scholarly journals Plasma renin activity determined by two different methods in spontaneously hypertensive rats.

1982 ◽  
Vol 23 (4) ◽  
pp. 587-592 ◽  
Author(s):  
Satoru KURIYAMA ◽  
Koichiro KAWASHIMA ◽  
Hirofumi SOKABE
1992 ◽  
Vol 82 (4) ◽  
pp. 389-395 ◽  
Author(s):  
C. Stonier ◽  
J. Bennett ◽  
E. A. Messenger ◽  
G. M. Aber

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.


1988 ◽  
Vol 75 (5) ◽  
pp. 527-534 ◽  
Author(s):  
Anne Barden ◽  
Lawrence J. Beilin ◽  
Robert Vandongen

1. Supplementation with 1% (w/v) KCl solution significantly attenuated the blood pressure rise with age normally observed in spontaneously hypertensive rats, resulting in a difference in blood pressure of 18 mmHg after 5 weeks. 2. Urinary 6-keto-prostaglandin F1α (the stable hydrolysis product of prostacyclin) and kallikrein excretion were significantly elevated in rats receiving potassium. 3. No difference was observed in sodium excretion during the initial days of potassium supplementation; however, the potassium-supplemented animals excreted relatively more sodium over the 5 week period. 4. Plasma renin activity was significantly reduced in those animals receiving potassium after 5 weeks. 5. It is proposed that a combination of increased systemic and/or renal prostacyclin and kallikrein synthesis may, in combination with reduced renin activity, contribute to the attenuation of blood pressure in potassium-supplemented spontaneously hypertensive rats.


1980 ◽  
Vol 59 (2) ◽  
pp. 123-129 ◽  
Author(s):  
A. R. Sinaiko ◽  
M. J. Cooper ◽  
B. L. Mirkin

1. Chemical sympathectomy was produced in spontaneously hypertensive rats by intraperitoneal injection of 6-hydroxydopamine hydrobromide (6-OHD) (100 μg/g body weight) on days 1, 4 and 7 of neonatal life and weekly thereafter until 6 weeks of age. The dose was then reduced to 50 μg/g body weight and injected every 2 weeks. 2. Studies were performed at 6 and 12 weeks of age in pentobarbital-anaesthetized rats. Plasma renin activity was measured before and 5 and 15 min after the administration of intravenous hydrallazine (5 mg/kg). Tissue noradrenaline concentration was determined in brains, hearts and kidneys from rats killed immediately upon completion of blood sampling. 3. The blood pressure of 6-OHD-treated rats was significantly lower than in untreated rats at 6 weeks (117 ± 3 and 146 ± 2 mmHg respectively) and 12 weeks (151 ± 5 and 196 ± 4 mmHg respectively). 4. Kidneys and hearts from 6-OHD-treated rats demonstrated a highly significant reduction in noradrenaline concentration at both 6 and 12 weeks; brain noradrenaline in treated rats was normal at 6 weeks and reduced only to 80% of normal at 12 weeks. 5. Control (pre-hydrallazine) plasma renin activity was significantly lower in 6-OHD-treated rats at 6 and 12 weeks. Nevertheless, renin release in response to intravenous hydrallazine, expressed in terms of absolute values of plasma renin activity, was not significantly different in the treated and untreated rats. When the percentage increase in plasma renin activity from control to 15 min post-hydrallazine samples was calculated, the response of the 6-OHD-treated rats was found to be significantly greater than the response in the untreated rats at each age. 6. These data show that treatment of neonatal rats with 6-OHD results in a significant reduction in basal activity of the renin-angiotensin system but does not interfere with the release of renin in response to hypotensive stress. In cases of severe compromise of adrenergic nervous system function, alternative mechanisms exist which allow the renin-angiotensin system to manifest a maximal response in order to maintain cardiovascular homeostasis.


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