l-proline supplementation improves nitric oxide bioavailability and counteracts the blood pressure rise induced by angiotensin II in rats

Nitric Oxide ◽  
2019 ◽  
Vol 82 ◽  
pp. 1-11 ◽  
Author(s):  
Joana Leal ◽  
Luísa Teixeira-Santos ◽  
Dora Pinho ◽  
Joana Afonso ◽  
Jorge Carvalho ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressure Rise ◽  
Blood Pressure Rise ◽  
Nitric Oxide Bioavailability

Effect of noradrenaline, vasopressin and angiotensin II on renal prostaglandins in man

1986 ◽  
Vol 70 (4) ◽  
pp. 371-377 ◽  
Author(s):  
Richard Loup ◽  
Laurent Favre ◽  
Michael B. Vallotton
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Urinary Excretion ◽  
Pressure Rise ◽  
Ang Ii ◽  
Weak Correlation ◽  
Renal Vasoconstriction ◽  
Blood Pressure Rise ◽  
Renal Prostaglandins ◽  
Healthy Female

1. To examine the response of renal prostaglandins (PG) to systemic and renal vasoconstriction noradrenaline (NA), arginine vasopressin (AVP) and angiotensin II (ANG II) were each infused into eight healthy female subjects for 3 h on different days. Urinary excretion of PGE2, PGF2α and 6-keto-PGF1α was determined hourly. 2. NA and ANG II stimulated excretion of PGF2α significantly, but not of PGE2 or 6-keto-PGF1α AVP stimulated renal PGF2α and 6-keto-PGF1α significantly, but not PGE2. 3. A weak correlation was found between urinary PGF2α and diastolic blood pressure during NA and ANG II infusions, but not during AVP infusion. 4. The release of renal PG does not appear to constitute an obligatory and concomitant response to the blood pressure rise induced by the pressor agonists. The greater response of PGF2α than of PGE2 may result from a preferential direct effect on PGF2α secretion or from an increased conversion of PGE2 into F2α.

Depletion of Resistance Vessel Polyamines Attenuates Angiotensin II Induced Blood Pressure Rise in Rats

1996 ◽  
Vol 18 (6) ◽  
pp. 811-830 ◽  
Author(s):  
Jamila Ibrahim ◽  
Alun D. Hughes ◽  
Michael Schachter ◽  
Peter S. Sever
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Pressure Rise ◽  
Resistance Vessel ◽  
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.

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