone-related protein (PTHrP) increases renin release from isolated perfused kidneys and may act as an autacoid regulator of renin secretion, but its effects on renin in vivo are unknown. In vivo, PTHrP causes hypercalcemia and anorexia, which may affect renin. We hypothesized that chronically elevated PTHrP would increase plasma renin activity (PRA) indirectly via its anorexic effects, reducing sodium chloride (NaCl) intake and causing NaCl restriction. We infused male Sprague-Dawley rats with the vehicle (control) or 125 μg PTHrP/day (PTHrP) via subcutaneous osmotic minipumps for 5 days. To replenish NaCl consumption, a third group of PTHrP-infused rats received 0.3% NaCl (PTHrP + NaCl) in their drinking water. PTHrP increased PRA from a median control value of 3.68 to 18.4 ng Ang I·ml−1·h−1 ( P < 0.05), whereas the median PTHrP + NaCl PRA value was normal (7.82 ng Ang I·ml−1·h−1, P < 0.05 vs. PTHrP). Plasma Ca2+ (median control: 10.2 mg/dl; PTHrP: 13.7 mg/dl; PTHrP + NaCl: 14.1 mg/dl; P < 0.05) and PTHrP (median control: 0.03 ng/ml; PTHrP: 0.12 ng/ml; PTHrP + NaCl: 0.15 ng/ml; P < 0.05) were elevated in PTHrP- and PTHrP + NaCl-treated rats. Body weights and caloric consumption were lower in PTHrP- and PTHrP + NaCl-treated rats. NaCl consumption was lower in PTHrP-treated rats (mean Na+: 28.5 ± 4.1 mg/day; mean Cl−: 47.8 mg/day) compared with controls (Na+: 67.3 ± 2.7 mg/day; Cl−: 112.8 ± 4.6 mg/day; P < 0.05). NaCl consumption was comparable with control in the PTHrP + NaCl group; 0.3% NaCl in the drinking water had no effect on PRA in normal rats. Thus, our data support the hypothesis that PTHrP increases PRA via its anorexic effects, reducing NaCl intake and causing NaCl restriction.

Effect of cyclooxygenase and thromboxane synthetase inhibition on furosemide-stimulated plasma renin activity

1987 ◽  
Vol 65 (1) ◽  
pp. 80-83 ◽  
Author(s):  
Sunil Datar ◽  
Frances A. McCauley ◽  
Thomas W. Wilson
Keyword(s):  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Cyclooxygenase Inhibitor ◽  
Sprague Dawley ◽  
Blood Samples ◽  
Sprague Dawley Rats ◽  
Thromboxane Synthetase ◽  
Serum Thromboxane

We studied the effects of a specific thromboxane (TX) synthetase inhibitor (U-63,557A) and a cyclooxygenase inhibitor on furosemide-induced renin release. Furosemide (2.0 mg∙kg−1) was injected into Sprague–Dawley rats pretreated with indomethacin (10 mg∙kg−1, i.v.), U-63,557A (1.0–32.0 mg∙kg−1, i.v.), or vehicle (Na2CO3 0.03 M). Plasma renin activity was measured in blood samples collected 0, 10, 20, and 40 min after the injection of furosemide. Blood was also collected after the administration of vehicle, indomefhacin, or U-63,557A for serum TXB2, a measure of platelet TXA2 synthesis. The results demonstrated that plasma renin activity rose with time following furosemide in the various groups of rats; indomethacin suppressed the furosemide-induced increments in plasma renin activity, while U-63,557A at doses of 4–8 mg∙kg−1 augmented it. At doses below 4 mg∙kg−1 or above 8 mg∙kg−1, U-63,557A did not augment renin secretion. Indomethacin and U-63,557A reduced serum thromboxane by 81 and 90%, respectively. Thus, these experiments suggest that thromboxane synthetase inhibition, within a narrow dosage range, potentiates furosemide-induced renin release while cyclooxygenase inhibition suppresses it.

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