scholarly journals Aortic and Carotid Arterial Stiffness and Epigenetic Regulator Gene Expression Changes Precede Blood Pressure Rise in Stroke-Prone Dahl Salt-Sensitive Hypertensive Rats

PLoS ONE ◽  
2014 ◽  
Vol 9 (9) ◽  
pp. e107888 ◽  
Author(s):  
Victoria L. Herrera ◽  
Julius L. Decano ◽  
Nicholas Giordano ◽  
Ann Marie Moran ◽  
Nelson Ruiz-Opazo
Keyword(s):  
Gene Expression ◽  
Blood Pressure ◽  
Arterial Stiffness ◽  
Pressure Rise ◽  
Regulator Gene ◽  
Hypertensive Rats ◽  
Blood Pressure Rise ◽  
Epigenetic Regulator ◽  
Carotid Arterial

Effect of potassium supplementation on blood pressure and vasodilator mechanisms in spontaneously hypertensive rats

1988 ◽  
Vol 75 (5) ◽  
pp. 527-534 ◽  
Author(s):  
Anne Barden ◽  
Lawrence J. Beilin ◽  
Robert Vandongen
Keyword(s):  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Hydrolysis Product ◽  
Pressure Rise ◽  
Plasma Renin ◽  
Renin Activity ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Potassium Supplementation ◽  
Blood Pressure Rise

1. Supplementation with 1% (w/v) KCl solution significantly attenuated the blood pressure rise with age normally observed in spontaneously hypertensive rats, resulting in a difference in blood pressure of 18 mmHg after 5 weeks. 2. Urinary 6-keto-prostaglandin F1α (the stable hydrolysis product of prostacyclin) and kallikrein excretion were significantly elevated in rats receiving potassium. 3. No difference was observed in sodium excretion during the initial days of potassium supplementation; however, the potassium-supplemented animals excreted relatively more sodium over the 5 week period. 4. Plasma renin activity was significantly reduced in those animals receiving potassium after 5 weeks. 5. It is proposed that a combination of increased systemic and/or renal prostacyclin and kallikrein synthesis may, in combination with reduced renin activity, contribute to the attenuation of blood pressure in potassium-supplemented spontaneously hypertensive rats.

scholarly journals Overexpression of proadrenomedullin N-terminal 20 peptide blunts blood pressure rise and attenuates myocardial hypertrophy and fibrosis in hypertensive rats

FEBS Letters ◽  
2005 ◽  
Vol 579 (22) ◽  
pp. 4997-5001 ◽  
Author(s):  
Yuan-Ning Cao ◽  
Kenji Kuwasako ◽  
Johji Kato ◽  
Kensaku Nishihira ◽  
Yujiro Asada ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Myocardial Hypertrophy ◽  
Pressure Rise ◽  
Hypertensive Rats ◽  
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.

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