Dose-response curves were obtained from dog anterior tibial artery rings at various lengths (L) to determine whether sensitivity to norepinephrine (NE) and potassium (K+) depends on arterial circumference. The dose for half maximal response (ED50) was determined by graphical estimation and by calculation from a best fit curve. For both NE and K+: 1) ED50 was lowest (most sensitive) at L for maximum active force (Lmax) and increased significantly as L decreased from Lmax; 2) ED50 at 1.0 and 1.15 Lmax was not significantly different; 3) ED50 of repeated dose-response curves at Lmax was not significantly different; and 4) when the direction of length change was reversed (from decreasing to increasing), the direction of change in ED50 was also reversed (from increasing to decreasing). Change in the dose for 10% maximal response was the same as ED50. The results did not depend on the method of determining ED50 or on whether responses were expressed as absolute values or as relative values. The results show that sensitivity of vascular smooth muscle depends on L and that the length-sensitivity relation is similar to the length-active tension relation. Similarity of results for NE and K+ indicate that length-dependent sensitivity does not depend on the method of stimulation.
Previous work has shown that vascular smooth muscle sensitivity depends on muscle length (arterial circumference) at lengths equal to and less than that for maximum active force (Lmax). In the present study dose-response curves were obtained from dog anterior tibial artery rings at lengths equal to or longer than Lmax. The curves were compared with dose-response curves obtained at lengths less than Lmax. The agonist concentration for half maximal response (ED50) was determined by graphical estimation and by calculation from a best-fit curve. The results show that with norepinephrine (NE) stimulation 1) ED50 decreased significantly at each step when the rings were stretched from Lmax to 1.15 Lmax and then to 1.30 Lmax; 2) ED50 increased significantly when length was decreased from 1.15 to 1.00 Lmax; 3) ED50 decreased significantly at each step when the rings were stretched from 0.70 Lmax to Lmax and then to 1.30 Lmax; and 4) for NE concentration greater than the ED50 at Lmax, active stress was significantly higher at Lmax than at 0.70 Lmax or 1.30 Lmax. For an NE concentration less than the ED50 at Lmax, the active stress at 1.30 Lmax was higher than the active stress at Lmax and at 0.70 Lmax. The results show that sensitivity of vascular smooth muscle continually increases with stretch and does not have a maximum at the length for maximum active force.
The production of constrictive responses limited to either arterial or venous segments of the vasculature of the dog paw was tested by stimulating various peripheral nerves of the hind leg. Resistance changes of the total vasculature of the paw, and of three of its component series-coupled segments (arterial, small vessel, and venous) were studied sequentially before and during stimulation of the sciatic nerve and of three of its branches (tibial, deep, and superficial fibular nerves). Stimulation characteristics (15 to 90 volts, 1-3 msec duration, 25/sec, and 30-second stimulation periods) were chosen to produce maximum vasoconstrictive responses. Tibial and deep fibular nerve stimulations produced constriction of the arterial segment but not of the venous segment. Superficial fibular nerve stimulation produced constriction of the venous segment but not of the arterial segment. All nerve stimulations produced constriction of small blood vessel segments. Thus, responses could be limited to either arterial (plus small vessel) or venous (plus small vessel) segments. Inability to localize response within small-vessel segments made it impossible to determine whether any peripheral nerve produced constrictive responses limited strictly to either pre-or postcapillary segments. No relationship was evident between control resistance values and the subsequent changes in resistance occurring in response to the standard stimulations.
Dog gracilis muscles were removed, enclosed in a plethysmograph and perfused at an inflow pressure of 110 mm Hg. Venous outflow pressure was 3 mm Hg. Circulating blood volumes were measured by the constant infusion technique using RBC-51Cr (9 muscles) or albumin-131I (11 muscles). Volumes were calculated from the infusion and from the washout of the indicator. Skeletal muscle contraction was produced by stimulation of the gracilis nerve stump with supramaximal stimuli at 2-15 Hz for 15-60 sec. Volume changes during and following the stimulations were measured by plethysmography and by changes in total muscle radioactivity. Inflow and outflow were also measured. Changes in interstitial fluid volume were calculated as the difference between total tissue and vascular volume changes. Blood volume increased at all contraction rates. Total tissue volume initially decreased during the contraction period and then returned to control. Extravascular volume decreased markedly during the initial period of contraction and then increased above control, returning to the control level following the end of the stimulation. The tissue pressure markedly increased during the contractions causing fluid movement into the vascular system. Minimal loss of labeled albumin during the period of contraction indicated capillary permeability was not altered.
Small vessel pressures and flows and changes in volume of the dog hind paw were recorded simultaneously to study the responses to various rates of sympathetic stimulation. Although a progressive change in small vessel responses occurred as the stimulation frequency was increased, the responses could be grouped into three categories. At the lowest stimulation frequencies (1–2/sec, and less) the constrictor response was predominantly arteriolar. During the stimulation period metatarsal vein pressures and paw volumes did not exceed prestimulation levels. At stimulation frequencies of 1–2/sec to 15–20/sec an initial arteriolar constriction was followed by appreciable arterial and venous constriction. Increases in venous resistance, coupled with continued arterial inflow, produced increased paw volume and pooling of blood in minute vessels. At stimulation frequencies of 20–25/sec marked arterial and venous constriction occurred. Arterial inflow was stopped and paw volumes were decreased even though venous resistance was increased.
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