ARTERIAL HYPERTENSION INDUCED BY 9α-FLUOROCORTISOL IN RATS

1974 ◽  
Vol 75 (3) ◽  
pp. 539-549 ◽  
Author(s):  
R. Hepp ◽  
K. Garbade ◽  
P. Oster ◽  
F. Gross

ABSTRACT In unilaterally nephrectomized rats, 9α-fluorocortisol (9α-FF), in doses of 0.3 and 1.0 mg given daily by intramuscular injection, induced an increase in blood pressure that was independent of additional sodium supply. 9α-FF reduced weight gain and, in the dose of 1.0 mg, increased fluid turnover when 0.9 % saline was given to drink. Haematocrit values were elevated, whether saline or water was given as drinking fluid. The serum sodium concentration was increased when saline was offered, but normal with water as drinking fluid. The serum potassium concentration was diminished in all groups that received 9α-FF. The renin content of the kidney was markedly depressed in all groups that had 9α-FF. The degree of suppression was similar in the groups that had saline and those that had water to drink. Under 9α-FF, plasma concentration of angiotensin II was virtually zero when saline was given to drink, but about ¼ to ½ normal when drinking fluid was water. It is concluded that the type of hypertension developing under high doses of 9α-FF resembles glucocorticoid rather than mineralocorticoid hypertension.

1957 ◽  
Vol 189 (3) ◽  
pp. 605-608 ◽  
Author(s):  
W. F. Rosse ◽  
A. L. Bennett ◽  
A. R. McIntyre

Shock was induced in dogs by the release of tourniquets which had been applied to the hind legs for 5 hours. The serum potassium level was followed by spaced sampling. It was seen to rise slightly (from an average of 4.02 mEq/l. to an average of 4.66 mEq/l.) during the prerelease period. Five minutes after the release of the tourniquets, the level had risen to an average of 7.50 mEq/l. and thirty minutes after the release, it had risen to an average of 8.56 mEq/l. At the critical point in the progress of the syndrome (when the mean blood pressure was approximately 50 mm Hg) the average value was 8.46 mEq/l. Ouabain was administered and the level of serum potassium was seen to rise, attaining values as high as 14.67 mEq/l. in one case. The results and significance of these increased levels are briefly discussed as well as an animadversion upon the effects of ouabain on the mean blood pressure.


1958 ◽  
Vol 195 (2) ◽  
pp. 445-447 ◽  
Author(s):  
S. Charles Freed ◽  
Shirley St. George ◽  
Ray H. Rosenman

The hypotension of potassium-deficiency is associated with a decrease in aorta potassium concentration, the sodium content remaining unchanged, resulting in a high sodium/potassium ratio. Loss of arterial tone may result and thus contribute to the lowering of blood pressure. Cortisone administration to such rats does not alter the low aorta potassium content but appreciably reduces the sodium concentration. The return to a more normal sodium/potassium ratio in the aorta following cortisone may restore the arterial tone and thus explain the blood pressure rise to normal levels.


1978 ◽  
Vol 55 (s4) ◽  
pp. 151s-153s ◽  
Author(s):  
J. K. McKenzie ◽  
E. Reisin

1. Six essential hypertensive patients (five with low renin) were treated in successive weeks with placebo; hydrochlorothiazide 100 mg (382 μmol)/day; hydrochlorothiazide and 50 mmol of sodium/day diet; hydrochlorothiazide, 50 mmol of sodium diet and propranolol 160 mg (544 μmol)/day; and hydrochlorothiazide, 50 mmol of sodium and indomethacin 100 mg (287 μmol)/day. 2. Although blood pressure remained unchanged and serum potassium fell on diuretic with or without low salt, there was a marked increase of active renin and a lesser increase of inactive renin, resulting in an increased proportion of active to total renin. 3. Propranolol decreased both active and inactive renin, but not significantly. 4. Indomethacin produced a marked suppression of active renin, a smaller reduction in inactive renin, and a reduction of the ratio of active to total renin almost to placebo values. 5. Blood pressure rose to control values on indomethacin despite the fall in renin whereas it fell with propranolol with little change in renin. 6. Serum aldosterone rose with stimulation but remained elevated despite effective renin suppression with indomethacin and continuing reduced serum potassium concentration.


1974 ◽  
Vol 76 (3) ◽  
pp. 539-555 ◽  
Author(s):  
D. Haack ◽  
E. Hackenthal ◽  
E. Homsy ◽  
B. Möhring ◽  
J. Möhring

ABSTRACT In normal rats on a standard sodium diet, the administration of 9-alpha-fluorohydrocortisone (9aFF) induced a rapid increase of blood pressure in parallel to an increase of plasma volume. Water and potassium balances became negative. Urinary sodium excretion remained unchanged or increased after high doses, whereas urinary sodium concentration and faecal sodium excretion were reduced. The diurnal rhythm of water and sodium excretion changed: during the night-period, renal water and sodium excretion were diminished, whereas during the day-period both were enhanced. Thus, some effects of 9aFF on electrolyte and water balance are similar to those of DOC, while other effects are similar to those of cortisone. It is postulated that a shift of fluid from intracellular to extracellular compartments, which increases plasma volume, is of critical importance for the 9aFF-induced blood pressure elevation in rats.


2021 ◽  
Vol 14 (3) ◽  
pp. e240898
Author(s):  
Katsunobu Yoshioka

A 53-year-old man was admitted to our hospital because of general fatigue and disorientation. He had been diagnosed with Bartter syndrome in his teens and had been taking potassium preparations since then. However, his serum potassium concentration (K+s) remained persistently low. Ten days before admission, he developed fever. He was diagnosed as having bronchitis and was treated with antibiotics. Although his fever subsided, general fatigue worsened. Laboratory examination showed hyponatraemia (127 mEq/L), while K+s was 2.3 mEq/L. C reactive protein was negative. On admission, laboratory examination revealed deterioration of hyponatraemia (125 mEq/L). Although his serum sodium concentration (Na+s) was refractory to electrolyte replacement, the level increased towards normal after spironolactone administration, following normalisation of K+s, suggesting that hyponatraemia was caused by K+ depletion. Physicians should be aware of the importance of the effects of exchangeable K+ (K+e) on Na+s.


1980 ◽  
Vol 18 (23) ◽  
pp. 92.1-92

Current 4-page advertisements1 for the diuretic xipamide (Diurexan - Merck) which we discussed last year2 cite “IMPORTANT NEW EVIDENCE (that) it is ‘as effective as many β-blockers but without their side effects, and produces better control of blood pressure throughout the whole day and night’”. This quotation comes from workers at Northwick Park3 and is accompanied by a photograph of the Clinical Research Centre. It is true that in their study the drug appeared to reduce blood pressure to much the same degree as β-blockers throughout the 24-hour cycle. But there is no reason to believe that xipamide differs from any other diuretic in its anti-hypertensive effect. As we noted some years ago, a thiazide diuretic alone can control even severely raised blood pressure in some patients.4 The advertising gives no prominence to the finding at Northwick Park (and elsewhere) that xipamide can cause a disturbing fall in the serum potassium concentration, and might thus be unsuitable for long-term anti-hypertensive therapy. It has still not been shown to have any advantage over other diuretics in the treatment of hypertension,2 and is relatively expensive.


1983 ◽  
Vol 61 (12) ◽  
pp. 1473-1477
Author(s):  
Raul Garcia ◽  
Georges Constantopoulos ◽  
Jolanta Gutkowska ◽  
Jacques Genest

Chronic potassium deficiency in one-kidney one-clip hypertensive dogs significantly reduces blood pressure and plasma potassium, with a simultaneous increase in plasma renin activity. Tissue potassium concentration was decreased and tissue sodium concentration was increased in striated muscle and adrenal glands, which may suggest that the sodium-potassium pump was inhibited. In myocardium the sodium concentration was higher but the potassium concentration was not significantly lower than in control hypertensive dogs on normal diets. Arterial cation concentrations in the potassium-deficient group were not significantly different from those in the control group. Tissue norepinephrine concentration was higher in arteries from potassium-deficient animals, significantly so in the mesenteric and femoral arteries. The conclusion is that potassium deficiency may decrease blood pressure in the one-kidney one-clip hypertensive dogs by impairing the release of norepinephrine.


1995 ◽  
Vol 31 (2) ◽  
pp. 151-155 ◽  
Author(s):  
MD McCabe ◽  
EC Feldman ◽  
RC Lynn ◽  
PH Kass

Twelve dogs with hypoadrenocorticism were treated with subcutaneous desoxycorticosterone pivalate (DOCP). Eight of these dogs were recently diagnosed and had not yet been treated. Four dogs previously had been diagnosed and treated (three with intramuscular DOCP, one with oral fludrocortisone acetate). History, physical examination, serum electrolytes, and blood urea nitrogen (BUN) were evaluated. Desoxycorticosterone pivalate (2.2 mg/kg body weight) was administered every 25 days. On day 0, recently diagnosed dogs had a median serum sodium concentration of 131.5 mEq/L, median serum potassium concentration of 6.6 mEq/L, and median BUN of 41.5 mg/dl. All subsequent median serum electrolyte and BUN concentrations were normal. All previously treated dogs had normal blood values which were maintained throughout the study.


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