Membrane electrical effects of histamine on vascular smooth muscle of canine coronary artery.

Outward membrane currents were characterized in single coronary smooth muscle cells of adult beagle dogs. The cells averaged 96.4 x 7.1 microns and had a resting potential of -50.7 mV, an input resistance of 307.9 M omega, a capacitance of 32.3 pF, and a calculated membrane surface area of 4,037 microns2. The cells contracted in response to external application of acetylcholine or high K+. In voltage clamp by use of the suction pipette method, outward current began to appear at -50 mV and reached 15.2 nA at 50 mV with a current density of 376.5 microA/cm2. The current was reduced by external tetraethylammonium, Ba2+, and internal Cs+, and its reversal potential had a Nernst relation to external K+ concentration. Elevation of external Ca2+ (Ca2+o) from 0 to 0.3 mM increased total K+ current by up to 300%; elevation of internal Ca2+ (Ca2+i) to 5 x 10(-7) M by internal perfusion increased total outward current to a similar extent, suggesting a large difference in Ca2+ transmembrane sensitivity. Total whole-cell K+ current consisted of two components: an initial time-independent current (Ii) followed by a time-dependent current (It). Ii and It were through separate K+ channels based on differences in a) sensitivity to Ca2+09b) modulation by an inward Ca2+ current, c) current amplitudes and activation kinetics, and d) responses to pharmacological agents. It was the largest component, measuring 4.5 nA in 0 mM Ca2+o but increasing to 11.9 nA in 0.3 mM Ca2+o with a steep 2.5 power function. It activated with a biexponential time course; in Ca2+o-free solution, its time course was relatively insensitive to voltage changes but became voltage sensitive in the presence of Ca2+o. Further, such sensitivity was abolished or enhanced by Co2+ or Bay K 8644, respectively. We concluded that there are two types of Ca2+-sensitive K+ currents, Ii and It, in coronary smooth muscle cells. Via an inward Ca2+ channel Ca2+o strongly modulates It, both in amplitude and kinetics.

Section: Outward Potassium Currents In Freshly Isolated Smooth Musclementioning

confidence: 88%

Outward potassium currents in freshly isolated smooth muscle cell of dog coronary arteries.

Wilde

Lee

1989

“…Histamine stimulation of arterial smooth muscle usually causes an initial rapid phase of contraction thought to correspond to the release of Ca ++ from internal stores, and a slower tonic phase thought to reflect the entry of Ca ++ from the extracellular space (Hudgins and Weiss, 1968;Watkins and Davidson, 1980 (Harder, 1980 ] o , was less than 1.2 ITIM. Potassium-free solutions usually depolarize vascular smooth muscle, whether through inhibition of an electrogenic Na-K pump, a decrease in potassium conductance, or indirectly, through norepinephrine release from nerve endings (for a review, see Hermsmeyer, 1983).…”

Section: Discussionmentioning

confidence: 99%

Histamine-induced rhythmic contraction of hog carotid artery smooth muscle.

Stein¹,

Driska²

1984

SUMMARY. Smooth muscle strips isolated from the hog common carotid artery can contract rhythmically, exhibiting low frequency, large amplitude oscillations in tension when stimulated with 10 IIM histamine. Strips required at least 1.45 ITIM calcium and 2.5 mM potassium to exhibit this rhythmic activity. Rhythmic contractions could be converted to tonic contractions by removal of potassium or ouabain treatment. Relaxation by 2 mM lanthanum, 1 mM manganese, or 1 fiM verapamil implies that the external medium is the source of calcium mediating the contractions. The involvement of adrenergic nerve terminals in this response was ruled out, since propranolol, phentolamine, tetrodotoxin, bretylium, or 6-hydroxydopamine treatment did not alter the oscillations. Blockade of H! receptors with 0.1 HM diphenhydramine relaxed the muscle strips. The H 2 receptor antagonist cimetidine (5 fiM) had no effects. Attempts to obtain rhythmic contractions by stimulating with other vasoactive agents (norepinephrine, acetylcholine, 5-hydroxytryptamine, angiotensin II, and elevated potassium concentrations) were unsuccessful, suggesting that this is a specific histamine response mediated solely by Hi receptors. These results show that this large artery, commonly considered a multi-unit smooth muscle, can sometimes exhibit single-unit behavior. (CircRes 55: 480-485, 1984)

“…Apparently, high-K + per se does not inhibit aerobic glycolysis as long as [Na + ]0 is not reduced. While the addition of histamine to K + -substituted saline (reduced [Na + ] o ) stimulates aerobic glycolysis, this could nonetheless be an effect of [Na + ]0, since histamine has been suggested to increase membrane permeability to Na + , as well as Ca ++ and K + (Casteels and Suzuki, 1980;Harder, 1980). The Ca ++ -sensitive excess ATPase induced by histamine might then reflect increased Ca ++ extrusion via a Na + / Ca ++ exchange mechanism (cf Lang and Blaustein, 1980) powered by the Na + /K + ATPase.…”

Section: Discussionmentioning

confidence: 99%

“…In the already K + -depolarized artery, histamine induces additional uptake of extracellular Ca ++ (Karaki and Weiss, 1980) and releases intracellularly bound Ca ++ from sites that are not sites of Ca ++ -sequestration (Deth and van Breeman, 1977), but does not further alter membrane potential (Suzuki and Casteels, 1979). The dependence of histamineinduced contraction on external [Ca ++ ] (Hudgins and Weiss, 1968;Watkins and Davidson, 1980) suggests that tonic histaminergic vasoconstriction (such as utilized here) is primarily the result of a voltage-independent increase in membrane permeability to external Ca ++ (Harder, 1980). Although the reactivity of blood vessels to histamine is highly variable (Vanhoutte 1978), the net systemic action of histamine is a vasodilation of the fine blood vessels, which is mediated primarily through H2-histaminergic receptors (cf Douglas, 1975;Levy, 1977).…”

mentioning

confidence: 88%

Effect of histamine on the energy metabolism of K+-depolarized hog carotid artery.

Peterson¹

1982

In a previous study (Peterson and Glück, 1982), activation of hog carotid artery with high-K+ medium caused no increase in aerobic glycolysis (lactic acid production). In contrast, histamine alone is found to stimulate aerobic glycolysis in a tension-dependent fashion (GLück and Paul, 1977). In this study, the addition of histamine to the already K+-depolarized hog carotid artery induced additional contraction, elevated tissue cyclic adenosine 3',5'-monophosphate [cAMP] levels, coupled the rate of aerobic glycolysis to external [Ca++] and isometric tension, and caused suprabasal energy utilization to exceed that required to support the contraction alone by approximately 25%. Increased cytoplasmic free-[Ca++] per se does not stimulate aerobic glycolysis. In the presence of histamine, however, aerobic glycolysis is Ca++-sensitive. Whereas a cycle of Ca++ depletion and restoration has only a small effect on basal metabolic rates in arteries activated with high-K+ alone, the same procedure with arteries stimulated by high-K+ with added histamine causes a dramatic shift in basal metabolic rates toward higher levels of glycolysis.