Noradrenaline contractions in rabbit mesenteric arteries skinned with saponin.

Abstract

SUMMARY1. In rings of small rabbit mesenteric arteries, noradrenaline induced oscillatory contractions. After depolarization with potassium, which produced in this preparation only a transient contraction, the arteries responded to noradrenaline with tonic contraction.2. Artery rings, skinned for 6 min with saponin (0-5 mg/ml.), were highly sensitive to calcium (half-maximum contraction at 4 x 10-7 M-Ca2+). In the skinned preparations, a contraction was still elicited by noradrenaline.3. Treatment with saponin renders virtually all smooth muscle cells of the mesenteric artery preparation hyperpermeable as indicated by both physiological and morphological criteria.4. While the Ca stores responsible for the noradrenaline-induced contraction of skinned arteries were depleted at a slow rate by 0.1 mM-EGTA, they were completely emptied by a 4 min exposure to 10 mM-EGTA. After release of intracellular Ca by noradrenaline, the Ca stores could be partially replenished by incubating the preparation in 10-6 M-Ca2+ for 4 min.5. Noradrenaline failed to contract skinned arteries after part of the intracellular Ca had been released by caffeine but not after Ca release by the ionophore X-537 A.6. The mitochondrial uncoupler, carbonyl cyanide m-chlorophenylhydrazone, inhibited noradrenaline-induced contractions of skinned arteries.7. Noradrenaline had no effect on 45Ca translocation in either membrane vesicles or mitochondria isolated from mesenteric arteries.8. The present results show that in vascular smooth muscle a certain degree of structural integrity of the cell membrane, but not its selective permeability, is required for the coupling between a-adrenoceptors and Ca release from intracellular stores; the data also suggest that axadrenoceptor stimulation results in release of Ca bound to the plasma membrane rather than indirect release of Ca accumulated in intracellular organelles.

Multiple sources of calcium for contraction of the human urinary bladder muscle

“…This occurred only at a low (25°C) bath temperature, while at 37°C a relaxant effect was observed. Caffeine has been shown to contract various smooth muscles by mobilizing an intracellular Ca pool from the sarcoplasmic reticulum (Weber & Hertz, 1968;Casteels & Raeymaekers, 1979;Haeusler et al, 1981;Itoh et al, 1982;Leijten & Van Breemen, 1984) but smooth muscle relaxation via inhibition of phosphodiesterases and other mechanisms has also been noted (Leijten & Van Breemen, 1984;Sato et al, 1988). We could speculate that at 37°C the relaxant effect of caffeine prevails while at 25$C the relaxant action is somehow slowed or inhibited thus unmasking a contractile effect.…”

Neurokinin A and Ca2+ current induce Ca(2+)‐activated Cl(‐) currents in guinea‐pig tracheal myocytes.

“…Similarly, Janssen & Sims (1992, 1994 in TSMCs (Janssen & Sims, 1992 (Iino, 1989); however, uncertainty remains as to the degree of overlap of the intracellular Ca2+ sources mobilized by neurotransmitters in TSMCs. In rabbit mesenteric artery, noradrenaline only partially depletes the caffeine-sensitive store (Haeusler, Richards & Thorens, 1981). In porcine coronary artery, and guinea-pig taenia coli (Casteels & Raeymaekers, 1979;Itoh, Kahiwara, Kitamura & Kuriyama, 1982), ACh appears to release Ca2+ from an additional caffeine-insensitive store.…”

Contractions of rat uterine smooth muscle induced by acetylcholine and angiotensin II in Ca2+‐free medium

“…The release of internal Ca2+ is also demonstrated by stimulating myometrial preparations in Ca2+-free solution with different agonists such as acetylcholine and angiotensin II (Edman & Schild, 1962;Hamon & Worcel, 1979). The mechanism of action of stimulant substances in uterus include activation of different excitation-contraction coupling mechanisms: (i) an acceleration of action potential discharge or an increase in spike amplitude may increase the cytoplasmic Ca2+ concentration since it is believed that Ca2+ ions carry the inward current responsible for the upstroke (Mironneau, 1974;Vassort, 1975; (ii) a direct increase in Ca2+ permeability may be produced through receptor-operated channel activation (Bolton, 1979;Bolton & Kitamura, 1983); (iii) a release of intracellular Ca2+ may be induced from a limited store whose characteristics of exchange have been recently studied in intestinal (Hurwitz, 1975;Casteels & Raeymaekers, 1979; and vascular smooth muscles (Deth & Van Breemen, 1977;Droogmans et al, 1977;Haeusler et al, 1981).…”