Abstract
We studied the effects of regular diet (035% NaCl/1.1% potassium), high sodium diet (4% NaCl/0.75% potassium), or high sodium and high potassium diet (4% NaCl/2.11% potassium) on blood pressure, plasma renin activity, renal and cerebrovascular lesions, and incidence of stroke and mortality in male stroke-prone spontaneously hypertensive rats (SHRSP). In the first 4 weeks, the rise in blood pressure was higher in high NaCl than in high NaCl/high potassium or regular diet groups. However, by 8 and 12 weeks, the blood pressure in all three groups was similar. After 4 weeks of diet, plasma renin activity was similar in the three groups (3.4±0.8, 4.1±0.9, and 5.2±1.6 ng/ml/hr, in high NaCl, high NaCl/high potassium, and regular diet groups, respectively) and were not related to sodium excretion. After 8 weeks, plasma renin activity was significantly increased only in the high NaCl group (13.7±3.7 ng/ml/hr), and by 12 weeks plasma renin activity was significantly higher in the high NaCl group (25.3±3.6 ng/ml/hr) than in the high NaCl/high potassium (11.1±2.9 ng/ml/hr) or in the regular diet (7.8±4.6 ng/ml/hr) groups. Moderate to severe renal vascular lesions were first detected in the high NaCl group by 8 weeks of diet. At 12 weeks, renal vascular damage index (RVDI), estimated histologically, was significantly higher in the high NaCl group (RVDI=79±14) than in the high NaCl/high potassium (RVDI=40±11) and regular diet (RVDI=7.8±4.6) groups. At this time, incidence of stroke was 81% in high NaCl, 24.5% in high NaCl/high potassium, and 7.7% in regular diet groups. The data demonstrate that: 1) the increase in mortality, stroke, and renal and cerebrovascular lesions in SHRSP fed a high sodium diet is associated with a paradoxical rise in plasma renin activity; 2) the protective effect of high potassium in SHRSP fed a high potassium diet is related to a lower blood pressure at 2-4 weeks and a lower plasma renin activity, but not a lower blood pressure at 8-12 weeks; 3) this rise in plasma renin activity demonstrates that a high potassium diet suppresses or delays a primary or secondary paradoxical rise in plasma renin activity and thus, angiotensin II in the rats fed a high sodium diet. This action together with possible direct effects of potassium in the vasculature contributes to the protective effect on end organ damage and stroke in SHRSP.
| Original language | English |
|---|---|
| Pages (from-to) | 318-326 |
| Number of pages | 9 |
| Journal | Hypertension |
| Volume | 15 |
| Issue number | 3 |
| Publication status | Published - Mar 1990 |
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Keywords
- Aldosterone
- Angiotensin II
- Atrial natriuretic factor
- Blood pressure
- Malignant hypertension
ASJC Scopus subject areas
- Internal Medicine
Cite this
Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats. / Volpe, Massimo; Camargo, Maria J F; Mueller, Franco B.; Campbell, Wallace G.; Sealey, Jean E.; Pecker, Mark S.; Sosa, R. Ernest; Laragh, John H.; Rookard, Antoinette.
In: Hypertension, Vol. 15, No. 3, 03.1990, p. 318-326.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Relation of plasma renin to end organ damage and to protection of K+ feeding in stroke-prone hypertensive rats
AU - Volpe, Massimo
AU - Camargo, Maria J F
AU - Mueller, Franco B.
AU - Campbell, Wallace G.
AU - Sealey, Jean E.
AU - Pecker, Mark S.
AU - Sosa, R. Ernest
AU - Laragh, John H.
AU - Rookard, Antoinette
PY - 1990/3
Y1 - 1990/3
N2 - We studied the effects of regular diet (035% NaCl/1.1% potassium), high sodium diet (4% NaCl/0.75% potassium), or high sodium and high potassium diet (4% NaCl/2.11% potassium) on blood pressure, plasma renin activity, renal and cerebrovascular lesions, and incidence of stroke and mortality in male stroke-prone spontaneously hypertensive rats (SHRSP). In the first 4 weeks, the rise in blood pressure was higher in high NaCl than in high NaCl/high potassium or regular diet groups. However, by 8 and 12 weeks, the blood pressure in all three groups was similar. After 4 weeks of diet, plasma renin activity was similar in the three groups (3.4±0.8, 4.1±0.9, and 5.2±1.6 ng/ml/hr, in high NaCl, high NaCl/high potassium, and regular diet groups, respectively) and were not related to sodium excretion. After 8 weeks, plasma renin activity was significantly increased only in the high NaCl group (13.7±3.7 ng/ml/hr), and by 12 weeks plasma renin activity was significantly higher in the high NaCl group (25.3±3.6 ng/ml/hr) than in the high NaCl/high potassium (11.1±2.9 ng/ml/hr) or in the regular diet (7.8±4.6 ng/ml/hr) groups. Moderate to severe renal vascular lesions were first detected in the high NaCl group by 8 weeks of diet. At 12 weeks, renal vascular damage index (RVDI), estimated histologically, was significantly higher in the high NaCl group (RVDI=79±14) than in the high NaCl/high potassium (RVDI=40±11) and regular diet (RVDI=7.8±4.6) groups. At this time, incidence of stroke was 81% in high NaCl, 24.5% in high NaCl/high potassium, and 7.7% in regular diet groups. The data demonstrate that: 1) the increase in mortality, stroke, and renal and cerebrovascular lesions in SHRSP fed a high sodium diet is associated with a paradoxical rise in plasma renin activity; 2) the protective effect of high potassium in SHRSP fed a high potassium diet is related to a lower blood pressure at 2-4 weeks and a lower plasma renin activity, but not a lower blood pressure at 8-12 weeks; 3) this rise in plasma renin activity demonstrates that a high potassium diet suppresses or delays a primary or secondary paradoxical rise in plasma renin activity and thus, angiotensin II in the rats fed a high sodium diet. This action together with possible direct effects of potassium in the vasculature contributes to the protective effect on end organ damage and stroke in SHRSP.
AB - We studied the effects of regular diet (035% NaCl/1.1% potassium), high sodium diet (4% NaCl/0.75% potassium), or high sodium and high potassium diet (4% NaCl/2.11% potassium) on blood pressure, plasma renin activity, renal and cerebrovascular lesions, and incidence of stroke and mortality in male stroke-prone spontaneously hypertensive rats (SHRSP). In the first 4 weeks, the rise in blood pressure was higher in high NaCl than in high NaCl/high potassium or regular diet groups. However, by 8 and 12 weeks, the blood pressure in all three groups was similar. After 4 weeks of diet, plasma renin activity was similar in the three groups (3.4±0.8, 4.1±0.9, and 5.2±1.6 ng/ml/hr, in high NaCl, high NaCl/high potassium, and regular diet groups, respectively) and were not related to sodium excretion. After 8 weeks, plasma renin activity was significantly increased only in the high NaCl group (13.7±3.7 ng/ml/hr), and by 12 weeks plasma renin activity was significantly higher in the high NaCl group (25.3±3.6 ng/ml/hr) than in the high NaCl/high potassium (11.1±2.9 ng/ml/hr) or in the regular diet (7.8±4.6 ng/ml/hr) groups. Moderate to severe renal vascular lesions were first detected in the high NaCl group by 8 weeks of diet. At 12 weeks, renal vascular damage index (RVDI), estimated histologically, was significantly higher in the high NaCl group (RVDI=79±14) than in the high NaCl/high potassium (RVDI=40±11) and regular diet (RVDI=7.8±4.6) groups. At this time, incidence of stroke was 81% in high NaCl, 24.5% in high NaCl/high potassium, and 7.7% in regular diet groups. The data demonstrate that: 1) the increase in mortality, stroke, and renal and cerebrovascular lesions in SHRSP fed a high sodium diet is associated with a paradoxical rise in plasma renin activity; 2) the protective effect of high potassium in SHRSP fed a high potassium diet is related to a lower blood pressure at 2-4 weeks and a lower plasma renin activity, but not a lower blood pressure at 8-12 weeks; 3) this rise in plasma renin activity demonstrates that a high potassium diet suppresses or delays a primary or secondary paradoxical rise in plasma renin activity and thus, angiotensin II in the rats fed a high sodium diet. This action together with possible direct effects of potassium in the vasculature contributes to the protective effect on end organ damage and stroke in SHRSP.
KW - Aldosterone
KW - Angiotensin II
KW - Atrial natriuretic factor
KW - Blood pressure
KW - Malignant hypertension
UR - http://www.scopus.com/inward/record.url?scp=0025217943&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0025217943&partnerID=8YFLogxK
M3 - Article
C2 - 2406201
AN - SCOPUS:0025217943
VL - 15
SP - 318
EP - 326
JO - Hypertension
JF - Hypertension
SN - 0194-911X
IS - 3
ER -