Effect of stretch on passive tension and contractility of isolated vascular smooth muscle

1962 ◽  
Vol 202 (5) ◽  
pp. 835-840 ◽  
Author(s):  
Harvey V. Sparks ◽  
David F. Bohr
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Standard Stimulus ◽  
Contractile Element ◽  
Passive Tension ◽  
Optimal Length ◽  
Length Variable

Helically cut strips of the wall of small branches of dog superior mesenteric artery were stretched in a stepwise fashion. Tension developed in response to stretch or to a standard stimulus (epinephrine or electricity) was recorded isometrically. The elastic diagram of the vessel is comparable to that reported by other investigators. Contraction in response to a standard stimulus increased with stretch, as much as 100% for a 10% increase in length. The increase in response continued until the strip reached a certain optimal length (variable from strip to strip), after which the response decreased with further stretch. When the strip was released in a stepwise fashion hysteresis was observed. Possible relationships of tension and length at the level of the contractile element are discussed together with ways in which the information presented here may relate to myogenic autoregulation.

Na+-H+ exchange is present in sarcolemmal vesicles from dog superior mesenteric artery

1986 ◽  
Vol 250 (2) ◽  
pp. H313-H319
Author(s):  
A. M. Kahn ◽  
H. Shelat ◽  
J. C. Allen
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Electrical Coupling ◽  
Proton Gradient ◽  
Ph Gradient ◽  
Differential Centrifugation ◽  
Na Transport ◽  
Vesicle Preparation

The Na+ concentration inside vascular smooth muscle cells is an important regulator of vascular smooth muscle function, but the mechanisms that mediate Na+ influx are not known. We studied Na+ transport in a newly described vesicle preparation preferentially enriched in sarcolemma and obtained by Mg2+ aggregation and differential centrifugation of homogenized dog superior mesenteric artery. In the presence of an outwardly directed proton gradient (pHout = 7.5, pHin = 5.0), 1 mM 22Na+ uptake was stimulated over twofold relative to the absence of a pH gradient (pHin = 7.5 or 5.0). pH gradient-stimulated Na+ uptake was inhibited by 1 mM amiloride. 22Na efflux was stimulated by an inwardly directed proton gradient (pHin = 7.5, pHout = 5.7 vs. 7.5). The rate of proton efflux from acid-loaded vesicles was measured by acridine orange fluorescence and was stimulated by 100 mM Naout but not by Nain = Naout = 100 mM. H+ gradient-stimulated Na+ transport and Na+ gradient-stimulated H+ transport were not due to electrical coupling between the two cations. The pH gradient-stimulated component of Na+ transport in the final vesicles, an intermediate fraction, and microsomes were proportional to the respective enzyme marker activities for sarcolemma but not for sarcoplasmic reticulum or mitochondrial membranes. We conclude that Mg2+ aggregation and differential centrifugation of homogenized vascular smooth muscle yield a vesicle preparation preferentially enriched in sarcolemma. Furthermore, the sarcolemma of vascular smooth muscle contains an amiloride-sensitive Na+-H+ proton countertransport system.

Isolation and culture of rat superior mesenteric artery smooth muscle cells

1993 ◽  
Vol 29 (2) ◽  
pp. 135-139 ◽  
Author(s):  
Paul G. McGuire ◽  
Helen M. Walker-Caprioglio ◽  
Sally A. Little ◽  
Linda J. McGuffee
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Muscle Cells

Evidence against the role of α1-adrenoceptor reserve in buffering the inhibitory effect of nifedipine on the contractility of canine vascular smooth muscle

1990 ◽  
Vol 68 (10) ◽  
pp. 1346-1350 ◽  
Author(s):  
Yong-Yuan Guan ◽  
Chiu-Yin Kwan ◽  
Edwin E. Daniel
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Saphenous Vein ◽  
Mesenteric Artery ◽  
Inhibitory Effect ◽  
Contractile Responses ◽  
Intracellular Ca ◽  
Adrenoceptor Agonists ◽  
The Difference ◽  
Muscle Calcium

The relationship between the postsynaptic α1-adrenoceptor reserve and the sensitivity of vasoconstriction induced by α-adrenoceptor agonists to the dihydropyridine Ca2+ entry blocker nifedipine was investigated in isolated muscle strips of dog mesenteric artery (DMA) and saphenous vein (DSV). The amplitudes of the contractile responses of DMA induced by phenylephrine were the same as those in DSV in the presence and in the absence of extracellular Ca2+. The use of 3 × 10−9 M phenoxybenzamine to irreversibly block the α1-adrenoceptors revealed a marked difference in the size of the α1-adrenoceptor reserve between DMA (40%) and DSV (7%). In spite of a larger receptor reserve, the contractile responses induced by phenylephrine in DMA were more sensitive to nifedipine compared with those in DSV. These results suggest that the postsynaptic α1-adrenoceptor reserve in vascular smooth muscle, at least in DMA and DSV, does not play an important role in buffering the inhibitory effect of nifedipine on the contractile response to a full agonist of α1-adrenoceptors. Other factors, such as the difference in the membrane depolarizing effect, the ability to utilize intracellular Ca2+ for contraction, and the possible existence of α1-adrenoceptor subtypes, may contribute to the different inhibitory effects of nifedipine on these blood vessels.Key words: adrenoceptors, nifedipine, smooth muscle, calcium, saphenous vein, mesenteric artery.

Inhibition of Ca2+-activated K+ channels by tyrosine phosphatase inhibitors in rat mesenteric artery

2000 ◽  
Vol 78 (9) ◽  
pp. 745-750 ◽  
Author(s):  
Hisashi Yokoshiki ◽  
Takashi Seki ◽  
Masanori Sunagawa ◽  
Nicholas Sperelakis
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Mesenteric Artery ◽  
Single Channel ◽  
Tyrosine Phosphatase ◽  
Phosphatase Inhibitors ◽  
Rat Mesenteric Artery ◽  
Dependent Signal ◽  
Single Channel Currents ◽  
Channel Currents

To investigate the possible regulation of large-conductance Ca2+-activated K+ channels (BKCa) by tyrosine phosphatases (Tyr-PPs), single-channel currents of myocytes from rat mesenteric artery were recorded in open cell-attached patches. Two structurally different Tyr-PP inhibitors, sodium orthovanadate (Na3VO4) and dephostatin, were used. The channels (236 pS) evoked at +40 mV and pCa 6, were significantly inhibited by 1 mM Na3VO4 (-81 ± 3%, n = 10; P < 0.005). Similarly, 100 µM dephostatin strongly inhibited the BKCa channels (-80 ± 7%, n = 7 ; P < 0.05). Therefore, BKCa channels in vascular smooth muscle cells may be regulated by tyrosine phosphatase-dependent signal transduction pathways, whose inhibition could attenuate the channel activity.Key words: Ca2+-activated K+ channel, vascular smooth muscle, tyrosine phosphatase, vanadate, dephostatin.

Sign in / Sign up

Export Citation Format

Share Document