Rhythmic activity in smooth muscle from small subcutaneous arteries

Johansson, Björn; Df, Bohr

doi:10.1152/ajplegacy.1966.210.4.801

Cited by 112 publications

(42 citation statements)

References 6 publications

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“…Unlike most arterial preparations, it is a spontaneously active tissue, and in this respect, it may well resemble the smaller blood vessels (Johansson & Bohr, 1966). It also differs from arterial preparations in its sensitivity to drugs; for instance histamine, 5-hydroxytryptamine, bradykinin and angiotensin all have relatively feeble effects when compared to the catecholamines.…”

Section: Discussionmentioning

confidence: 99%

An Analysis of the Responses of the Isolated Portal Vein of the Rabbit to Electrical Stimulation and to Drugs

Hughes

Vane

1967

British Journal of Pharmacology and Chemotherapy

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Transmural electrical stimulation has been used to investigate responses of isolated intestinal smooth muscle preparations to nerve stimulation (Paton, 1955;Day & Vane, 1963;Paton & Vane, 1963;Birmingham & Wilson, 1965;Burnstock, Campbell & Rand, 1966). Paterson (1965) stimulated isolated arterial strips transmurally and showed that the ensuing contractions were probably caused by excitation of post-ganglionic adrenergic neurones in the vessel wall.Isolated venous muscle reacts to drugs (Franklin, 1925;Sutter, 1965) but little is known about its response to electrical excitation. We have, therefore, investigated the effects of transmural stimulation on the portal vein of the rabbit; the results show that this tissue has an innervation which can cause both excitatory and inhibitory effects. In addition, there is a non-adrenergic non-cholinergic inhibitory innervation. METHODSMale albino rabbits weighing 2-3 kg were killed by breaking the neck. The abdomen was opened and the portal vein was exposed and cleared of surrounding tissue. The length of portal vein, starting at the junction of the splenic and the superior mesenteric veins and ending at its bifurcation into right and left branches, was cut out and washed in cold Krebs solution. The vein was opened along its longitudinal axis to form a flat strip of tissue 3-4 cm long. Threads were attached to each end, and the strip was suspended vertically in a 50 ml. organ bath containing Krebs solution at 37' C, gassed with 95% oxygen and 5% carbon dioxide. The lower end of the strip was tied to a glass rod, while the upper end was attached to an isometric transducer (tensile sensor, Type S.T.I. Ether-Langham Thompson Ltd.). The transducer formed part of a bridge circuit, the output of which was recorded on a potentiometric millivolt recorder (Texas Instruments ServoRiter) through suitable attenuation. To stimulate the isolated vein, two pairs of parallel platinum wires, 3 cm long, were mounted longitudinally on opposite internal faces of a Perspex cylinder 4 cm long and 1 cm internal diameter. The cylinder was fixed in the organ-bath and the vein was suspended within it. Thus the electrodes lay parallel to the vein on each side of it but not touching it. For transmural stimulation, two stimulators with identical outputs were connected in parallel, in order to give sufficient power output to ensure maximal excitation.The vein was stimulated with rectangular pulses of 0.5-1 msec duration and full voltage output from the stimulators (80 V). Stimulus frequencies varying from 15/min to 50/sec were used. It was

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Section: Discussionmentioning

confidence: 99%

An Analysis of the Responses of the Isolated Portal Vein of the Rabbit to Electrical Stimulation and to Drugs

Hughes

Vane

1967

British Journal of Pharmacology and Chemotherapy

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“…Many investigators have shown that potassium at the increased concentrations observed in venous blood during exercise and hypoxia can relax smooth muscle both in vivo (5)(6)(7)(8)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) and in vitro (21)(22)(23)(24)(25)(26)(27)(28)(29)(30)(31). Therefore, this ion.…”

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confidence: 99%

Effects of potassium ion on the microcirculation of the hamster.

Duling¹

1975

Circulation Research

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The vasoactive properties of potassium were assessed in the microcirculation of the hamster cremaster muscle and the muscular and epithelial portions of the hamster cheek pouch. Tissues were transilluminated and suffused with a physiological salt solution whose potassium concentration varied from 0 to 20 mM. Vessel diameters were measured and normalized as a percent of the control diameter (± SE) observed during exposure to 4.7 mM K + . Altering the potassium concentration in the suffusion solution caused a transient vascular response. The peak changes in the vascular diameter of the arterioles supplying striated muscle varied directly with the suffusion solution potassium concentration from a minimum of 78 ± 3% in 0 mM K + to 155 ± 15% in 15 mM K". Vascular diameter increases were sustained for the full 5-minute test period only in 15 mM K+. In the epithelial portions of the cheek pouch, only the constrictor component of the potassium response was observed. The data indicate that potassium is sufficiently potent to participate in initiating functional hyperemia in striated muscle and might cause as much as a 6.3-fold increase in flow. Functional hyperemias exceeding approximately 3 minutes cannot be due to potassium ion, since the dilation induced by this agent is transient.• Cells contain a large store of labile potassium that can be released by various stimuli such as muscle contraction and hypoxia (1-9). Many investigators have shown that potassium at the increased concentrations observed in venous blood during exercise and hypoxia can relax smooth muscle both in vivo (5)(6)(7)(8)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19)(20) and in vitro (21-31). Therefore, this ion. may be important in the local control of blood flow. However, further quantification of the reactivity of resistance vessels to the ion must be carried out before accurate estimates of the importance of potassium in blood flow regulation can be made. These data can be obtained by studying microvessel responses to alterations in suffusion solution potassium concentrations, but such experiments have only been performed on pial vessels (11,16,17). Furthermore, no data are currently available showing the temporal response pattern of microvessels during variations in potassium concentration. These data are of particular interest in view of the transient potassium ion release during functional hyperemia in striated muscle (7,8) and the transient vascular smooth muscle response to potassium both in vitro (26-32) and in vivo (10). A preliminary report of this work was presented at the Fall Meeting of the American Physiological Society, August, 1974. This work was done during Dr. Duling's tenure as an Established Investigator of the American Heart Association.Received September 20, 1974. Accepted for publication June 4, 1975. I have therefore studied the responses of the arterioles of the hamster cremaster muscle and cheek pouch to changes in the potassium concentration of a superfusion solution. The aims of the experiment were to: (1) estab...

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“…Because there is evidence that the magnitude of vascular response (-AR) to K+ is a function of the 1.7 (8) 139.3±1.6 (17) [Ca++], meq/liter 3.7+0.1 (22) 3.9i0.1 (8) 3.7+0.1 (18) [Mg++], meq/liter 1.8240.02 (22) 1.8540.12 (8) 1.85±0.06 (18) Hct, ml/100 ml 42.1+0.5 (74) 42.840.9 (24) 42.8+0.8 (25) 43.241.1 (25) Means±SEM; number of observations indicated in parentheses. Because there were significant correlations between IR and AR and because IR was significantly greater in hypertensives than in normotensives, we also compared responses in hypertensives and normotensives by using analysis of covariance, which adjusted responses for their regression on initial resistance.…”

Section: Resultsmentioning

confidence: 99%

“…These observations have naturally led us to speculate that there may be an underlying defect in Na+-K+-ATPase enzyme systems in vascular smooth muscle in renal hypertensives (9). Such a defect could decrease the activity of the cellular electrogenic pump, tending to depolarize cell membranes, either generally, or in specific "pacemaker" cells (25). Membrane depolarization might account for the impaired vascular relaxation and decreased stimulatory thresholds (26) in hypertension.…”

Section: Resultsmentioning

confidence: 99%