Blood pressure control and erythrocytosis in rats: theory and observations

1994 ◽  
Vol 72 (6) ◽  
pp. 679-686 ◽  
Author(s):  
Anne B. Gould ◽  
Susan Goodman ◽  
Charles Swartz

We compared some of our latest experiments on blood pressure control and erythrocytosis in spontaneously hypertensive rats with Gaar's computer-simulated studies, which suggest that erythrocytosis is a key to understanding the hemodynamic changes in hypertension. We tested two of Gaar's several predictions: (i) peripheral vascular resistance decreases when the feedback control of erythrocytosis is blocked and (ii) in primary hypertension, blood volume is increased slightly. We also studied the interrelation of systolic blood pressure and plasma renin substrate in spontaneously hypertensive rats, and the effect of diet on renin, blood pressure, and erythrocytosis. Our data showed that (i) on a percentage basis the renin system supports blood pressure essentially in the same manner in normal and hypertensive rats, (ii) peripheral vascular resistance decreased when erythrocytosis was partially blocked by feeding a low-iron diet, (iii) blood volume was similar in normal and hypertensive rats, and (iv) dextrin stimulates plasma renin, packed cell volume, and blood pressure in hypertensive rats. We conclude that blood pressure and erythrocytosis are interrelated, that the combined data of simulated and experimental studies support the notion that primary hypertension is a blood-vessel adaptation in response to a renal energy need that may require additional oxygen.Key words: angiotensinogen, renin, dextrin, packed cell volume.

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.


1979 ◽  
Vol 236 (3) ◽  
pp. H409-H416 ◽  
Author(s):  
M. Shibota ◽  
A. Nagaoka ◽  
A. Shino ◽  
T. Fujita

The development of malignant hypertension was studied in stroke-prone spontaneously hypertensive rats (SHR) kept on 1% NaCl as drinking water. Along with salt-loading, blood pressure gradually increased and reached a severe hypertensive level (greater than 230 mmHg), which was followed by increases in urinary protein (greater than 100 (mg/250 g body wt)/day) and plasma renin concentration (PRC, from 18.9 +/- 0.1 to 51.2 +/- 19.4 (ng/ml)/h, mean +/- SD). At this stage, renal small arteries and arterioles showed severe sclerosis and fibrinoid necrosis. Stroke was observed within a week after the onset of these renal abnormalities. The dose of exogenous angiotensin II (AII) producing 30 mmHg rise in blood pressure increased with the elevation of PRC, from 22 +/- 12 to 75 +/- 36 ng/kg, which was comparable to that in rats on water. The fall of blood pressure due to an AII inhibitor, [1-sarcosine, 8-alanine]AII (10(microgram/kg)/min for 40 min) became more prominent with the increase in PRC in salt-loaded rats, but was not detected in rats on water. These findings suggest that the activation of renin-angiotensin system participates in malignant hypertension of salt-loaded stroke-prone SHR rats that show stroke signs, proteinuria, hyperreninemia, and renovascular changes.


1989 ◽  
Vol 257 (2) ◽  
pp. F197-F203 ◽  
Author(s):  
R. Rettig ◽  
H. Stauss ◽  
C. Folberth ◽  
D. Ganten ◽  
B. Waldherr ◽  
...  

We determined whether transplantations of kidneys from stroke-prone spontaneously hypertensive rats (SPSHR) and from normotensive Wistar-Kyoto rats (WKY) alter blood pressure in renal graft recipients. Kidneys taken from seven male SPSHR and seven male WKY rats (blood pressure 186 +/- 4.8 and 111 +/- 3.7 mmHg, respectively) at the age of 20 wk were transplanted, using microsurgical techniques, to bilaterally nephrectomized age-matched male F1 hybrids (blood pressure 136 +/- 2.6 and 138 +/- 6.3 mmHg, respectively) bred from SPSHR and WKY parents. After renal transplantation, blood pressure in recipients of SPSHR kidneys rose to 146 +/- 11.8 (week 2), 163 +/- 16.4 (week 3), 192 +/- 17.1 (week 4), 222 +/- 17.7 (week 5), 221 +/- 12.6 (week 6), 218 +/- 20.3 (week 7), and 239 +/- 9.2 mmHg (week 8). There was no significant change in blood pressure in recipients of WKY kidneys. All rats recovered rapidly from surgery. After renal transplantation, there was a significant increase in daily water intake, a decrease in plasma renin activity, and a slight rise in plasma urea concentration. Our data show that transplantation of kidneys from adult SPSHR causes hypertension in normotensive recipients, indicating a major function for the kidney in SPSHR hypertension.


Molecules ◽  
2020 ◽  
Vol 25 (16) ◽  
pp. 3758 ◽  
Author(s):  
Paola Marcolongo ◽  
Alessandra Gamberucci ◽  
Gabriella Tamasi ◽  
Alessio Pardini ◽  
Claudia Bonechi ◽  
...  

Blood pressure control in hypertensive subjects calls for changes in lifestyle, especially diet. Tomato is widely consumed and rich in healthy components (i.e., carotenoids, vitamins and polyphenols). The aim of this study was to evaluate the chemical composition and antihypertensive effects of locular gel reconstituted in serum of green tomatoes of “Camone” variety. Tomato serum and locular gel were chemically characterised. The antihypertensive effects of the locular gel in serum, pure tomatine, and captopril, administered by oral gavage, were investigated for 4 weeks in male spontaneously hypertensive and normotensive rats. Systolic blood pressure and heart rate were monitored using the tail cuff method. Body and heart weight, serum glucose, triglycerides and inflammatory cytokines, aorta thickness and liver metabolising activity were also assessed. Locular gel and serum showed good tomatine and polyphenols content. Significant reductions in blood pressure and heart rate, as well as in inflammatory blood cytokines and aorta thickness, were observed in spontaneously hypertensive rats treated both with locular gel in serum and captopril. No significant effects were observed in normotensive rats. Green tomatoes locular gel and serum, usually discarded during tomato industrial processing, are rich in bioactive compounds (i.e., chlorogenic acid, caffeic acid and rutin, as well as the glycoalkaloids, α-tomatine and dehydrotomatine) that can lower in vivo blood pressure towards healthier values, as observed in spontaneously hypertensive rats.


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