The effect of potassium on the tone of isolated arteries

Konold, P.; Gebert, G; Brecht, K.

doi:10.1007/bf00362638

Cited by 48 publications

(19 citation statements)

References 14 publications

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“…The direct effects of elevated potassium concentration on vascular smooth muscle appear to result from two separate actions of this ion: the well-known depolarizing effect and a second, hyperpolarizing effect resulting from stimulation of an electrogenic pump. The net effect of potassium on the smooth muscle cell has, in fact, been interpreted quantitatively as the sum of opposing actions of the ion (27,30,39). In support of this concept is the fact that the vascular smooth muscle relaxation induced by potassium can be eliminated or converted to a constriction by the administration of ouabain (10,12,25).…”

Section: Dulingmentioning

confidence: 99%

“…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.…”

mentioning

confidence: 99%

“…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)(27)(28)(29)(30)(31)(32) and in vivo (10).…”

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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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Section: Dulingmentioning

confidence: 99%

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confidence: 99%

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confidence: 99%

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Effects of potassium ion on the microcirculation of the hamster.

Duling¹

1975

Circulation Research

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“…It is likely that the response we observed is, at least in part, independent of local neural structures (20), because in the dog the response is not blocked by phentolamine or nerve section (3). Furthermore, the response is observed in vitro and is not blocked by tetrodotoxin (18).…”

Section: Resultsmentioning

confidence: 74%

“…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%