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.

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.

Chronic central potassium infusion prevents deoxycorticosterone-salt hypertension in rats

1995 ◽  
Vol 268 (2) ◽  
pp. H646-H652 ◽  
Author(s):  
S. A. Klarr ◽  
R. F. Keep ◽  
A. L. Betz
Keyword(s):  
Blood Pressure ◽  
Animal Model ◽  
Cerebrospinal Fluid ◽  
Systolic Blood Pressure ◽  
Potassium Concentration ◽  
Pressure Rise ◽  
Blood Pressure Rise ◽  
Lower Blood ◽  
Salt Hypertension ◽  
Blood Pressures

Although it has long been established that cerebrospinal fluid potassium concentration (CSF [K]) is very tightly regulated, it has been reported that rats made hypertensive by central infusions of aldosterone have significantly lower CSF [K] compared with normotensive controls. We investigated whether reduced CSF [K] is also present in another animal model of hypertension, the deoxycorticosterone acetate (DOCA)-salt rat, and we hypothesized that chronic intracerebroventricular (IVT) infusion of potassium with miniosmotic pumps might attenuate the rise in blood pressure observed in these rats. DOCA-salt rats without IVT infusions or with control CSF infusions (0.5 microliter/h of 2.9 mM K for 2 wk) had a significantly increased systolic blood pressure and a significantly lower CSF [K] compared with their respective sham groups. In contrast, DOCA-salt rats receiving IVT infusions with elevated [K] (10, 30, or 150 mM) had significantly lower blood pressures compared with those receiving control CSF. They also did not exhibit decreased CSF [K] compared with their respective sham groups. At 10 and 150 mM K, the blood pressure rise in DOCA-salt rats was not significantly different from shams. At 30 mM K, there was a slight, but significant, increase in blood pressure in the DOCA-salt rats compared with their shams, but this rise was still much less than in DOCA-salt rats infused with 2.9 mM K. Infusions with elevated [K] had no effect on blood pressure in the sham animals. These studies suggest that altered brain potassium homeostasis may play an important role in the development of DOCA-salt hypertension.

Arterial blood pressure responses to graded transient arousal from sleep in normal humans

1993 ◽  
Vol 74 (3) ◽  
pp. 1123-1130 ◽  
Author(s):  
R. J. Davies ◽  
P. J. Belt ◽  
S. J. Roberts ◽  
N. J. Ali ◽  
J. R. Stradling
Keyword(s):  
Blood Pressure ◽  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Confidence Interval ◽  
Rem Sleep ◽  
High Frequency ◽  
Pressure Rise ◽  
Nrem Sleep ◽  
Blood Pressure Rise ◽  
Obstructive Sleep

During obstructive sleep apnea, transient arousal at the resumption of breathing is coincident with a substantial rise in blood pressure. To assess the hemodynamic effect of arousal alone, 149 transient stimuli were administered to five normal subjects. Two electroencephalograms (EEG), an electrooculogram, a submental electromyogram (EMG), and beat-to-beat blood pressure (Finapres, Ohmeda) were recorded in all subjects. Stimulus length was varied to produce a range of cortical EEG arousals that were graded as follows: 0, no increase in high-frequency EEG or EMG; 1, increased high-frequency EEG and/or EMG for < 10 s; 2, increased high-frequency EEG and/or EMG for > 10 s. Overall, compared with control values, average systolic pressure rose [nonrapid-eye-movement (NREM) sleep 10.0 +/- 7.69 (SD) mmHg; rapid-eye-movement (REM) sleep 6.0 +/- 6.73 mmHg] and average diastolic pressure rose (NREM sleep 6.1 +/- 4.43 mmHg; REM sleep 3.7 +/- 3.02 mmHg) over the 10 s following the stimulus (NREM sleep, P < 0.0001; REM sleep, P < 0.002). During NREM sleep, there was a trend toward larger blood pressure rises at larger grades of arousal (systolic: r = 0.22, 95% confidence interval 0.02–0.40; diastolic: r = 0.48, 95% confidence interval 0.31–0.62). The average blood pressure rise in response to the grade 2 arousals was approximately 75% of that during obstructive sleep apnea. Arousal stimuli that did not cause EEG arousal still produced a blood pressure rise (mean systolic rise 8.6 +/- 7.0 mmHg, P < 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

SP052SALT-SENSITIVE BLOOD PRESSURE RISE IN TYPE 1 DIABETES IS ACCOMPANIED BY INCAPACITY FOR VASODILATION – A RANDOMIZED EXPERIMENTAL CROSS-OVER STUDY

2019 ◽  
Vol 34 (Supplement_1) ◽  
Author(s):  
Eliane Wenstedt ◽  
Nienke Rorije ◽  
Kim Van Der Molen ◽  
Youssef Chahid ◽  
Bert-Jan Van Den Born ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Type 1 Diabetes ◽  
Pressure Rise ◽  
Experimental Cross ◽  
Blood Pressure Rise

An induced blood pressure rise does not alter upper airway resistance in sleeping humans

1998 ◽  
Vol 84 (1) ◽  
pp. 269-276 ◽  
Author(s):  
Christine R. Wilson ◽  
Shalini Manchanda ◽  
David Crabtree ◽  
James B. Skatrud ◽  
Jerome A. Dempsey
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Eye Movement ◽  
Airway Resistance ◽  
Pressure Rise ◽  
Upper Airway ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Upper Airway Resistance ◽  
Blood Pressure Rise

Wilson, Christine R., Shalini Manchanda, David Crabtree, James B. Skatrud, and Jerome A. Dempsey. An induced blood pressure rise does not alter upper airway resistance in sleeping humans. J. Appl. Physiol. 84(1): 269–276, 1998.—Sleep apnea is associated with episodic increases in systemic blood pressure. We investigated whether transient increases in arterial pressure altered upper airway resistance and/or breathing pattern in nine sleeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nose or face mask. During non-rapid-eye-movement sleep, we injected 40- to 200-μg iv boluses of phenylephrine. Parasympathetic blockade was used if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 ± 5 (mean ± SD) mmHg (range 12–37 mmHg) within 12 s and remained elevated for 105 s. There were no significant changes in inspiratory or expiratory pharyngeal resistance (measured at peak flow, peak pressure, 0.2 l/s or by evaluating the dynamic pressure-flow relationship). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20–25 s. At 26 s after peak MAP, tidal volume fell by 19%, consistent with hypocapnic ventilatory inhibition. We conclude that transient increases in MAP of a magnitude commonly observed during non-rapid-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.

ON THE HYPERTENSIVE ACTION OF TOLAZOLINE AND HYDERGINE

1963 ◽  
Vol 41 (1) ◽  
pp. 941-946 ◽  
Author(s):  
B. G. Benfey ◽  
D. R. Varma
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Contractility ◽  
Pressure Rise ◽  
Pressor Effect ◽  
Blood Pressure Rise ◽  
Chronotropic Effects

The effects of tolazoline and Hydergine on blood pressure, cardiac contractility, and heart rate have been studied in dogs under pentobarbitone anesthesia. Whereas in the absence of reserpine, tolazoline had a pressor effect in two of four dogs, following reserpine it had a marked pressor action in each of eight dogs. The blood pressure rise was associated with positive inotropic and negative chronotropic effects. Phenoxybenzamine abolished these effects of tolazoline. Hydergine had pressor and negative chronotropic effects in the absence of reserpine. Following reserpine these effects were associated with positive inotropic actions. Phenoxybenzamine reduced these effects of Hydergine. It is concluded that the pressor action of tolazoline is wholly due to adrenergic vasoconstriction, whereas that of Hydergine is only partly an adrenergic effect.

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