Rat Vascular Smooth Muscle Research Articles

Na-H exchange is a major pathway for Na influx in rat vascular smooth muscle

Rat aortic segments and aortic smooth muscle cells in primary culture were used to examine the importance of the Na-H exchange system in transporting Na into smooth muscle. Ethylisopropylamiloride was approximately 100 times more potent than amiloride at inhibiting Na influx into smooth muscle. In a 135 mM Na-containing medium approximately 80% of the Na influx rate could be inhibited by 100 microM ethylisopropylamiloride. The rate of Na entry into cells was markedly influenced by extracellular and intracellular pH. Elevating extracellular pH from 6.0 to 8.0 increased the Na influx rate. The dependence of the Na influx rate on intracellular pH was demonstrated by acidification of cells with nigericin or preincubation with ammonium chloride. These two procedures increased 22Na+ influx rate by about 3.5-fold. In both instances the increases in 22Na+ influx rate could be completely attenuated by ethylisopropylamiloride. Increases in Na influx rate via the Na-H exchange also increased the activity of the Na-K pump, thereby maintaining intracellular Na content approximately constant. These results indicate that Na-H exchange is a major influx pathway for Na in rat vascular smooth muscle. Activation of this system activates the Na-K pump, which maintains intracellular Na constant.

Amiloride-sensitive sodium-hydrogen exchange is a major pathway for sodium influx in rat vascular smooth muscle

Amiloride-sensitive sodium-hydrogen exchange is a major pathway for sodium influx in rat vascular smooth muscle

Effect of a Low Concentration of Angiotensin II on Vascular Smooth Muscle Tone

We have previously found that long-term blockade of angiotensin II (AII) formation by captopril suppresses the "leakiness" of vascular smooth muscle membrane from spontaneously hypertensive rats. The present study was undertaken to examine whether a subpressor concentration of AII alters the membrane permeability and the tension of vascular smooth muscle of rats. The isometric tensions of rat aortic strips were recorded and the cellular Na contents in the muscles were measured by the "cold Li-exchange method." Lowering external K+ concentration to 0 or 0.5 mM produced slowly developing contractions in the muscles. These contractions were significantly enhanced by 4 h of pretreatment with 3 X 10(-10) M AII, whereas there were no contractions in normal Tyrode solution. Increase in cellular Na during incubation in K+-free solution was greater in AII-pretreated muscles and the cellular Na in these muscles leaked out more rapidly into cold Li solution than it did in untreated muscles. These findings suggest that the subpressor concentration of AII increases the passive permeability of vascular smooth muscles to Na and, if the Na pump activity is partially impaired, elevates the vascular tone.

The anatomical location of the series elastic component in rat vascular smooth muscle.

1. Flash photomicrographs using Nomarski optics have been taken of the smooth muscle cells in an activated arterial resistance vessel preparation (i.d. approximately 150 micrometers) before and after a quick release of internal circumference in an attempt to determine the location of the series elastic component (s.e.c.). 2. If the s.e.c. lies mainly within the smooth muscle cells, then, while the position of an intracellular structure would change during a release, there would be little change in its position after the release during tension recovery. 3. The movement of intracellular structures during a quick release, x, and the corresponding movement during tension recovery, y, was determined by taking double flash exposures at the appropriate times and measuring the separation of the double images on the film. In eighty-five pairs of measurements from seven vessels the ratio y/x was equal to 0.21 +/- 0.02 (S.E.). 4. The results show that less than half of the smooth muscle s.e.c. resides in extracellular components. The active dynamic stiffness of smooth muscle cells is substantially less than that of skeletal muscle fibres.

Parenteral Linoleic and gamma-linolenic acids ameliorate the gross effects of zinc deficiency.

AbstractZinc deficiency and essential fatty acid deficiency in rats have gross effects which are very similar. Zinc, prostaglandin E1, and dihomo-γ-linolenic acid (prostaglandin E1 precursor) all have very similar effects on rat vascular smooth muscle. Zinc deficiency has no consistent effect on tissue zinc or zinc enzymes. These observations suggest that the mechanism by which zinc deficiency affects growth and metabolism may be via inhibition of prostaglandin synthesis from essential fatty acids. This hypothesis was examined using zinc deficient rats supplemented with oils containing various concentrations of essential fatty acids. Male Wistar rats were maintained on a zinc deficient diet for 5 weeks and supplemented daily with one of three oils containing different concentrations of essential fatty acids: olive oil (mainly oleic acid), safflower oil (mainly linoleic acid), or evening primrose oil (mainly linoleic and γ-linolenic acids). The olive oil treated rats did not benefit from this treatment in ...

Effect of isomers of octopamine on in vitro reactivity of vascular smooth muscle of rats.

The vascular reactivity to DL-ortho-, meta-, and para-octopamine was tested in vitro in aortic smooth muscle of the rat. When reactivities were compared on a molar basis with L-phenylephrine, an alpha-adrenergic agonist, the potencies of the three isomers were: 0.7500, 0.0075 and 0.0038 times that of phenylephrine for the m-, p- and o-isomer, respectively, Thus, of the three isomers, DL-m-octopamine had the greatest alpha-adrenergic activity in vitro as it did in vivo in earlier studies. Additional studies showed L-phenylephrine to induce about one-third the vascular response induced by L-norepinephrine.

Vasorelaxant action of caroverine fumarate (a quinoxaline derivative), a calcium-blocking agent.

1 Caroverine fumarate, 1-(2-diethylaminoethyl)-3-(p-methoxy-benzyl)-1,2-dihydro-2-quinoxalinone fumarate, caused a greater inhibition of the pressor response to KCl (8 x 10(-2) M) than that to noradrenaline (10(-6) M) in the rat hindquarter preparation. 2 In the isolated aorta of the rat, caroverine (up to 10(-6) M) markedly suppressed the contraction caused by KCl (4 x 10(-2) M) (high-K) but had little effect on the contractile response to noradrenaline (10(-6) M) whether added before the spasmogen or in its presence. 3 In the high-K-treated aorta, caroverine shifted the concentration-response curve for external calcium to the right, competitively. The negative logarithm of the affinity (pA2) of caroverine was calculated to be approx. 7. 4 Increased 45Ca uptake of the high-K-treated aorta measured by a modified lanthanum method was inhibited by either caroverine (3 x 10(-6) M) or verapamil (10(-6) M). 5 Concentrations of caroverine and verapamil reducing high-K-induced aortic contraction to 50% of its maximum were 2.4 x 10(-7) and 6.6 x 10(-8) M respectively. 6 Following washout the caroverine-induced inhibition of high-K-induced aortic contraction was more rapidly restored than the verapamil-induced inhibition. 7 These results suggest that caroverine fumarate is a specific and readily reversible calcium influx inhibitor in the rat vascular smooth muscle.