Changes in the Renin-Angiotensin-Aldosterone System and in Sodium and Potassium Balance during Development of Renal Hypertension in Rats

1975 ◽  
Vol 48 (1) ◽  
pp. 17-26 ◽  
Author(s):  
F. H. H. Leenen ◽  
J. W. Scheeren ◽  
D. Omylanowski ◽  
J. D. Elema ◽  
B. Van Der Wal ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Systolic Blood Pressure ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Potassium Balance ◽  
Peripheral Plasma ◽  
Sodium And Potassium

1. The relationships between the renin-angiotensin-aldosterone system, sodium and potassium balance and systolic blood pressure were studied during development of moderate (160–180 mmHg; clip i.d. 0.25 mm) and severe (200–230 mmHg; clip i.d. 0.20 mm) renal hypertension in rats with an undisturbed contralateral kidney. 2. In severely hypertensive rats renin activity in the peripheral plasma increased from day 9, by which time the systolic blood pressure was elevated to 160–180 mmHg. The rate of total corticosteroid and aldosterone production in vitro increased from day 14 and plasma renin substrate concentration increased from day 24. In moderately hypertensive rats, none of these changes occurred. 3. During the first 10 days after the application of 0.25 and 0.20 mm clips, sodium and potassium retention/g gain in body weight were higher than in sham-operated controls. During the next 10 days, the positive balance stabilized in animals with a 0.25 mm clip whereas, in animals with a 0.20 mm clip, sodium and potassium balance returned to the level of the sham-operated controls through increased renal losses. Despite these changes the systolic pressure rose further in animals with a 0.20 mm clip. 4. The initial sodium retention could be a factor in the early rise of blood pressure and could account for the delay in the rise of peripheral plasma renin activity. The subsequent loss of the retained sodium and potassium during the development of severe hypertension could have facilitated the rise in peripheral plasma renin activity, but did not initiate this rise.

Plasma Renin Activity and Sodium, Potassium and Water Excretion during Reversal of Hypertension in the One-Clip, Two-Kidney Hypertensive Rat

1979 ◽  
Vol 57 (1) ◽  
pp. 47-52 ◽  
Author(s):  
R. G. M. Ten Berg ◽  
F. H. H. Leenen ◽  
W. De Jong
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Internal Diameter ◽  
Hypertensive Rats ◽  
Water Excretion ◽  
Contralateral Kidney ◽  
Sodium And Potassium ◽  
Renal Hypertensive Rats

1. The effect of removal of the clip on blood pressure, plasma renin activity and the excretion of water, sodium and potassium was studied in renal hypertensive rats. Hypertension was induced by application of a clip with an internal diameter of 0·20 mm, which was removed after 1, 2 or 3 weeks, and by using a clip with an internal diameter of 0·25 mm, which was removed after 2 weeks. The contralateral kidney remained undisturbed. 2. Blood pressure was almost normal 24 h after the removal of the clip; 70–90% of the total decrease in blood pressure occurred within 2–5 h. 3. The increased plasma renin activity, which was observed 2 and 3 weeks after application of a 0·20 mm clip, had returned to control values 24 h after removal of the clip. One week after application of a 0·20 mm clip, and 2 weeks after a 0·25 mm clip, plasma renin activity did not differ significantly from control values, before as well as after unclipping. 4. No significant differences were found between unclipped and sham-operated renal hypertensive rats, nor between the latter and the sham-operated normotensive control rats for water, sodium and potassium excretion, and for change in body weight, during the 24 h after the removal of the clip. 5. It is concluded that urinary loss of water and/or sodium does not play an important role in the acute decrease of blood pressure which occurs after the removal of a renal artery clip in one-clip, two-kidney hypertensive rats. A decrease in peripheral plasma renin activity can only partly explain the reversal of the hypertension.

Alpha 1-adrenoceptor blockade in renal hypertensive rats with low and high renin levels

1984 ◽  
Vol 246 (4) ◽  
pp. H573-H578
Author(s):  
B. Waeber ◽  
J. Nussberger ◽  
H. R. Brunner
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Renal Hypertension ◽  
Plasma Renin ◽  
Renin Activity ◽  
Plasma Norepinephrine ◽  
Hypertensive Rats ◽  
Blood Pressure Elevation ◽  
Significant Difference ◽  
Renal Hypertensive Rats

A total of 75 male Wistar rats with one-kidney, one-clip renal hypertension was maintained on either a regular (RNa) or a low-salt (LNa) diet for 3 wk after clipping. Blood pressure in the unanesthetized rats was equally elevated independent of sodium intake. Plasma renin activity was higher in LNa animals, and blood pressure was renin dependent only in this group, as evidenced by the blood pressure response to 10 mg/kg captopril iv. There was no significant difference in plasma catecholamines between RNa and LNa rats, although in the former the sympathetic nervous system is believed to play a major role in sustaining high blood pressure. The acute intravenous administration of 0.5 mg/kg prazosin did not induce a more pronounced blood pressure fall in the RNa rats. Prazosin enhanced plasma norepinephrine levels similarly in both groups, but epinephrine levels only rose in the LNa animals. Prazosin also markedly stimulated plasma renin activity rendering blood pressure renin dependent even in RNa rats. Thus, using alpha 1-adrenoceptor blockade, it has not been possible to demonstrate that the blood pressure elevation of salt-repleted one-kidney, one-clip renal hypertensive rats is due to an enhanced sympathetic nerve activity. Data obtained with sympatholytic agents must be interpreted with great caution if renin activity cannot be kept unchanged.

scholarly journals Chronic effects of Bunitrolol and Pindolol on blood pressure,heart rate,vascular lesions,and plasma renin activity in hypertensive rats.

1982 ◽  
Vol 32 (4) ◽  
pp. 742-745 ◽  
Author(s):  
Yukio HASEGAWA ◽  
Takushi X. WATANABE ◽  
Koichiro KAWASHIMA ◽  
Hirofumi SOKABE ◽  
Ken SAITO
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Plasma Renin Activity ◽  
Plasma Renin ◽  
Renin Activity ◽  
Vascular Lesions ◽  
Hypertensive Rats ◽  
Chronic Effects

Oestradiol-induced hypotension in spontaneously hypertensive rats: putative role for intracellular cations, sodium-potassium flux and prostanoids

1992 ◽  
Vol 82 (4) ◽  
pp. 389-395 ◽  
Author(s):  
C. Stonier ◽  
J. Bennett ◽  
E. A. Messenger ◽  
G. M. Aber
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cell Volume ◽  
Packed Cell Volume ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Angiotensin I ◽  
Spontaneously Hypertensive

1. The effect of oestradiol alone and in combination with indomethacin on blood pressure, erythrocyte cation concentration and Na+−K+ flux has been studied in adult female normotensive and spontaneously hypertensive rats. 2. Oestradiol alone resulted in a significant decrease in blood pressure in spontaneously hypertensive rats (from 165.3 ± 3.9 to 146.4 ± 2.7 mmHg, P < 0.001), whereas it induced a significant increase in normotensive rats (from 111.8 ± 1.8 to 124.1 ± 3.6 mmHg, P < 0.001). When indomethacin and oestradiol were administered simultaneously or when indomethacin was given alone, no change in blood pressure occurred in spontaneously hypertensive rats (158.6 ± 6.9 and 159.8 ± 6.2 mmHg, respectively). 3. The fall in blood pressure induced by oestradiol in spontaneously hypertensive rats was associated with significant reductions in erythrocyte K+ concentration (from 127.4 ± 1.2 to 116.9 ± 1.7 mmol/l of cells, P < 0.001), in erythrocyte Na+ concentration (from 14.3 ± 0.8 to 13.0 ± 0.6 mmol/l of cells, P < 0.02), in ouabain-sensitive erythrocyte Na+ flux (from 17.8 ± 0.3 to 16.0 ± 0.4 mmol h−1 (1 of cells)−1, P < 0.01) and in ouabain-sensitive erythrocyte K+ flux (from 11.4 ± 0.2 to 10.4 ± 0.2 mmol h−1 (1 of cells)−1, P < 0.01). No change in blood pressure, erythrocyte cation concentration or Na+−K+ flux occurred when oestradiol and indomethacin were given together or when indomethacin was administered alone. 4. The hypertensive influence of oestradiol in normotensive rats was unaccompanied by any changes in erythrocyte K+ concentration, erythrocyte Na+ concentration and total, ouabain-sensitive and ouabain-resistant Na+−K+ flux. 5. The divergent changes in blood pressure noted in the two strains occurred despite comparable changes in plasma renin activity after oestradiol, with significant increases in plasma renin activity in normotensive rats (from 16.4 ± 4.2 to 28.4 ± 6.6 ng of angiotensin I h−1 ml−1, P < 0.05) and in spontaneously hypertensive rats (from 28.3 ± 2.7 to 39.5 ± 5.7 ng of angiotensin I h−1 ml−1, P < 0.01). The plasma renin activity in spontaneously hypertensive rats receiving oestradiol or indomethacin and oestradiol were similar with values of 39.5 ± 5.7 and 40.6 ± 5.7 ng of angiotensin I h−1 ml−1, respectively, but were significantly higher than that seen in control animals (28.3 ± 2.7 ng of angiotensin I h−1 ml−1, P < 0.01). Similarly, indomethacin alone induced a significant increase in plasma renin activity in spontaneously hypertensive rats to 35.8 ± 7.6 ng of angiotensin I h−1 ml−1 (P < 0.05). 6. The contrasting effects of oestradiol on blood pressure in the two rat strains occurred without any change in packed cell volume. Likewise, the changes in blood pressure in spontaneously hypertensive rats with either oestradiol alone or in combination with indomethacin occurred without any change in packed cell volume, although indomethacin alone resulted in a significant reduction in packed cell volume (from 30.9 ± 1.6 to 26.8 ± 2.0, P < 0.01). 7. The results suggest that the hypotensive action of oestradiol in spontaneously hypertensive rats might be mediated through its influence on erythrocyte cation concentration and/or the modulation of Na+−K+ flux either directly or via the action of prostanoids.

Influence of Family History of Hypertension on the Relationships between Blood Pressure, Body Weight, Electrolyte Metabolism, Renin, Prolactin and Parathormone

1981 ◽  
Vol 61 (s7) ◽  
pp. 359s-362s ◽  
Author(s):  
F. Wessels ◽  
D. Hoffmann ◽  
H. Wagner ◽  
H. Zumkley
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Family History ◽  
Plasma Renin Activity ◽  
Systolic Blood Pressure ◽  
Plasma Renin ◽  
Renin Activity ◽  
Creatinine Ratio ◽  
History Of ◽  
Family History Of Hypertension

1. The influence of family history of hypertension on the relationships between blood pressure, relative body weight, sodium/creatinine ratio of the 24 h urine, plasma renin activity and the plasma concentration of prolactin and parathormone were examined in 102 healthy male students. 2. Grouping together results from all students showed significant positive correlations between systolic blood pressure and prolactin, parathormone as well as relative body weight, between plasma renin activity and prolactin and a significant negative correlation between plasma renin activity and sodium/creatinine ratio of the 24 h urine. 3. By dividing the students into two groups according to their family history of hypertension we could demonstrate in those with family history of hypertension a highly significant positive correlation between mean blood pressure and sodium/creatinine ratio of the 24 h urine and an improvement of the correlations between systolic blood pressure and prolactin and between sodium/creatinine ratio of the 24 h urine and plasma renin activity. In students without family history of hypertension these relationships were no longer detectable. In the students without family history of hypertension the correlations between systolic blood pressure and relative body weight as well as between plasma renin activity and prolactin gained substantially in significance. In students with positive family history of hypertension these correlations could no longer be demonstrated. The correlations between systolic blood pressure and parathormone remained unaffected by family history of hypertension. 4. The results suggest that a genetic predisposition to essential hypertension is able to intensify the blood pressure effect of Na intake and of prolactin, which, besides its function as a sex hormone, is presumed additionally to be able to retain salt. However, the positive relationship between body weight and blood pressure, as well as between plasma renin activity and prolactin, the significance of which increases greatly in subjects without family history of hypertension, appears to be lost as the result of the increased sensitivity to salt in positive family history of hypertension.

Racial differences in blood pressure in evans county, Georgia: Relationship to sodium and potassium intake and plasma renin activity

1980 ◽  
Vol 33 (2) ◽  
pp. 87-94 ◽  
Author(s):  
C.E. Grim ◽  
F.C. Luft ◽  
J.Z. Miller ◽  
G.R. Meneely ◽  
H.D. Battarbee ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Racial Differences ◽  
Plasma Renin ◽  
Renin Activity ◽  
Potassium Intake ◽  
Sodium And Potassium

Effects of salmon calcitonin on plasma renin activity and systolic blood pressure in the rat

1986 ◽  
Vol 66 (3) ◽  
pp. 351-355 ◽  
Author(s):  
G. Clementi ◽  
E. Rapisarda ◽  
C.E. Fiore ◽  
A. Prato ◽  
M. Amico-Roxas ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Systolic Blood Pressure ◽  
Salmon Calcitonin ◽  
Plasma Renin ◽  
Renin Activity
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