The immediate cardiovascular responses on active change from the squatting (control) to the standing position differ from those obtained in the lying-to-standing manoeuvre. Without exception, the first beat after changing from squatting to standing showed a decrease in systolic, diastolic and mean pressure by 2.0 +/- 1.1 kPa (14.6 +/- 8.3 mm Hg), 1.4 +/- 1.7 kPa (10.6 +/- 12.6 mm Hg) and 1.9 +/- 1.0 kPa (13.9 +/- 7.3 mm Hg), respectively. During the 4th or 5th pulse after standing the pulse pressure was significantly higher than when lying (P less than 0.01). Mean pressure reached a minimum of 7.7 +/- 1.9 kPa (57.8 +/- 14.4 mm Hg) after 7.1 +/- 1.1 s. Thereafter the blood pressure increased to a new level within about 15 s. 11 of 16 subjects demonstrated a biphasic heart rate (HR) response. The maximum HR was reached after 11.0 +/- 2.4 s of standing. In all experiments, the peaks in HR were distinctly delayed after the blood pressure dips. We conclude that an arterial baroreflex could be implicated in the immediate HR increase after a squatting-to-standing manoeuvre. The subsequent time course of the initial HR response, however, might be induced by other mechanisms.
With continuous perfusion at transmural pressures of 0.1 and 0.5 kPa, beta-homobetaine methylester (HBM) decreased the rate of spontaneously beating atria significantly with an ED50 of about 5 X 10(-6) mol/l. The dose-dependent decrease in the atrial rate was stronger at an intraluminal pressure of 0.5 kPa, at this pressure the dose-response curve sloped more steeply. The stretch acceleration of the atrial rate was also significantly inhibited by HBM. In comparison with acetylcholine, the HBM was over 10 times more effective. Atropine blocked the interactions of the HBM with the muscarinic cholinergic receptors of the pacemaker cells.
The initial heart rate response to rapid passive changing of posture was analysed in 43 normal subjects. The tilting (mean tilt time: 1.7 s) was applied during expiration or inspiration. As compared to inspiration, the 70 degrees head-up tilt during expiration resulted in significantly higher values of heart rate increase and longer duration of the "initial complex", i.e. the immediate increase and the following decrease of heart rate to a minimum after tilting. The heart rate response to tilting from erect to supine position was not symmetrical to that during head-up tilt: at first the heart rate increased, about 6 s after the change of body position heart rate decreased suddenly, mostly below the recumbent control value, which was attained again after about 20-30 s. The distinct initial heart rate response to the head-up tilt probably can be explained in part by the hydrostatically caused drop of the mural pressure at the level of carotid artery and the different sensitivity of arterial baroreflex during the respiratory cycle. Other mechanisms, e.g. the participation of chronotropic autoregulation are discussed.
With continuous perfusion at defined intraluminal pressures of 0.1 and 0.5 kPa, the effect of the calcium ion antagonist verapamil on the chronotropic autoregulation mediated by stretch was investigated in right atrial preparations. At both intraluminal pressures verapamil at a concentration of 4 X 10(-7) mol/l decreased the atrial rate progressively with increasing duration of verapamil perfusion. Time-dependent the stretch acceleration was also inhibited significantly at 50-72% of the control values. The findings of the present study support the hypothesis of the participation of a calcium current in the origin of stretch-induced chronotropic autoregulation.
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