Summary. The functional importance of an increased wall/lumen ratio due to e. g. hypertrophy of the walls of the resistance vessels in hypertensive disease has been dealt with. Ito is theoretically highly probable that the mere existence of an increased wall mass must cause a proportionally bigger lumen decrease for a given smooth muscle shortening, so that a structurally based “potentiation” of the vasoconstrictor reeponse is obtained. For this reason a given level of smooth muscle tone will probably result in a higher flow resistance in hypertensive disease, where vascular wall hypertrophy has taken place, as compared with the normal vascular bed, provided that the maximally dilated vessels do not show an increase of the lumen as a result of the hypertrophic change. Experimental evidence suggests that this is not the case; if anything the maximally dilated resistance vessels seem to be slightly narrowed in cases of well‐established essential hypertension. In addition it is pointed out that a primary increase of pressure may in many haemodynamically important regions raise the vascular tone, simply due to some strictly local influences on the resistance vessels, where no engagement of specific vasoconstrictor agents or increased smooth muscle sensitivity is implied. Such more chronic and acute secondary consequences of a primary rise of blood pressure may importantly contribute to the increased flow resistance, and possibly most, so in so‐called essential hypertension.

The present study compared the haemodynamic pattern of active and passive standing. We used non-invasive techniques with beat-to-beat evaluation of blood pressure, heart rate and stroke volume. Seven healthy subjects, aged 24-41 (mean 30) years were examined. Finger blood pressure was continuously recorded by volume clamp technique (Finapres), and simultaneous beat-to-beat beat stroke volume was obtained, using an ultrasound Doppler technique, from the product of the valvular area and the aortic flow velocity time integral in the ascending aorta from the suprasternal notch. Measurements were performed at rest, during active standing and following passive tilt (60 degrees). Active standing caused a transient but greater reduction of blood pressure and a higher increase of heart rate than passive tilt during the first 30s (delta mean blood pressure: -39 +/- 10 vs. -16 +/- 7 mmHg, delta heart rate: 35 +/- 8 vs. 12 +/- 7 beats m-1 (active standing vs. passive tilt; P < 0.01). There was a significantly larger increase in cardiac output during active standing (37 +/- 24 vs. 0 +/- 15%, P < 0.01) and a more marked decrease in total peripheral resistance (-58 +/- 11 vs. -16 +/- 17%, P < 0.01). A precipitous rise in intra-abdominal pressure (43 +/- 22 mmHg) could be observed upon rising only in active standing. This was interpreted as an indication of translocation of blood to the thorax. There was no significant difference in haemodynamic changes during the later stage of standing (1-7 min) between both manoeuvres. These results suggest that active standing causes a marked blood pressure reduction in the initial phase which seems to reflect systemic vasodilatation caused by activation of cardiopulmonary baroreflexes, probably due to a rapid shift of blood from the splanchnic vessels in addition to the shift from muscular vessels associated with abdominal and calf muscle contraction. Moreover, the ultrasound Doppler technique was found to be a more adequate method for rapid beat-to-beat evaluation of cardiac output during orthostatic manoeuvres.

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