Effects of Bradykinin on Short-Term Variability in Blood Pressure and Heart Rate in Rats

1995 ◽  
Vol 25 (6) ◽  
pp. 914-923 ◽  
Author(s):  
Pascal Ponchon ◽  
Marie-Laure Grichois ◽  
Jean-Pierre Girolami ◽  
Jean-Luc Elghozi
1999 ◽  
Vol 17 (8) ◽  
pp. 1135-1143 ◽  
Author(s):  
P Verwaerde ◽  
J M. Sénard ◽  
M Galinier ◽  
P Rougé ◽  
P Massabuau ◽  
...  

1998 ◽  
Vol 8 (3) ◽  
pp. 181-186 ◽  
Author(s):  
Arlette Girard ◽  
François-Claude Hugues ◽  
Claire Le Jeunne ◽  
Jean-Luc Elghozi

1999 ◽  
Vol 96 (6) ◽  
pp. 613 ◽  
Author(s):  
Djillali ANNANE ◽  
Véronique BAUDRIE ◽  
Anne-Sophie BLANC ◽  
Dominique LAUDE ◽  
Jean-Claude RAPHAL ◽  
...  

2000 ◽  
Vol 278 (1) ◽  
pp. R215-R225 ◽  
Author(s):  
Ben J. A. Janssen ◽  
Peter J. A. Leenders ◽  
Jos F. M. Smits

Knowledge on murine blood pressure and heart rate control mechanisms is limited. With the use of a tethering system, mean arterial pressure (MAP) and pulse interval (PI) were continuously recorded for periods up to 3 wk in Swiss mice. The day-to-day variation of MAP and PI was stable from 5 days after surgery. Within each mouse ( n = 9), MAP and PI varied by 21 ± 6 mmHg and 17 ± 4 ms around their respective 24-h averages (97 ± 3 mmHg and 89 ± 3 ms). Over 24-h periods, MAP and PI were bimodally distributed and clustered around two preferential states. Short-term variability of MAP and PI was compared between the resting (control) and active states using spectral analysis. In resting conditions, variability of MAP was mainly confined to frequencies <1 Hz, whereas variability of PI was predominantly linked to the respiration cycle (3–6 Hz). In the active state, MAP power increased in the 0.08- to 3-Hz range, whereas PI power fell in the 0.08- to 0.4-Hz range. In both conditions, coherence between MAP and PI was high at 0.4 Hz with MAP leading the PI fluctuations by 0.3–0.4 s, suggesting that reflex coupling between MAP and PI occurred at the same frequency range as in rats. Short-term variability of MAP and PI was studied after intravenous injection of autonomic blockers. Compared with the resting control state, MAP fell and PI increased after ganglionic blockade with hexamethonium. Comparable responses of MAP were obtained with the α-blocker prazosin, whereas the β-blocker metoprolol increased PI similarly. Muscarinic blockade with atropine did not significantly alter steady-state levels of MAP and PI. Both hexamethonium and prazosin decreased MAP variability in the 0.08- to 1-Hz range. In contrast, after hexamethonium and metoprolol, PI variability increased in the 0.4- to 3-Hz range. Atropine had no effect on MAP fluctuations but decreased those of PI in the 0.08- to 1-Hz range. These data indicate that, in mice, blood pressure and its variability are predominantly under sympathetic control, whereas both vagal and sympathetic nerves control PI variability. Blockade of endogenous nitric oxide formation by N G-nitro-l-arginine methyl ester increased MAP variability specifically in the 0.08- to 0.4-Hz range, suggesting a role of nitric oxide in buffering blood pressure fluctuations.


2004 ◽  
Vol 22 (Suppl. 2) ◽  
pp. S206
Author(s):  
J. Freitas ◽  
R. Santos ◽  
E. Azevedo ◽  
M. Carvalho ◽  
C. Abreu-Lima ◽  
...  

1999 ◽  
Vol 96 (6) ◽  
pp. 613-621 ◽  
Author(s):  
Djillali ANNANE ◽  
Véronique BAUDRIE ◽  
Anne-Sophie BLANC ◽  
Dominique LAUDE ◽  
Jean-Claude RAPHAËL ◽  
...  

The effect of Guillain-Barré syndrome (GBS) on the short-term variability of blood pressure and heart rate was evaluated in six patients presenting with a moderate form of the syndrome, i.e. unable to stand up unaided and without respiratory failure, at the height of the disease and during recovery. The patients were compared with six age-matched healthy volunteers. During the acute phase of the syndrome, GBS patients exhibited a significant heart rate elevation (+26 beats/min compared with healthy subjects), but the acceleratory response to atropine, or to 60 ° head-up tilt, was maintained. Resting plasma noradrenaline levels were high in acute GBS, but the secretory response to tilt was preserved. Desensitization to noradrenaline was observed in acute GBS with a reduced pressor action of this α-adrenoceptor agonist. Blood pressure levels were normal and head-up tilt did not induce orthostatic hypotension in this moderate form of GBS. Power spectral analysis demonstrated marked alterations in cardiovascular variability. The overall heart period variability was markedly reduced with the reduction predominantly in the high-frequency (respiratory) range (-73%). The low-frequency component of heart period variability was also reduced (-54%). This cardiovascular profile of moderate GBS at the height of the disease could result from a demyelination of the reflex loop controlling respiratory oscillations in heart rate and from a desensitization of the arterial tree to an elevated plasma noradrenaline. Sympathetic nervous activation may contribute to the high resting heart rate in acute GBS.


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