Electron-impact ionization of CCl4 and CCl2F2.

Absolute partial and total cross sections for electron-impact ionization of CCl4 and CCl2F2 are reported for electron energies from threshold to 1000 eV. The product ions are mass analyzed using a time-of-flight mass spectrometer and detected with a position-sensitive detector whose output demonstrates that all product ion species are collected with equal efficiency irrespective of their initial kinetic energies. Data are presented for production of CCl3(+), CCl2(+), CCl+, C+, Cl2(+), and CCl3(2+) from CCl4; and for production of CCl(2)F+, CClF2(+), CClF(+), (CCl+ + CF2(+)), Cl+, CF+, F+, and C+ from CCl2F2. Data are also reported for formation of (CCl2(+),Cl+) and (CCl+, Cl+) ion pairs from CCl4. The total cross section for each target is obtained as the sum of the partial cross sections. The overall uncertainty in the absolute cross sections for most of the singly charged ions is +/- 5-7 %. The present partial cross sections for lighter fragment ions are found to be considerably greater than had been previously reported but the most recent total cross section measurements agree well with those reported here. Neither the binary-encounter-Bethe theory nor the Deutsch-Mark theory reproduces the experimental cross sections correctly for both targets.

Negative ion formation and motion in a mixture of CCl4 and Ar.

This paper deals with the measurement of the mobility of negative ions in the mixtures of CCl4 with Ar with the CCl4 ratio up to 33.3%. The pulsed Townsend technique was employed to produce an integrated ionic avalanche over a range of the density-reduced electric field E/N for which ionization is either negligible or absent, and attachment processes are dominant, leading to the formation of mostly CCl-4. The E/N range of measurement was 1-50 Td (1 Td=10(-17) V cm(2)). Our measurements strongly suggest that attachment is the dominant process and only negative ions are formed.

Negative ion motion in the mixtures of SF6 with CF4 and CH4-Ar.

This paper deals with the measurement of the mobility of negative ions in the mixtures of SF6 with CF4 and the CH4-Ar (50:50) binary mixture with SF6 contents up to 50%. The pulsed Townsend technique was used to observe the integrated ionic avalanches over a range of the density-reduced electric field E/N for which ionization is either negligible or absent, and attachment processes are significant, leading to the formation of mostly SF-6. The E/N range of measurement was from 1 to 70 Td (1 Td=10(-17) V cm(2)), over which the measured mobilities were found to be almost constant. The mobility of the negative ions was also measured for trace amounts of SF6 in CH4 and Ar and 1% CF4, thereby providing a good value of the mobility of SF-6 in these pure gases, in order to test the measured mobilities with Blanc's law. We have found good agreement, within quoted experimental uncertainties, between calculated and measured values.

In vitro and in vivo characterization of 2,6-dimethyl-3,5-dicarbomethoxy-4-(2-isothiocyano)phenyl-1,4- dihydropy ridine as a Ca2+ channel antagonist.

The actions of 2,6-dimethyl-3,5-dicarbomethoxy-4-(2-isothiocyano)phenyl-1,4- dihydropyridine (o-NCS-DHP), a nifedipine analog bearing a reactive group, have been characterized in vitro by pharmacological and radioligand binding techniques in a number of smooth muscles and in vivo by blood pressure and radioligand binding. o-NCS-DHP exhibits persistent, but slowly reversible, antagonism in guinea pig ileal longitudinal smooth muscle, guinea pig bladder, taenia coli, rat portal vein, and rat tail artery to receptor responses (muscarinic and alpha-adrenoceptor) and K+ depolarization initiated responses. Duration of response was significantly longer than that of equivalent concentrations of nifedipine. In many tissues a component of antagonism produced by o-NCS-DHP was not reversed by repeated washing over the duration of the experiment (up to 2 or 7 h). A comparison of the actions of o-NCS-DHP and its isomers m-NCS-DHP and p-NCS-DHP revealed the former to be significantly longer lasting in rat tail artery against K+ depolarization induced responses. A similar profile was exhibited when the Ca2+ channel activator Bay K 8644 was employed as the stimulant, but the antagonism produced by all three compounds was fully reversed with sufficiently prolonged washing. In vivo administration of o-NCS-DHP (5-25 mg/kg) produced a persistent reduction of [3H]nitrendipine binding in rat brain, gut, and heart characterized as Bmax, but not KD, changes. No effects on [3H]dihydroalprenolol or [3H]quinuclidinyl benzilate binding were detected. Binding site recoveries were characterized by t1/2 values of 35-50 h, and these were significantly prolonged to 91-107 h in animals treated with cycloheximide. Recovery of [3H]nitrendipine binding sites correlated with blood pressure restoration in spontaneously hypertensive rats. These data suggest that o-NCS-DHP possesses both reversible and irreversible actions. The reversible actions are unusually persistent compared with nifedipine and other 1,4-dihydropyridine analogs. This persistent, but reversible component, may be accompanied by an irreversible action particularly at the higher concentrations employed in the in vivo experiments.

Inhibitory actions of a series of Ca2+ channel antagonists against agonist and K+ depolarization induced responses in smooth muscle: an assessment of selectivity of action.

The inhibitory effects of the Ca2+ channel antagonists D-600, diltiazem, nifedipine and seven 1,4-dihydropyridine analogs of nifedipine against 80 mM K+ depolarization induced responses in guinea pig trachea, parenchyma, and pulmonary artery and rat renal and mesenteric artery preparations were determined. Together with similar data previously obtained for guinea pig ileum and bladder, these data permitted an assessment of tissue selectivity of action in smooth muscles of a series of Ca2+ channel antagonists under constant conditions (saline composition) and an identical challenge (K+ depolarization). Very similar rank orders of activity were expressed in all tissues suggesting that the same basic structure-activity relationship operates. However, the series of antagonists were significantly less active in respiratory smooth muscle than in other visceral or vascular smooth muscles. pA2 values for a series of 1,4-dihydropyridine antagonists measured in guinea pig taenia coli against Ca2+-induced responses in K+-depolarizing media correlated with mean inhibitory concentration values against K+-induced responses, suggesting that the latter were an appropriate measure of antagonist potency. pA2 values measured for nifedipine, D-600, and diltiazem against Ca2+-induced responses in taenia coli in the presence of a depolarizing K+ saline, or methylfurmethide, histamine, or 5-hydroxytryptamine did not differ, suggesting that the same channels were activated regardless of stimulant.

Ca2+ channel antagonist actions in bladder smooth muscle: comparative pharmacologic and [3H]nitrendipine binding studies.

The actions of a series of 15 Ca2+ channel antagonists including D-600, nifedipine, and diltiazem were examined against K+ depolarization and muscarinic receptor induced responses in guinea pig bladder smooth muscle. Responses of bladder are very dependent upon extracellular Ca2+ and sensitive to the Ca2+ channel antagonists, the tonic component more than the phasic component of response. Regardless of stimulant, K+ or methylfurmethide (MF), or component of response, the same rank order of antagonist activities is expressed, suggestive of a single structure-activity relationship and the existence of a single category of binding site which may, however, exist in several affinity states. High affinity binding of [3H]nitrendipine (KD = 1.1 X 10(-10) M) occurs in bladder membranes, and similar high affinity binding was found in microsomal preparations from other smooth muscles including guinea pig and rat lung, rat vas deferens, uterus, and stomach. [3H]nitrendipine binding in the bladder was sensitive to displacement by other 1,4-dihydropyridines, paralleling their pharmacologic activities and showing excellent agreement with binding data previously obtained for guinea pig ileal smooth muscle. Comparison of pharmacologic data for inhibition of K+- and MF-induced responses by a common series of Ca2+ channel antagonists in bladder and ileum revealed excellent correlations. Neither pharmacologic nor binding studies suggest significant differences in Ca2+ channel antagonist properties in smooth muscle from bladder and intestine.