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Biomedical subjects

S Sunano

Publications and source records attributed to S Sunano.

At least 55 records · Page 3Linked to original sources
PubMed1991

Caffeine-induced contraction of rat portal vein and effects of K-depolarization, Na-removal and low temperature.

Contribution of Ca influx from extracellular pool and Ca-release from store sites in caffeine-induced contraction of rat portal vein longitudinal muscle were examined. At 37 degrees C caffeine induced a phasic contraction and the contraction was inhibited by verapamil or in the absence of Ca. Under low temperature, it was not decreased remarkably by verapamil or by the removal of extracellular Ca. Na-removal potentiated caffeine-induced contraction in the absence of Ca. Caffeine-induced contraction was also potentiated by high-K-depolarization. These contractions were at both temperature inhibited greatly by ryanodine. Caffeine induced the burst of the action potential at 37 degrees C but it was not remarkable at 17 degrees C. These results indicate that both extracellular Ca influx and release of stored Ca are involved in the caffeine-induced contraction. However, dependence of the contraction on Ca sources are influenced by temperature, extracellular Na and membrane potential.

Action Potentials↗
PubMed1990

Effects of Bay K 8644 on the spontaneous electrical and mechanical activities of the rat portal vein.

Effects of Bay K 8644 on the spontaneous electrical and mechanical activities of the rat portal vein were studied. Bay K 8644 enhanced contractions in amplitude and duration. Bay K 8644 prolonged the duration of the spontaneous spike potential bursts and increased the number of spike potentials in a burst. These results indicate that the increase in the amplitude and duration of spontaneous contractions of the rat portal vein induced by Bay K 8644 are mediated mainly by the facilitation of the membrane electrical activity.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1990

Relaxation of mesenteric artery of stroke prone spontaneously hypertensive rats by calcium removal.

1. The time courses of the relaxation, induced by removal of extracellular Ca2+, of K-depolarized mesenteric artery preparations from stroke prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY) were compared. 2. The time course of the decline in extracellular Ca2+ was estimated from the time course of the relaxation and the concentration-response curve of K(+)-depolarized preparations to Ca2+. The time course of the decline in the intracellular free Ca2+ concentration was also estimated from the reported relation between Ca2+ concentration and the contraction of skinned vascular smooth muscle. 3. The time course of relaxation was exponential, the curve being made up of three components. The time course was slower in preparations from SHRSP, especially the first component of the relaxation curve. 4. The time courses of the decline in the intracellular and extracellular Ca2+ concentrations were also exponential, being made up of three components and were also slower in the preparation made from SHRSP. 5. The wall and muscle layer of the mesenteric arteries used in the present experiments were significantly thicker in the SHRSP preparations. 6. Calculation of the half relaxation time, based on the diffusion of Ca2+ across the blood vessel wall, suggested that the slower relaxation in preparations from SHRSP is due largely to the thicker muscle layer, although differences in Ca2+ sequestration by the smooth muscle cells may also be involved.

Animals↗
PubMed1990

Intranephron PGE2 production in stroke-prone spontaneously hypertensive rats.

To investigate whether intranephron prostaglandin E2 (PGE2) production in stroke-prone spontaneously hypertensive rats (SHRSP) differs from that in Wistar-Kyoto rats (WKY), we measured PGE2 accumulation rates in microdissected nephron segments from 4- to 6- and 12- to 14-wk-old male rats by radioimmunoassay. In both young and adult WKY, PGE2 accumulation was highest in the papillary collecting duct (PCD) and outer medullary and cortical collecting tubules, intermediate in the glomerulus (Glm), medullary and cortical thick ascending limbs of Henle's loop, and distal tubule, and negligible in the proximal tubule. PGE2 accumulation in adult WKY was severalfold higher than that in young WKY. PGE2 accumulation in adult and prehypertensive young SHRSP was significantly lower than that of respective WKY in most segments, whereas urinary PGE2 excretion was significantly higher in SHRSP than in age-matched WKY. Plasma arginine vasopressin concentrations in adult SHRSP were significantly higher than in WKY. PGE2 accumulation stimulated by 5 microM arachidonic acid was significantly lower in SHRSP than in WKY in most segments of young rats but was lower only in Glm and PCD of adult rats. PGE2 accumulation stimulated by 2 microM Ca2+ ionophore A23187 was significantly lower in most segments of adult and young SHRSP. These results indicate that a decrease in renal tubular PGE2 productive activities in SHRSP might not be caused by secondary adaptation to hypertension.

Aging↗
PubMed1989

Blood pressure and impairment of endothelium-dependent relaxation in spontaneously hypertensive rats.

Correlation between hypertension and impairment of endothelium-dependent relaxation was demonstrated using aortae from certain strains of rats with various levels of spontaneous hypertension. It was also observed that the impairment of endothelium-dependent relaxation is the secondary change due to hypertension, and the level and duration of hypertension is the determinant factor of the impairment.

Animals↗
PubMed1989

Electrical and mechanical properties of spontaneous contraction in hypertensive rat portal vein.

Contractile and electrical activities of longitudinal smooth muscle of portal vein from normotensive Wistar Kyoto rats (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were compared. Amplitude and duration of spontaneous contraction of SHRSP portal vein were greater than those of WKY portal vein. No significant differences were observed in the resting membrane potentials between these preparations. Spontaneous spike activity appeared as a form of bursts. Duration of the burst and the number of spikes in each burst was greater in the portal vein of SHRSP than that of WKY. The amplitude of phasic and tonic components of K-contracture was also greater in SHRSP portal vein. Adrenergic and cholinergic nerves were not involved in the differences in contractions of the portal vein of these animal strains. Cross-sectional area of the longitudinal muscle layer was greater in SHRSP portal vein. These results suggest that the differences in spontaneous electrical activity are the cause of the differences in force and duration of the spontaneous contraction of portal vein from WKY and SHRSP, although the difference in excitation-contraction coupling of smooth muscle may be involved in much less extent.

Animals↗
PubMed1989

Caffeine-induced contraction in arteries from stroke-prone spontaneously hypertensive rats.

Differences in caffeine-induced contraction in smooth muscle of resistance vessels from stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar Kyoto rats (WKY) were investigated by using mesenteric artery preparations. The contraction induced by caffeine (10 mM) was greater in SHRSP preparations, both in the presence and absence of Ca (10 min after Ca removal). Caffeine-induced contraction was gradually decreased by the removal of extracellular Ca. No significant difference was observed in the time course of the decay of the contraction between SHRSP and WKY preparations, and the contraction disappeared when the time in Ca-free solution exceeded 80 min. The contraction induced by high-K-Tyrode's solution was completely abolished within 10 min after Ca removal, both in SHRSP and WKY preparations. Caffeine-induced contraction could be blocked by procaine or ryanodine. The results suggest that caffeine induces contraction by releasing Ca from sarcoplasmic reticulum, and that the release of Ca is greater in SHRSP vascular smooth muscle. It is also suggested that sarcoplasmic reticulum is leaky for stored Ca when extracellular Ca is removed, and that the rate of leakage does not differ between smooth muscle cells of SHRSP and WKY mesenteric arteries.

Animals↗
PubMed1989

[Actions of vanadate on muscles].

Vanadate, a trace element of biological tissues and fluid, has been known to be a potent inhibitor of Na, K-ATPase in various tissues. In skeletal muscle, it inhibits the Na, K-ATPase of the membrane fraction, whereas it can not inhibit the Na, K-pump in an intact preparation. It inhibits the Ca-ATPase of the sarcoplasmic reticulum and that of contractile proteins. Vanadate potentiates the contraction of some heart muscles, while it depresses the contraction in some other heart muscles. The positive and negative inotropic effects are mediated by changes in the action potential. The inhibition of Na, K-ATPase is not always involved in the inotropic actions. The inhibition of the Ca-ATPase of the sarcoplasmic reticulum and plasma membrane can be the causes of positive inotropic action. Actions on adenylate cyclase can also be the cause of inotropism. In smooth muscle, vanadate induces contractions with and/or without membrane excitation. The contractions are initiated by both the influx of extracellular Ca2+ and the release of intracellular bound Ca2+. The inhibition of Na, K-ATPase is not involved in the contraction but the inhibition of the Ca-pump of membranous systems can be the cause of the contraction. Vanadate is a useful tool for studies on the excitation-contraction coupling in muscles.

Animals↗
PubMed1988

Effects of sodium vanadate on the smooth muscle of the rat portal vein.

The effects of vanadate on the mechanical and electrical activity of the rat portal vein were examined. Vanadate increased the height of the spontaneous contractions of the portal vein without affecting basal tension. This effect was not blocked by alpha-blockers or atropine. Vanadate did not exert any effect when the spontaneous contractions were abolished by high concentrations of verapamil or in the absence of Ca. Vanadate did not change the resting membrane potential of the smooth muscle cells of the vein, but it increased the rate of rise and the amplitude of the action potentials and the number of action potentials per burst. The intracellular Na content was increased slightly by vanadate. However, the effects of Na,K-pump inhibition by ouabain or K-removal were quite different from those of vanadate, and these procedures did not block the effect of vanadate, although they attenuated it. Vanadate also potentiated the K-contracture of the portal vein. These results indicate that vanadate increases the amplitude of the spontaneous contractions through an increase in the number of action potentials per burst which underly the contraction. These effects are not mediated by intrinsic nerve excitation or inhibition of Na,K pump activity. The facilitation of Ca entry through the voltage dependent Ca channel may be the main cause of the effect of vanadate on mechanical activity.

Animals↗
PubMed1988

Extra- and intracellular calcium in vanadate-induced contraction of vascular smooth muscle.

The effects of extracellular Ca and Ca antagonists on vanadate-induced contractions of vascular smooth muscles of aortae and mesenteric arteries from rabbits, guinea pigs, and Wistar-Kyoto (WKY) and stroke-prone spontaneously hypertensive rats (SHRSP) were studied. Vanadate-induced contractions of aortae were greatly diminished by extracellular Ca removal; the size of the remaining contraction was variable. Vanadate-induced contractions of mesenteric arteries, which were only observed in the presence of elevated K, were suppressed by the removal of Ca. Verapamil and nifedipine depressed vanadate-induced contractions of aortae from WKY and SHRSP, whereas they produced no or only slight inhibition of responses in guinea pig and rabbit aortae. Ca uptake into smooth muscle cell increased in the presence of vanadate, but the increase was much less than that induced by high K. In saponin-skinned smooth muscle, vanadate depressed the Ca-induced contraction. It is concluded that the vanadate-induced contraction utilizes both extracellular and intracellularly bound Ca, the relative contribution of which varies from preparation to preparation.

Animals↗
PubMed1988

[Vanadate and smooth muscles].

Vanadate is a trace element in biological tissues which has inhibitory actions on various enzymes. It inhibits Na, K-ATPase of smooth muscle membrane. Ca-ATPase and Ca-uptake of membranous systems of smooth muscle cells are also inhibited by vanadate. Vanadate induces contractions in various smooth muscles. These contractions are not mediated by the inhibition of Na, K-ATPase. The contractions are induced by both the influxed Ca from extracellular space and the released Ca from intracellular binding sites. In certain smooth muscles, the changes in electrical activities are also involved. These effects of vanadate are not mediated by the release of transmitter from intrinsic nerves. The direct actions on contractile proteins is inhibitory and cannot be the cause of the contraction. Thus, vanadate induces contraction in various smooth muscles, by increasing Ca permeability of cell membrane and by releasing intracellular bound Ca. In addition, the inhibition of Ca-pump may also be involved in the initiation or potentiation of contraction by vanadate. The degree of each action varies among various smooth muscles.

Animals↗
PubMed1987

Noradrenaline content and release in the mesenteric artery of stroke-prone spontaneously hypertensive rats (SHRSP) and a new strain of SHRSP (M-SHRSP).

Adrenergic innervation in the main trunk of the mesenteric artery was studied in stroke-prone spontaneously hypertensive rats (SHRSP) as well as in a new strain of SHRSP (M-SHRSP) and was compared with that of normotensive Wistar Kyoto rats (WKY). Noradrenaline (NA) content and high K-induced NA release in the artery of 6-week-old SHRSP and M-SHRSP were greater than those in the artery of WKY. These results suggest that a higher adrenergic innervation of the artery might be involved in the development of hypertension in SHRSP and M-SHRSP.

Animals↗
PubMed1987

Effects of vanadate on vascular smooth muscles of WKY and SHRSP.

The effects of vanadate on the vascular smooth muscle of Wistar Kyoto rats (WKY) and stroke prone spontaneously hypertensive rats (SHRSP) were examined. It was shown that sodium vanadate caused contraction of the aortae, mesenteric and basilar arteries of both strains, and that the reactivity was higher in SHRSP in the aorta and mesenteric artery. The vanadate-induced contractions were not blocked by 6-hydroxydopamine, adrenergic blocking agents, indomethacin or ouabain, while 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene did. An increase in K+-concentration potentiated the vanadate-induced contractions of the mesenteric arteries and minimized the difference between preparations from WKY and SHRSP. In depolarized preparations incubated in K-Tyrode's solution (140 mM KCl), vanadate induced phasic contractions followed by marked relaxation in the aortae of both species, the relaxation being more prominent in SHRSP aorta, while depolarized mesenteric arteries showed sustained contractions. It was revealed that vanadate caused contractions by acting inside the cell, and membrane permeability to vanadate might be higher in the vascular smooth muscle of SHRSP. The findings also suggested that vanadium, an inorganic element, can be involved in the initiation of hypertension in SHRSP when it acts on vascular smooth muscle.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗