BLOOD-PRESSURE RISE WITH AGE—A WESTERN DISEASE?

The Lancet ◽  
1981 ◽  
Vol 318 (8248) ◽  
pp. 693-694
Author(s):  
Hugh Trowell ◽  
Denis Burkitt
Keyword(s):  
Blood Pressure ◽  
Pressure Rise ◽  
Blood Pressure Rise

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.

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.

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.

Antihypertensive Effect of Guanfacine: Long-Term ‘Once-a-Day’ Treatment and Sudden Withdrawal

1981 ◽  
Vol 61 (s7) ◽  
pp. 469s-471s
Author(s):  
I. Szám ◽  
J. Holló
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Antihypertensive Effect ◽  
Clinical Symptoms ◽  
Day Treatment ◽  
Pressure Rise ◽  
Common Side Effect ◽  
Blood Pressure Rise ◽  
Abrupt Discontinuation

1. Twenty patients with essential hypertension were treated with guanfacine given in single daily doses of 1–5 mg over a period of 24 weeks. Compared with the initial values at the end of the first wash-out period, there was a significant decrease of blood pressure and heart rate. The most common side effect, dryness of the mouth, usually disappeared after 8–10 weeks of treatment. No changes in laboratory values were seen. In the post-treatment placebo period there were significant increases in blood pressure and heart rate compared with the last readings during the treatment period. However, these never exceeded the pretreatment values. 2. In a second trial guanfacine (1–5 mg daily) was abruptly discontinued in 11 patients after 6–20 weeks' treatment. Blood pressure was measured twice a day, in lying and standing positions, during the 4 days before abrupt withdrawal of guanfacine and for 7 days after discontinuation. Clopamide was given concurrently to two patients, and this was continued after withdrawal of guanfacine. Only in two patients did the blood pressure rise to values above the initial levels (30 mmHg systolic and 10 mmHg diastolic), but no clinical symptoms were observed during the withdrawal. A transitory increase of heart rate of between 10 and 30 beats/min was observed in five patients after abrupt discontinuation of the drug.

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