scholarly journals Hypertension, transmural pressure, and vascular smooth muscle response in rats.

1975 ◽  
Vol 36 (5) ◽  
pp. 590-598 ◽  
Author(s):  
T R Hansen ◽  
D F Bohr
2013 ◽  
Vol 45 (2) ◽  
pp. 375-383 ◽  
Author(s):  
Zhaoxia Wang ◽  
Weidong Wu ◽  
Maoping Tang ◽  
Ying Zhou ◽  
Lianyun Wang ◽  
...  

1993 ◽  
Vol 73 (6) ◽  
pp. 1113-1120 ◽  
Author(s):  
L Stewart ◽  
C Hamilton ◽  
J Ingwall ◽  
S Naomi ◽  
S Graves ◽  
...  

1990 ◽  
Vol 259 (1) ◽  
pp. H29-H33 ◽  
Author(s):  
J. H. Lombard ◽  
H. Eskinder ◽  
K. Kauser ◽  
J. L. Osborn ◽  
D. R. Harder

The electrical and mechanical responses of vascular smooth muscle to norepinephrine were compared at three different levels of transmural pressure (60, 100, and 140 mmHg) in cannulated small arteries that were isolated from dog kidneys. Elevation of transmural pressure caused depolarization of the vascular smooth muscle and a significant increase in vessel sensitivity to norepinephrine. Norepinephrine produced less depolarization as transmural pressure was elevated. Comparison of the relationship between transmembrane potential and norepinephrine concentration at these different transmural pressures suggests that membrane depolarization contributes to, but is not the sole explanation of, the increased norepinephrine sensitivity at higher transmural pressures. The results of this study suggest that transmural pressure in a blood vessel may be an important determinant of its sensitivity to vasoactive agonists.


1987 ◽  
Vol 253 (4) ◽  
pp. F778-F781 ◽  
Author(s):  
D. R. Harder ◽  
R. Gilbert ◽  
J. H. Lombard

The goal of this study was to define some of the cellular and ionic mechanisms of smooth muscle cell activation in dog renal arteries exposed to physiological levels of transmural pressure. Isolated interlobular arteries were cannulated and connected to a pressure reservoir to allow manipulation of transmural pressure in 20-mmHg increment steps from 20 to 120 mmHg. As transmural pressure was increased, vascular smooth muscle exhibited a linear depolarization from an average resting potential of -57+/- 2 mV at 20 mmHg to -38+/- 2.4 mV at 120 mmHg. Spontaneous action potentials could often be recorded at pressures greater than 80 mmHg. These appeared to occur primarily at bifurcation points of branching arteries. Vascular smooth muscle depolarization and action potentials occurring in response to increases in transmural pressure were associated with a maintenance of internal diameter of the vessel segments despite increases in transmural pressure in the range between 60 and 120 mmHg. The “pressure-induced” activation of vascular smooth muscle contraction and spontaneous action potentials of small renal arteries at higher transmural pressures were blocked on Ca2+ channel inhibition with verapamil (10(-6) M). These data document a membrane ionic mechanism (probably increased Ca2+ influx) for pressure-induced myogenic activation of isolated renal arteries. It is interesting that the contraction of these vessels occurs over the pressure range in which autoregulation of renal blood flow normally occurs. The physiological significance of these responses needs to be determined.


1987 ◽  
Vol 252 (3) ◽  
pp. H671-H673 ◽  
Author(s):  
Z. S. Katusic ◽  
J. T. Shepherd ◽  
P. M. Vanhoutte

Stretch applied to isolated canine basilar arteries caused the development of active tension in rings with endothelium but not in those in which the endothelium had been removed. Blockade of calcium entry with diltiazem or inhibition of cyclooxygenase with indomethacin abolished the endothelium-dependent response to stretch. These observations suggest that the endothelium may contribute to the autoregulation of cerebral blood flow during increases in transmural pressure by the increased production and/or release of prostaglandins, which causes activation of the underlying vascular smooth muscle.


2016 ◽  
Vol 207 ◽  
pp. 154-159 ◽  
Author(s):  
Simona Punzi ◽  
Chiara Belloli ◽  
Marc Gogny ◽  
Jean-Claude Desfontis ◽  
Mohamed Y. Mallem

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