• The Korean Journal of Physiology
• /
• v.28 no.2
• /
• pp.159-167
• /
• 1994

The contraction of rabbit basilar artery was examined as a function of changes in the $Na^+$ electrochemical gradient in order to determine the contribution of $Na^+/Ca^{2+}$ exchange to the modulation of contractility. Ouabain $(10^{-5}\;M)$ or $K^+-free$ Tyrode solution caused an increase in tonic tension even in the presence of a $Ca^{2+}$ channel blocker $(10^{-6}\;M\;verapamil)$ and an ${\alpha}-receptor$ blocker $(10^{-5}\;M\;phentolamine)$. After treatment with ouabain $(10^{-5}\;M)$, contractions were augmented by reduction of external $Na^+$ concentration. The longer the treatment with ouabain $(10^{-5}\;M)$ was, the larger the amplitude of $Na^+-free$ contracture was. $Na^+-free$ contracture wag induced by either substitution of equimolar Tris for $Na^+$ or substitution of equimolar $Li^+\;for\;Na^+$. The competition between $Na^+\;and\;Ca^{2+}$ for the $Na^+/Ca^{2+}$ exchange carrier would exist, because it was observed that contractility was dependent on the $Na^+$ electrochemical gradient or the extracellular $Ca^{2+}$ concentration (2 mM, 4 mM). Ryanodine $(10^{-7}\;M)$, the blocker of intracellular $Ca^{2+}$ release from the sarcoplasmic reticulum, did not suppress the development of $Na^+-free$ contracture. The contractile response to norepinephrine $(10^{-6}\;M)$ was augmented by reducing the extracellular $Na^+$ concentration. The relaxation rate from caffeine-induced contraction was dependent on the extracellular $Na^+$ concentration (0 mM, 140 mM). From the above results, it could be suggested that $Na^+/Ca^{2+}$ exchange can move $Ca^{2+}$ either into or out of rabbit basilar arterial smooth muscle. $Ca^{2+}$ entry or extrusion is dependent upon the $Na^+$ electrochemical gradient. $Na^+/Ca^{2+}$ exchange plays a significant role in the regulation of contractility in rabbit basilar arterial smooth muscle.

• The Korean Journal of Pharmacology
• /
• v.26 no.1
• /
• pp.25-33
• /
• 1990

The responsiveness of various arterial smooth muscles isolated from rabbit to peptide YY (PYY) and the calcium source responsible for the muscles to contract were studied in vitro. PYY contracted the muscle strips of femoral, basilar and common iliac arteries more sensitively than renal, superior mesenteric and common carotid arteries. Common carotid and renal arteries were less sensitive to PYY $(p{\leqslant}0.05)$ than to NE; and basilar artery was more sensitive to PYY$(p{\leqslant}0.01)$ than to NE. A calcium channel blocker, verapamil and an inhibitor of intracellular calcium release, 3, 4, 5-Trime-thoxybenzoic arid 8-(diethylamino)octyl ester [TMB-8] significantly $(p{\leqslant}0.001)$ suppressed the concentration-response of the strips from femoral artery to PYY. When both verapamil and TMB-8 existed in normal PSS, the concentration-response to PYY was inhibited almost completely; and a similar suppression was observed when the muscle was incubated in calcium-free, ethyleneglycol-bis-(beta-aminoethyl ether)N,N,N',N'-tetraacetic acid [EGTA] containing PSS. The results of these experiments suggest that increased PYY activity in circulation may result in the more sensitive increase in the intracranial vascular resistance and the cerebral arterial pressure than the increased sympathetic activity and that both intra- and extracellular calcium are to be utilized for the PYY-induced contraction on arterial smooth muscle.