We have studied the nitroso group transfer from substituted N-methyl-N-nitrosobenzenesulfonamides to primary and secondary amines, observing that the rate of the reaction increases as a consequence of the presence of electron withdrawing groups on the aromatic ring of the nitrosating agents. The rate constants determined for the nitroso group transfer, ktr, give good Bronsted-type relationships between log ktr (rate constant for nitroso group transfer) and pKaR2NH2+ and pKaleaving group. The study of the nitrosation processes of secondary amines catalyzed by ONSCN and denitrosation catalyzed by SCN-, in combination with the formation equilibrium of ONSCN, has enabled us to calculate the value of the equilibrium constant for the loss of the NO+ group from a protonated N-nitrosamine (pKNOR2N+HNO), which can be defined by analogy with pKaR2NH2+. The value of pKNOX-NO for the loss of the NO+ group from an N-methyl-N-nitrosobenzenesulfonamide was obtained in a similar way. By using values of delta pKNO = pKNOR2N+HNO - pKNOX-NO, we were able to calculate the equilibrium constant for the nitroso group transfer and characterize the transition state. On the basis of Bronsted-type correlations, we have obtained values of beta nuclnorm and alpha lgnorm approximately equal to 0.55, showing a perfectly balanced transition state. In terms of the Marcus theory, the calculation of the intrinsic barriers for the nitroso group transfer reaction shows that the presence of electron withdrawing groups on the aromatic ring of the N-methyl-N-nitrosobenzenesulfonamides does not cause these barriers to vary.

The kinetics of the nitrosation reaction of several substituted sulfonamides and of the denitrosation of the resulting products have been studied. The denitrosation rate is first-order with respect to both the nitroso compound and acid concentration and no effect of added nucleophiles was observed. The denitrosation reaction is general-acid catalysed, with a Brønsted parameter, d , of 0.7, which is independent of the substituents on the aromatic ring. Kinetic solvent isotope effects range from1.20 ± 0.05 to 2.04 ± 0.06 for denitrosation by L 3 O ϩ and from k d AH /k d AD ‫؍‬ 1.5 ± 0.2 to 2.3 ± 0.3 for denitrosation by dichloroacetic acid, which suggest that a rate-determining proton transfer is involved in this reaction. For nitrosation reaction, the absence of catalysis by nucleophilic anions, the observed general-base catalysis ( NO ‫؍‬ 0.3) and the substituent effects suggest a concerted nitrosationdenitrosation process. The Leffler parameters obtained for N ؒ ؒ ؒ H bond formation ( nuc ‫؍‬ 0.7) as well as for N ؒ ؒ ؒ N᎐ ᎐ O bond breaking ( lg ‫؍‬ 0.17) are in favour of an imbalance in the transition state ( imbalance ‫؍‬ 0.53) with the development of a positive charge on the nitrogen adjacent to the nitroso group.

Kinetic measurements for the acid-catalysed decomposition of N-nitroso-2-arylimidazolines are reported. Reactions are first-order in both [substrate] and [H+]. Two products are formed; an oxazoline, which is the product of hydrolysis of the amidine moiety, and the parent imidazoline formed by denitrosation of the substrate. These products arise from two competing pathways both of which are acid catalysed. The solvent isotope effects for the denitrosation, k&/k$, and amidine hydrolysis, kE'/ki ', are 3.1 and 3.5, respectively. The denitrosation pathway, but not amidine hydrolysis, is catalysed by nucleophilic anions, and a value of 1.7 for the Swain-Scott constant, s, is obtained. In the absence of nucleophilic anions, amidine hydrolysis is preferred over denitrosation, k i t being twice as large as k:;) at 25°C. Substitutents in the 2-aryl ring affect the rate of decomposition giving Hammett p values of 0.7 for denitrosation and 1.0 for amidine hydrolysis, which reflect the proximity of the reacting centres to the substituents. Values of the activation parameters are AHRo 74 kJ mol-', AH1 74 kJ mot-', Asko -48 J K-l mol-' and A S i -43 J K-l mol-l. The data are interpreted in terms of a fast equilibrium protonation of the substrate, followed by competitive attack at the protonated substrate, either of water or nucleophilic anions at the nitroso nitrogen atom, or of water at the amidine carbon atom. Protonation is required to activate the substrate, the substrate being recovered from neutral or alkaline solutions unchanged. The mechanism is discussed with reference to the analogous reactions of N-nitrosoamines and Nn it rosoam ides.Imidazolines [ e g . (l)] are cyclic amidines that have a variety of biological effects.' For example, fenmetozole (2) and dazadrol (3) are examples of antidepressive imidazolines, whereas tolazoline (4) and phentolamine (5) are known vasodilator^.'-^ Many

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Nitrosation of clonidine has been studied kinetically both in acid medium (with nitrous acid) and in basic medium (with 2.2-dichloroethyl nitrite). The reactive form in acid medium was found t o be the protonated clonidine (pK, 8.18). The absence of catalysis by halides or thiocyanate, the existence of general base catalysis, and the measured solvent isotope effect all indicate that the reaction mechanism is different from that for the N-nitrosation of amines. Specifically, kinetic results indicate that the attack of the nitrosating agent on the substrate is not the rate determining step of the process, and suggest a mechanism that shows parallels with that found for ureas. However, in slightly basic medium, the reaction of clonidine with the alkyl nitrite occurs through the free base form of clonidine, as shown by the influence of acidity upon the reaction rate. In this case, the kinetic behaviour is similar to that exhibited by amines.