Rat venular pressure-diameter relationships are regulated by sympathetic activity.
The hypothesis that the pressure-diameter relationship of intestinal venules in rats is primarily determined by sympathetic nervous system activity was tested. The pressure-diameter relationship of the smallest to largest diameter (20-100 microns) intestinal venules of the rat was measured at rest, during hemorrhage to increase sympathetic neural activity, and during saline volume expansion to decrease sympathetic activity. During hemorrhage, the diameter of all venules decreased approximately 10% at 10 mmHg venous pressure, and the slope of the pressure-diameter relationship increased approximately 50% above control. Blood volume expansion led to an approximately 10% increase in venule diameter at 10 mmHg and a 25% decrease in slope. Denervation of the vessels causes concomitant vasodilation, which was greater than the vasodilation caused by blood volume expansion. Hemorrhage after denervation caused no significant changes in the relationship when compared with denervated control. Nitroprusside caused an even greater vasodilation when compared with the pressure-diameter relationship after denervation. The results suggest that the slope and 10-mmHg intercept of the pressure-diameter relationship for the largest through smallest intestinal venules and, therefore, their vascular compliance and capacitance characteristics are primarily determined by sympathetic activity.
Shoukas
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AA
Department of Biomedical Engineering, School of Medicine, Johns Hopkins University, Baltimore, Maryland 21205.
Bohlen
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HG
D000818:Animals; D001794:Blood Pressure; D003714:Denervation; D006470:Hemorrhage / Q000503:physiopathology; D007422:Intestines / Q000098:blood supply; D008297:Male; D008955:Models, Cardiovascular; D009599:Nitroprusside / Q000494:pharmacology; D010952:Plasma Substitutes / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012146:Rest; D012965:Sodium Chloride / Q000494:pharmacology; D013564:Sympathetic Nervous System / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects; D014680:Veins / Q000502:physiology*; D014699:Venules / Q000294:innervation / Q000502:physiology*
D010952:Plasma Substitutes; D009599:Nitroprusside; D012965:Sodium Chloride