The Autoregulation of Blood Flow through Organs

Clinical Science (1971) 40, 1 ~ 8 ~ .
MEDICAL RESEARCH SOCIETY
The Annual General Meeting of the Medical Research Society was held on 11-12 December
1970, at the Hammersmith Hospital. The following Symposium was held and Communications and Demonstrations given:
SYMPOSIUM ON AUTOREGULATION
Chairman: M. FLOYER,
Medical Unit, LondonHospital
A. VASCULAR SMOOTH MUSCLE I N
EXPERIMENTAL HYPERTENSION
D. F. BOHR,M. D. S
~ andNT. R. HANSEN
Department of Physiology, University of Michigan,
Ann Arbor
One of three mechanisms may cause the increase in
total peripheral resistance of chronic experimental
hypertension: (1) structural changes in the vessel wall
that encroach on the lumen; (2) increase in extrinsic
activation of vascular smooth muscle (humoral or
neurogenic); or (3) intrinsic change in vascular
smooth muscle responsiveness. In the current work
the possibility of an intrinsic change was studied in
isolated vascular smooth muscle from rats with DCA
hypertension. This muscle was found to be more
responsive than that from control rats to all agents
which caused vasoconstriction. Vascular smooth
muscle from the hypertensive rat was particularly
responsive to smallincreases incalciumconcentration.
In a preliminary experiment the increased responsiveness was found to be present in vascular smooth
muscle above aortic coarctation but not in that from
a vessel below the coarctation. This observation
suggests that the increase in responsiveness of vascular smooth muscle in experimental hypertension
may be secondary to the increase in wall tension.
viewed under which this mechanism appears to
operate.
The calibre of a vessel may be determined by,
amongst other factors, the concentration of local
vasodilator metabolites and by local mechanical
forces. Both may play a part in autoregulation.
Alterations in the local concentration of vasoactive
metabolites which follow a change in blood flow,
metabolism being unchanged, may lead to adjustments of vessel calibre and the return of flow to the
original level (Haddy & Scott, 1968, Physiologicd
Reviews, 48,688). The calibre will also be determined
by the balance between the two opposing forces
acting on the vessel wall, namely the balance between
the circumferential wall tension and the transmural or
distending pressure. Vascular smooth muscle contracts in response to passive stretching (Johannson &
Bohr, 1966,American Journal of Physiology, 210,801).
It is possible that the local vascular control which
occurs in response to changes in distending pressure is
achieved because of a myogenic reaction of the blood
vessels. This reaction has been investigated in man by
changing perfusion pressure and by local exposure of
a limb to subatmospheric pressure (Greedeld, 1964,
Circulation Research, Suppl. 1, 70; Mellander, Oberg
& Odelram, 1964,Acta Physiologica Scandinavica, 61,
34; Ardill, Fentem, Findlay & Isaac, 1969,Journalof
Physiology, 203, 31; Fentem & Matthews, 1970,
Journal of Physiology, 210, 65~).
Some of the authors’ work was supported by a grant
from the British Heart Foundation.
C. THE NATURE OF THE INCREASED
PERIPHERAL RESISTANCE I N
HYPERTENSION
B. THE AUTOREGULATION OF BLOOD
FLOW THROUGH ORGANS AND TISSUES
J. CONWAY
P. H. FENTEM
and A. D. M. GREEN~ELD
Department of Medicine, Georgetown University, and
V.A. Hospital, Washington D.C., U.S.A.
Department of Physiology, The Medical School, The
University of Nottingham, Nottingham NG7 2RD
The blood flow through various organs and tissues is,
under many conditions, maintained relatively constant despite variations in perfusion pressure. This
autoregulation of blood flow must generally depend
upon adjustments of the calibre of resistance blood
vessels (Mellander & Johannson, 1968, Pharmacological Reviews, 20, 117). The conditions will be re-
Although an increased peripheral resistance is present
in all but the earliest stages of hypertension, the nature
of the change in the vascular tree which might be
responsible €or it has not been elucidated. While an
increase in vascular smooth muscle tone has commonly been assumed to be present, evidence from
three different experimental situations suggests that
this is not so.
First, the level of resistance after maximal dilatation
in the forearm (Folkow, Grimby & Thulesius, 1958,
1P