Effect of a potassium-deficient diet on arterial blood pressure, plasma and tissue cations, and tissue norepinephrine in the hypertensive dog

1983 ◽  
Vol 61 (12) ◽  
pp. 1473-1477
Author(s):  
Raul Garcia ◽  
Georges Constantopoulos ◽  
Jolanta Gutkowska ◽  
Jacques Genest
Keyword(s):  
Blood Pressure ◽  
Potassium Concentration ◽  
Plasma Renin ◽  
Sodium Concentration ◽  
Potassium Deficiency ◽  
Simultaneous Increase ◽  
Control Group ◽  
Deficient Diet ◽  
Arterial Blood ◽  
Tissue Norepinephrine

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.

Aorta Electrolytes of Hypotensive Potassium-Deficient Rats

1958 ◽  
Vol 195 (2) ◽  
pp. 445-447 ◽  
Author(s):  
S. Charles Freed ◽  
Shirley St. George ◽  
Ray H. Rosenman
Keyword(s):  
Blood Pressure ◽  
Potassium Concentration ◽  
Pressure Rise ◽  
Sodium Concentration ◽  
Sodium Content ◽  
Potassium Deficiency ◽  
Sodium Potassium ◽  
High Sodium ◽  
Blood Pressure Rise ◽  
Arterial Tone

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.

Effect of Low Electrolyte Feeding on Development of Potassium Deficiency

1957 ◽  
Vol 191 (3) ◽  
pp. 610-614 ◽  
Author(s):  
Malcolm A. Holliday ◽  
William E. Segar
Keyword(s):  
Potassium Concentration ◽  
Sodium Intake ◽  
Extracellular Volume ◽  
Sodium Concentration ◽  
Potassium Deficiency ◽  
Electrolyte Composition ◽  
Urine Excretion ◽  
Deficient Diet ◽  
Sodium Potassium ◽  
Low Sodium

Rats fed a diet deficient in sodium, potassium and chloride were observed for 3, 6, 12, 28, 60 and 110 days. Urine excretion of these ions was observed during the initial adjustment to the diet. Serum and muscle electrolyte composition was determined at the end of each interval. Initially the loss of sodium and chloride constituted a loss of extracellular volume without change in concentration. The loss of potassium in this period resulted in a decrease in the intracellular concentration of potassium. Subsequent conservation of all three substances was very effective. No alkalosis developed during the first 28 days on the deficient diet despite an 18% reduction in muscle potassium concentration. A minimal increase in muscle sodium concentration was observed at this level of potassium deficiency. Evidence indicates that this minimal increase was not a function of the low sodium intake per se but rather was characteristic of the magnitude of potassium deficiency, since a similar minimal increase in muscle sodium occurs when an adequate sodium intake is provided.

scholarly journals Accumulation of Prostacyclin in Rat Brain during Haemorrhagic Hypotension—Possible Role of PGI2 in Autoregulation

1984 ◽  
Vol 4 (1) ◽  
pp. 107-109 ◽  
Author(s):  
E. Shohami ◽  
A. Sidi
Keyword(s):  
Blood Pressure ◽  
Steady State ◽  
Control Group ◽  
Prostaglandin E ◽  
Cortical Tissue ◽  
Arterial Blood ◽  
Haemorrhagic Hypotension ◽  
Potent Vasodilator ◽  
Prostaglandin F

The effect of haemorrhagic hypotension on the levels of prostaglandin E2 (PGE2), thromboxane B2 (TXB2), and 6-keto prostaglandin F1α (6-keto-PGF1α) in cortical tissue of rats was studied. Lightly anesthetized rats were subjected to steady-state hypotension for 15 min, with a mean arterial blood pressure of 80, 60, and 40 mm Hg, and compared to a control group of normotensive rats. No significant change was found in the levels of PGE2 and TXB2. The level of 6-keto-PGF1α increased from 7.8 ± 0.9 to 14.1 ± 1.9 pg/mg protein (p < 0.02) at 80 mm Hg. Our findings suggest that prostacyclin, which is a potent vasodilator, might play a role in setting the lower limit of the autoregulation range.

Enhancement of the Antihypertensive Effect of Hydrochlorothiazide in Dogs after Suppression of Renin Release by Beta-Adrenergic Blockade

1975 ◽  
Vol 48 (2) ◽  
pp. 147-151
Author(s):  
C. S. Sweet ◽  
M. Mandradjieff
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Arterial Blood Pressure ◽  
Antihypertensive Effect ◽  
Plasma Renin ◽  
Renin Activity ◽  
Renin Release ◽  
Antihypertensive Activity ◽  
Adrenergic Blockade ◽  
Arterial Blood

1. Renal hypertensive dogs were treated with hydrochlorothiazide (8−2 μmol/kg or 33 μmol/kg daily for 7 days), or timolol (4.6 μmol/kg daily for 4 days), a potent β-adrenergic blocking agent, or combinations of these drugs). Changes in mean arterial blood pressure and plasma renin activity were measured over the treatment period. 2. Neither drug significantly lowered arterial blood pressure when administered alone. Plasma renin activity, which did not change during treatment with timolol, was substantially elevated during treatment with hydrochlorothiazide. 3. When timolol was administered concomitantly with hydrochlorothiazide, plasma renin activity was suppressed and blood pressure was significantly lowered. 4. These observations suggest that compensatory activation of the renin-angiotensin system limits the antihypertensive activity of hydrochlorothiazide in renal hypertensive dogs and suppression of diuretic-induced renin release by timolol unmasks the antihypertensive effect of the diuretic.

scholarly journals Salt sensitivity of blood pressure in NKCC1-deficient mice

2008 ◽  
Vol 295 (4) ◽  
pp. F1230-F1238 ◽  
Author(s):  
Soo Mi Kim ◽  
Christoph Eisner ◽  
Robert Faulhaber-Walter ◽  
Diane Mizel ◽  
Susan M. Wall ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Wheel Running ◽  
Plasma Renin ◽  
Pressure Change ◽  
Standard Diet ◽  
Wild Type ◽  
Vascular Effects ◽  
Arterial Blood ◽  
Deficient Mice

NKCC1 is a widely expressed isoform of the Na-2Cl-K cotransporter that mediates several direct and indirect vascular effects and regulates expression and release of renin. In this study, we used NKCC1-deficient (NKCC1−/−) and wild-type (WT) mice to assess day/night differences of blood pressure (BP), locomotor activity, and renin release and to study the effects of high (8%) or low (0.03%) dietary NaCl intake on BP, activity, and the renin/aldosterone system. On a standard diet, 24-h mean arterial blood pressure (MAP) and heart rate determined by radiotelemetry, and their day/night differences, were not different in NKCC1−/− and WT mice. Spontaneous and wheel-running activities in the active night phase were lower in NKCC1−/− than WT mice. In NKCC1−/− mice on a high-NaCl diet, MAP increased by 10 mmHg in the night without changes in heart rate. In contrast, there was no salt-dependent blood pressure change in WT mice. MAP reductions by hydralazine (1 mg/kg) or isoproterenol (10 μg/mouse) were significantly greater in NKCC1−/− than WT mice. Plasma renin (PRC; ng ANG I·ml−1·h−1) and aldosterone (aldo; pg/ml) concentrations were higher in NKCC1−/− than WT mice (PRC: 3,745 ± 377 vs. 1,245 ± 364; aldo: 763 ± 136 vs. 327 ± 98). Hyperreninism and hyperaldosteronism were found in NKCC1−/− mice during both day and night. High Na suppressed PRC and aldosterone in both NKCC1−/− and WT mice, whereas a low-Na diet increased PRC and aldosterone in WT but not NKCC1−/− mice. We conclude that 24-h MAP and MAP circadian rhythms do not differ between NKCC1−/− and WT mice on a standard diet, probably reflecting a balance between anti- and prohypertensive factors, but that blood pressure of NKCC1−/− mice is more sensitive to increases and decreases of Na intake.

scholarly journals EFFECT OF DIFFERENT OCCLUSION PRESSURE ON PECULIARITIES OF MUSCLE BLOOD FLOW

2018 ◽  
Vol 1 (108) ◽  
pp. 2-8
Author(s):  
Kęstutis Bunevičius ◽  
Albinas Grunovas ◽  
Jonas Poderys
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Arterial Blood Pressure ◽  
Arterial Blood Flow ◽  
Control Group ◽  
Reactive Hyperaemia ◽  
Occlusion Pressure ◽  
Arterial Blood ◽  
Flow Intensity ◽  
Blood Flow Intensity

Background. Occlusion pressure intensity influences the blood flow intensity. Immediately after the cuff pressure is released, reactive hyperaemia occurs. Increased blood flow and nutritive delivery are critical for an anabolic stimulus, such as insulin. The aim of study was to find which occlusion pressure was optimal to increase the highest level of post occlusion reactive hyperaemia. Methods. Participants were randomly assigned into one of the four conditions (n = 12 per group): control group without blood flow restriction, experimental groups with 120; 200 or 300 mmHg occlusion pressure. We used venous occlusion plethysmography and arterial blood pressure measurements. Results. After the onset of 120 and 200 mm Hg pressure occlusion, the blood flow intensity significantly decreased. Occlusion induced hyperaemia increased arterial blood flow intensity 134 ± 11.2% (p < .05) in the group with 120 mmHg, in the group with 200 mmHg it increased 267 ± 10.5% (p < .05), in the group with 300 mmHg it increased 233 ± 10.9% (p < .05). Applied 300 mmHg occlusion from the 12 minute diastolic and systolic arterial blood pressure decreased statistically significantly. Conclusions. Occlusion manoeuvre impacted the vascular vasodilatation, but the peak blood flow registered after occlusion did not relate to applied occlusion pressure. The pressure of 200 mmHg is optimal to impact the high level of vasodilatation. Longer than 12 min 300 mmHg could not be recommended due to the steep decrease of systolic and diastolic blood pressures.

Pharmacological and genetic evidence that cathepsin B is not the physiological activator of rodent prorenin

2010 ◽  
Vol 391 (12) ◽  
Author(s):  
M. David Percival ◽  
Sylvie Toulmond ◽  
Nathalie Coulombe ◽  
Wanda Cromlish ◽  
Sylvie Desmarais ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Plasma Renin Activity ◽  
Cathepsin B ◽  
Plasma Renin ◽  
Renin Activity ◽  
Spontaneously Hypertensive ◽  
Protein Levels ◽  
Arterial Blood ◽  
Gene Compensation

Abstract Renin is the first enzyme in the renin-angiotensin-aldosterone system which is the principal regulator of blood pressure and hydroelectrolyte balance. Previous studies suggest that cathepsin B is the activator of the prorenin zymogen. Here, we show no difference in plasma renin activity, or mean arterial blood pressure between wild-type and cathepsin B knockout mice. To account for potential gene compensation, a potent, selective, reversible cathepsin B inhibitor was developed to determine the role of cathepsin B on prorenin processing in rats. Pharmacological inhibition of cathepsin B in spontaneously hypertensive and double transgenic rats did not result in a reduction in renal mature renin protein levels or plasma renin activity. We conclude that cathepsin B does not play a significant role in this process in rodents.

The use of propofol as an induction agent for halothane and isoflurane anesthesia in dogs

1998 ◽  
Vol 34 (1) ◽  
pp. 84-91 ◽  
Author(s):  
A Bufalari ◽  
SM Miller ◽  
C Giannoni ◽  
CE Short
Keyword(s):  
Blood Pressure ◽  
Wave Activity ◽  
Simultaneous Increase ◽  
Induction Agent ◽  
Total Amplitude ◽  
Brain Wave ◽  
Isoflurane Anesthesia ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Brain Wave Activity

Cardiovascular, pulmonary, and quantitative electroencephalographic parameters were assessed in 12 anesthetized dogs to determine the compatibility of the injectable anesthetic propofol with halothane and isoflurane. No cases of apnea were observed during induction of anesthesia. An adequate level of anesthesia was established in each protocol as judged by both the lack of response to mechanical noxious stimuli (i.e., tail clamping) and evidence of reduction in total amplitude of brain wave activity. The initial propofol-mediated decrease in arterial blood pressure continued during either halothane (52.4%) or isoflurane (38%) anesthesia without a simultaneous increase in heart rate. The results of this study suggest that propofol, in combination with inhalant agents, can be used effectively and safely for canine anesthesia in veterinary practice.

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