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The effects of the ionophore, RO 2-2985 (X537A, RO) were studied on isolated coronary, renal and femoral arteries in two types of experiments: (1) the effect of RO as a modulator of various contractile effects of KCl and phenylephrine (PE), and (2) the effect of RO itself as a contractile agonist. The effect of the ionophore A23187 was observed in similar experiments to help determine the nature of the RO response. In the first type of experiment, RO was found to have a differential effect upon the arteries contracted with KCl. The coronary arteries relaxed upon addition of the ionophore, whereas, the femoral and renal arteries did not. A23187 had only a transient effect on KCl-contracted coronary arteries. RO relaxed femoral and renal arteries contracted with PE, and A23187 had only a transient effect. RO attenuated ED50 values and maximum tension developments to both KCl and PE, and A23187 had no effect on these parameters. In the second type of experiment, RO (only at 10-5 M) was found to contract femoral and coronary arteries, but had no effect on renal arteries. Experiments with alpha-blocking agents and calculations using association constants of RO for catecholamines suggest that RO is not acting via catecholamine chelation. The dissimilarity between the effects of RO and A23187 suggest that RO may not be working through a specific effect on Ca++. These differential responses to RO suggest variations in intervessel regulation of PE- AND KCl-induced contradictions and can explain, in part, the in vivo effects of RO on regional blood flow.

The purpose of this work was to test the hypothesis that stress relaxation (SR) in vascular smooth muscle is related to the amount of contractile activity (developed stress) and perhaps a property of the contractile element (CE). Using medial-intimal strips from the hog carotid artery, a strain (delta 1/l0, where l0 equals optimal length for force development) of 2% was applied at two different rates in the presence of various levels of developed or passive stress. Developed stress was altered either by changing the extracellular K-ion concentration with the strip length equal to l0 or by stimulating with a salt solution containing 30 mM KCl at various strip lengths. Passive stress was altered by varying strip length. At each level of developed or passive stress the magnitude of the increment in stress due to the strain (induced stress) and the SR were noted. SR varied directly with the magnitude of the developed stress, but there was a small and relatively unchanging amount of SR when passive stress was varied. At a given level of developed stress, the magnitude of SR was greater at a strain rate of 0.016 than at 0.001 l0/sec. When developed stress was altered, the magnitude of SR was essentially equal to the amount of induced stress; however, when passive stress was varied, SR was always less than induced stress. These observations are consistent with the hypothesis that, in the presence of developed stress, a large fraction of the SR represents the lengthening of the CE. This increased CE length allows a reequilibration of stress between the series elastic element and the contractile element. In the absence of developed stress, SR may represent a passive, physical property of this heterogeneous tissue.

It has been reported by several investigators that the maximum active force generating ability (i.e., force/tissue cross-sectional area) of the aorta increases as the animal matures and then declines later in life. The purpose of this work was to determine if changes in the actomyosin content of the aorta occur during maturation which could contribute to the observed changes in force generating ability. The actin and myosin contents of rat thoracic aorta obtained from animals 3, 5, 7, 16 and 43 weeks of age were determined by quantitative gel electrophoresis, and were normalized with respect to tissue mass and protein and DNA contents. The results indicate that the amount of actomyosin (i.e., actin + myosin heavy chains) per tissue mass, protein and DNA increases rapidly during the first 5 weeks after birth and then remains constant. These observations suggest that the increasing actin and myosin heavy chain content of aorta observed early in life could explain in part the increasing force generating ability reported during this period, but that a loss of contractile material is not responsible for the reduction in force generating ability seen later in life.