Inhibitory effect of potassium on blood pressure in DOCA salt hypertension in rats

1981 ◽  
Vol 97 (4) ◽  
pp. 525-532 ◽  
Author(s):  
Hiromichi Suzuki ◽  
Kazuoki Kondo ◽  
Takao Saruta

Abstract. The present study was performed to assess the influence of potassium on blood pressure in deoxycorticosterone (DOCA) salt hypertensive rats. The effects of potassium administration on the systolic blood pressure, fluid intake, urine volume, excretion of sodium and potassium, serum sodium and potassium, plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were investigated both during the first 2 weeks of development of DOCA salt hypertension and during the next 2 weeks of established DOCA salt hypertension. Potassium administration prevented the development of DOCA salt hypertension and reduced the blood pressure in established DOCA salt hypertension. Fluid intake, urine volume, and excretion of sodium and potassium appeared to be markedly increased in rats treated with potassium. The levels of serum sodium and potassium were unchanged by potassium loading. Both the PRA and PAC which were suppressed in DOCA salt hypertensive rats, were reversed in rats treated by potassium loading. It is suggested that the elevation of blood pressure may be prevented and the increased blood pressure reduced mainly by the diuresis and natriuresis caused by potassium loading.

1983 ◽  
Vol 245 (6) ◽  
pp. F755-F762 ◽  
Author(s):  
B. M. Iversen ◽  
L. Morkrid ◽  
J. Ofstad

The afferent arteriolar diameter (dAA) was investigated during development of hypertensive renal disease in normal and uninephrectomized control rats, in chronic DOCA-salt (DOCA), post-DOCA (p-DOCA), and chronic two-kidney one-clip (2K-1C) hypertensive rats, and in post-two-kidney one-clip (p-2K-1C) normotensive rats. dAA was measured by the microsphere method. Nephron loss was present in the kidneys exposed to elevate blood pressure. The dAA was reduced from 19.9 to 17.2 micron in the DOCA group (P less than 0.001) and from 19.1 to 16.3 micron in the nonclipped kidneys in the 2K-1C group (P less than 0.001). The dAA increased from 19.9 to 20.7 micron in the p-DOCA group. Afferent arteriolar dilatation from 19.1 to 21.0 micron (P less than 0.001) was present about 50 days after clipping in the 2K-1C group; in the clipped kidneys the dAA returned to normal (18.9 micron) after declipping. No relation between the dAA and plasma renin concentration was observed. In all models dAA was the same in three cortical layers of equal thickness. Accordingly, chronic renal DOCA-salt hypertension constricts the afferent arteriole with angiotensin-independent mechanisms. Autoregulatory dilatation of the afferent arteriole seems to be maintained for at least 50 days. When the hypertension is moderate, dAA in damaged kidneys may be dilated.


1981 ◽  
Vol 61 (s7) ◽  
pp. 335s-338s ◽  
Author(s):  
R. F. Bing ◽  
G. I. Russell ◽  
J. D. Swales ◽  
H. Thurston ◽  
A. Fletcher

1. Chemical renal medullectomy was produced in rats by injection of 2-bromoethylamine hydrobromide. Plasma creatinine and blood pressure were unchanged although urine volume was increased fourfold. 2. Left renal artery constriction resulted in similar degrees of hypertension in both intact and medullectomized rats. This was associated with a significantly smaller rise in plasma renin concentration in the latter. 3. Blood pressure in conscious intact hypertensive rats became normal within 24 h of unclipping whereas blood pressure of medullectomized rats remained significantly elevated. 4. The presence of an intact renal medulla is essential to the complete reversal of two-kidney, one-clip hypertension in the rat. This may reflect the loss of a medullary vasodepressor system.


1979 ◽  
Vol 57 (1) ◽  
pp. 47-52 ◽  
Author(s):  
R. G. M. Ten Berg ◽  
F. H. H. Leenen ◽  
W. De Jong

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.


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 ◽  
...  

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.


1982 ◽  
Vol 63 (s8) ◽  
pp. 265s-267s ◽  
Author(s):  
H. Witzgall ◽  
B. Scherer ◽  
P. C. Weber

1. Haemodynamic and hormonal actions of 100 mg of captopril (SQ 14 225) orally were tested in 12 healthy volunteers with and without indomethacin pretreatment. 2. Without indomethacin, mean arterial blood pressure was reduced at 30 and 60 min after captopril (P < 0.02). Heart rate did not change. Plasma renin activity (PRA) increased (P < 0.002), and plasma and urinary aldosterone as well as plasma 18-hydroxycorticosterone (18- OH-B) decreased after captopril (P < 0.02). Prostaglandin (PG) E2, kallikrein, urine volume, sodium and potassium excretion rates remained constant after captopril. 3. Under indomethacin pretreatment, blood pressure was reduced to a smaller degree at 30 and 60 min after captopril (P < 0.05). Heart rate was constantly lower than without indomethacin (P < 0.05). Indomethacin decreased basal PGE2 and kallikrein excretion (P < 0.02) and reduced basal PRA as well as the increase of PRA after captopril (P < 0.05). Basal mineralocorticoid levels were significantly lower than without indomethacin. Aldosterone did not decrease further after captopril, and 18-OH-B fell only slightly. 4. The results suggest that prostaglandins may be involved in the haemodynamic and hormonal actions of captopril.


1986 ◽  
Vol 251 (2) ◽  
pp. H261-H268 ◽  
Author(s):  
Y. Itaya ◽  
H. Suzuki ◽  
S. Matsukawa ◽  
K. Kondo ◽  
T. Saruta

The antihypertensive effect of blockade of the brain renin-angiotensin system (brain RAS) was investigated in DOCA (deoxycorticosterone acetate)-salt hypertensive rats. Continuous intracerebroventricular (ICV) administration of SQ14225 (SQ; 1.25 micrograms X 0.5 microliter-1 X h-1) for 7 days attenuated the increase in blood pressure (99 +/- 5 vs. 116 +/- 4 mmHg on the 7th day) and also reduced the elevation of blood pressure (157 +/- 7 vs. 138 +/- 6 mmHg) in these hypertensive rats. Attenuation of increasing blood pressure in the developing phase following ICV SQ treatment was accompanied by decrease of fluid intake and prevention of elevation of the plasma vasopressin. In the established phase, in addition to reduction of the plasma vasopressin and decrease of fluid intake, restoration of the impaired baroreceptor reflexes was brought about by ICV SQ treatment. These results indicate that the brain RAS strongly influences the regulation of blood pressure in DOCA-salt hypertensive rats and that its mechanism of action is closely related to changes in sodium excretion, vasopressin, and the baroreceptor reflexes.


1987 ◽  
Vol 72 (3) ◽  
pp. 313-319 ◽  
Author(s):  
A. Louise Sugden ◽  
James A. Straw ◽  
Barbara L. Bean

1. Blood pressure was measured after treatment with a high K+, a low Na+ and a combined high K+/low Na+ diet in young spontaneously hypertensive rats (SHR). 2. A high K+ diet reduced blood pressure by approximately 10 mmHg during the development of hypertension. This decrease was accompanied by a significant increase in water intake and urine volume and a significant decrease in plasma renin activity (PRA). 3. A low Na+ diet also decreased blood pressure significantly, but, in contrast to the high K+ diet, water intake and urine volume significantly decreased and PRA increased. 4. When both diets were given together, the antihypertensive effects of both were eliminated. Thus while an increase in dietary K+ and a decrease in dietary Na+ are both effective antihypertensive regimens in SHR, the mechanism of action of each appears to be different and may be antagonistic in these animals.


2011 ◽  
Vol 27 (6) ◽  
pp. 266-268 ◽  
Author(s):  
Tony Joseph Eid ◽  
Amanda A Morris ◽  
Sachin A Shah

Objective: To report a case of hypertension secondary to ingestion of licorice root tea. Case Summary: A 46-year-old African American female with newly diagnosed stage 1 hypertension presented with a blood pressure measurement of 144/81 mm Hg and a reduced plasma potassium level of 3.2 mEq/L. The patient attempted lifestyle modifications prior to initiating an antihypertensive agent, but at a follow-up appointment, her blood pressure remained elevated. A current laboratory panel revealed a depressed morning plasma aldosterone concentration (PAC) of 5 ng/dL and low morning plasma renin activity (PRA) of 0.13 ng/mL/h. Later it was revealed that the patient regularly (1–2 cups/day) consumed “Yogi Calming” tea, a blend of herbs, including licorice root. The patient was advised to discontinue consumption of the herbal tea, and at a subsequent appointment, her blood pressure was 128/73 mm Hg and her laboratory panel had improved, including serum potassium concentration of 4.1 mEq/L, PAC of 6 ng/dL, and PRA of 0.19 ng/mL/h. Discussion: Excessive consumption of licorice has been well documented to cause pseudohyperaldosteronism, characterized by hypertension, hypokalemia, and suppressed plasma renin and aldosterone levels. Glycyrrhizin, the active ingredient in licorice, inhibits 11β-hydroxysteroid dehydrogenase type 2, an oxidase responsible for the conversion and inactivation of cortisol to cortisone. Chronic ingestion of licorice-containing foods has been demonstrated to cause pseudohyperaldosteronism. These include soft candies, lozenges, and dietary supplements, but licorice-containing teas have been infrequently described. Based on the Naranjo probability score, our patient's hypertension appears to have been a probable licorice-induced reaction secondary to a licorice-containing tea. Conclusions: Herbal and dietary supplements are frequently consumed by patients without full knowledge of the contents of the products or the impact on their health. In clinical practice, when hypertension is accompanied by hypokalemia and reduced PRA and PAC, licorice consumption should be investigated and causal hypertension ruled out.


1987 ◽  
Vol 72 (3) ◽  
pp. 321-327 ◽  
Author(s):  
A. Louise Sugden ◽  
Barbara L. Bean ◽  
James A. Straw

1. These studies were designed to investigate the effects of high dietary K+ on electrolyte and water balance in young spontaneously hypertensive rats (SHR) and to relate these effects to changes in blood pressure. 2. The high K+ diet reduced blood pressure by approximately 10 mmHg during the development of hypertension. Blood pressure, however, plateaued at the same maximum level as control by age 13 weeks. 3. Rats fed the high K+ diet showed a significant increase in water intake and urine volume throughout the treatment period but no change in plasma volume or extracellular fluid volume occurred. 4. A slight natriuresis was also observed in rats on the high K+ diet, but this was not of sufficient magnitude to decrease total body Na+. 5. These results confirm previous findings that K+ causes a diuresis and a natriuresis, but demonstrate that the diuretic action of K+ cannot explain its antihypertensive properties in young SHR.


1984 ◽  
Vol 66 (6) ◽  
pp. 659-663 ◽  
Author(s):  
L. T. Bannan ◽  
J. F. Potter ◽  
D. G. Beevers ◽  
J. B. Saunders ◽  
J. R. F. Walters ◽  
...  

1. Sixty-five alcoholic patients admitted for detoxification had blood pressure, withdrawal symptoms, plasma cortisol (PC) and plasma aldosteron (PA) levels, plasma renin activity (PRA), and serum dopamin β-hydroxylase (DBH) levels measured on the first and fourth days after admission. 2. On the morning after admission blood pressure was elevated (>140/90) in 32 patients (49%) and was 160/95mmHg or more in 21 (32%). PRA was initially elevated in 41 patients, PA levels in 14, and 13 patients had raised PC levels. By the fourth day, blood pressure and bio-chemical measures had fallen significantly while urine volume and sodium output, low on admission, had increased significantly. On admission urinary metanephrine levels were raised in four out of the 31 patients who had them measured. 3. The height of both the systolic and diastolic blood pressures was significantly related to the severity of the alcohol. withdrawal symptoms. Of the biochemical parameters measured, PC level correlated with systolic but not diastolic pressure, and urinary volume was inversely correlated with the height of the diastolic pressure. No relationship was found between blood pressure and PRA or PA level. 4. The pressor effect of alcohol withdrawal could be due to sympathetic nervous system overactivity, or possibly to hypercortisolaemia. The first hypothesis seems more likely.


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