Steroids during development of genetic hypertension in rats of Lyon strain

1989 ◽  
Vol 257 (2) ◽  
pp. H506-H510 ◽  
Author(s):  
M. Vincent ◽  
C. E. Gomez-Sanchez ◽  
A. Bataillard ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Urinary Excretion ◽  
Male Rats ◽  
Hydroxylase Activity ◽  
Full Development ◽  
Genetically Hypertensive Rats ◽  
Low Blood Pressure ◽  
Doc Concentration ◽  
Low Levels ◽  
Genetically Hypertensive

The urinary excretion and the plasma concentration of deoxycorticosterone (DOC), corticosterone, 18-hydroxy-DOC (18-OH-DOC), aldosterone, and 19-nor-DOC were measured by specific radioimmunoassays in genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) male rats of the Lyon strains at two ages that characterize the development of their systolic blood pressure (SBP). When compared with both LN and LL controls, 5-wk-old LH rats exhibited an increased urinary DOC and decreased urinary corticosterone excretions, which were significantly related to the SBP level (r' = 0.618 and -0.520; n = 23; P less than 0.01 for DOC and corticosterone, respectively). In addition, the adrenal synthesis of LH rats was found to rely on an increased 18-hydroxylase activity as indicated by elevated urinary 18-OH-DOC/corticosterone and aldosterone/corticosterone associated with a lower 11-beta-hydroxylase activity shown by the decreased urinary corticosterone/DOC. Twenty-wk-old LH rats with fully developed hypertension exhibited normal urinary excretion of steroids and a decrease in plasma DOC concentration, which negatively correlated with the SBP level (r' = -0.574; n = 25; P less than 0.01). In conclusion, the present study demonstrates that in the Lyon model of genetically hypertensive rats, compared with two genetically different control strains and maintained under physiological unstressed conditions, the development of hypertension is associated with an increased urinary excretion of DOC. After the full development of their hypertension, the mineralocorticoid synthesis in LH rats returns to normal or low levels which could, however, remain inappropriately high for their sodium body content.

NE turnover in genetically hypertensive rats of Lyon strain. I. Brain nuclei

1988 ◽  
Vol 255 (4) ◽  
pp. H729-H735 ◽  
Author(s):  
M. Sautel ◽  
J. Sacquet ◽  
M. Vincent ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Hypothalamic Nucleus ◽  
Primary Role ◽  
Hypertensive Rats ◽  
Brain Areas ◽  
Brain Nuclei ◽  
Genetically Hypertensive Rats ◽  
Low Blood Pressure ◽  
Genetically Hypertensive

Several indirect evidences of alterations in the central catecholaminergic structures were obtained in genetically hypertensive rats. Because they could be of pathogenetic value, we measured, in the present work, the in vivo turnover (TO) of norepinephrine (NE) in brain areas of 5- and 22-wk-old genetically hypertensive (LH) rats of the Lyon strain, and their simultaneously selected normotensive (LN) and low blood pressure (LL) controls. Among the changes observed, the increased TO of NE in the A2 and A6 regions of 5-wk-old LH rats and its decrease in the posteroventral hypothalamic nucleus of 22-wk-old LH animals appeared likely to compensate for hypertension. On the contrary, the decreased TO of NE in the anterior hypothalamic nucleus observed at 5 wk and in the A6 and A1 areas at 22 wk of age in LH rats could participate in the development or the maintenance of hypertension. Above all, it was postulated that the increased TO of NE found in the A7 region of 5-wk-old LH rats could play a primary role in the pathogenesis of hypertension in the Lyon model.

Urinary 6-Ketoprostaglandin F1α in Genetically Hypertensive Rats of the Lyon Strain

1984 ◽  
Vol 66 (4) ◽  
pp. 453-457 ◽  
Author(s):  
D. Benzoni ◽  
M. Vincent ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Urinary Excretion ◽  
Female Rats ◽  
Primary Role ◽  
Hypertensive Rats ◽  
Genetically Hypertensive Rats ◽  
Pathophysiological Role ◽  
Low Blood Pressure ◽  
Old Rats ◽  
Genetically Determined

1. In order to assess the pathophysiological role of renal prostacyclin in genetic hypertension, the urinary excretion of its main stable metabolite, 6-ketoprostaglandin F1α, was followed in 12 hypertensive, normotensive and low blood pressure female rats of the Lyon strains at the ages of 5,9, 21, 32 and 45 weeks. 2. The urinary excretion of 6-ketoprostaglandin F1α, which progressively decreased in the three strains between 5 and 21 weeks of age, was found to be increased in 5- and 9-week-old hypertensive rats and it was reduced in 5-week-old low blood pressure rats, compared with age-matched normotensive controls. 3. The urinary 6-ketoprostaglandin F1α was found to be significantly related to the systolic blood pressure in 5- and 9-week-old rats of the three strains (r = 0.42; n = 71; P<0.001). 4. These results exclude a primary role in the development of hypertension for a genetically determined defect in the renal biosynthesis of prostacyclin in the spontaneous hypertensive rat of the Lyon strain.

NE turnover in genetically hypertensive rats of Lyon strain. II. Peripheral organs

1988 ◽  
Vol 255 (4) ◽  
pp. H736-H741
Author(s):  
M. Sautel ◽  
J. Sacquet ◽  
M. Vincent ◽  
J. Sassard
Keyword(s):  
Blood Pressure ◽  
Kidney Cortex ◽  
Cardiac Innervation ◽  
Hypertensive Rats ◽  
Genetically Hypertensive Rats ◽  
Low Blood Pressure ◽  
Cervical Ganglia ◽  
Peripheral Sympathetic Nervous System ◽  
Genetically Hypertensive

The peripheral sympathetic nervous system (SNS) is a major determinant of blood pressure and is likely to be involved in the pathophysiology of hypertension. Because SNS activity varies among organs, we measured the in vivo turnover (TO) of norepinephrine (NE) in seven organs of 5- and 22-wk-old genetically hypertensive (LH), normotensive (LN), and low blood pressure (LL) rats of the Lyon strains. The TO of NE was found normal in the superior cervical ganglia and decreased in the heart of 5-wk-old LH rats compared with both LL and LN controls. This suggests that sympathetic cardiac innervation may not be involved in the development of hypertension. On the contrary, an increased TO of NE in the kidney cortex and an elevated TO of dopamine associated with an increased epinephrine content in the adrenal medulla were observed in 5-wk-old LH rats, which could participate in the development of hypertension in the Lyon model.

Blood Pressure in Genetically Hypertensive Rats

Hypertension ◽  
1995 ◽  
Vol 26 (3) ◽  
pp. 452-459 ◽  
Author(s):  
Anne O. Davidson ◽  
Nicholas Schork ◽  
Bryon C. Jaques ◽  
Andrew W. Kelman ◽  
Roger G. Sutcliffe ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hypertensive Rats ◽  
Genetically Hypertensive Rats ◽  
Genetically Hypertensive

High blood pressure maintenance in transgenic mRen-2 vs. Lyon genetically hypertensive rats

1993 ◽  
Vol 265 (1) ◽  
pp. R180-R186 ◽  
Author(s):  
M. Lo ◽  
I. A. Medeiros ◽  
J. J. Mullins ◽  
D. Ganten ◽  
C. Barres ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Sprague Dawley ◽  
Hypertensive Rats ◽  
Renal Handling ◽  
Genetically Hypertensive Rats ◽  
Pressure Natriuresis ◽  
Genetically Hypertensive

The present work was aimed to assess the factors involved in the maintenance of hypertension in adult transgenic mRen-2 (TG) rats. Special attention was paid to the renal handling of sodium, the sympathetic, and the renin-angiotensin system (RAS) activity. TG rats were compared with age-matched Lyon genetically hypertensive rats (LH), as both are of Sprague-Dawley origin. Blood pressure (BP), heart rate, and renal sympathetic nerve activity (RSNA) were recorded in conscious freely moving animals. Kidneys were isolated and single-pass perfused at different pressure levels. It was observed that the peripheral sympathetic drive was identical in TG and LH rats as indicated by their similar 24-h urinary excretion of catecholamines and methoxylated metabolites, baseline RSNA and its control by the baroreflex, and hypotensive response to ganglion-blockade. On the contrary, TG rats differed from LH rats by a more rapid excretion of an oral isotonic sodium load, a greater hypotensive and natriuretic response to furosemide, and a more marked BP response to acute RAS blockade. The TG kidney responses to stepwise changes in renal perfusion pressure (RPP) differed from those of LH rats by significantly higher perfusate flow and glomerular filtration rate. However, the pressure natriuresis curve of TG kidneys did not differ from that of LH rats because of an elevated tubular sodium reabsorption rate. These results suggest that adult TG rats, compared with LH rats, exhibit a tendency toward sodium and water retention, which may explain that despite low renal and circulating renin levels, the RAS remains involved in the maintenance of high BP in that model.

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