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28 Anwar H. Subratty and Fawzia B. H. Gunny Figure 1: Cumulative dose response curve showing effects of ACE inhibitor, captopril (1M) on TAME-induced contractions on rat aorta. Figure 2: Tracing showing effects of captopril 0.01 M on TAME-induced contractions on rat aorta in vitro. show that contractile responses induced by TAMEesterase could be the result of degradation of kinins by kininase. The latter hypothesis is confirmed from experiments using the ACE inhibitor. Findings from these experiments have shown that when strips were pre-incubated with Captopril (1M), there was a definite significant inhibition of the contractile responses previously seen with TAME alone. Based on our findings we thus postulate the following mechanism for TAME-esterase induced contractions. During the conversion of high molecular weight kininogens to kinins in the presence of kallikreins whereby TAME-esterase is a zymogen, bradykinin which is released is degraded by a kininase (kininase II). In the presence of a sufficient dose of a kininase II inhibitor, namely Captopril, the contractile effects of the kininase is substantially attenuated to the extent that no significant contractions were observed. As mentioned earlier, we have already reported two different mechanisms by which TAME-esterase induce contraction in-vitro. Through the present study, we are describing a third pharmacological pathway showing that TAME-esterase induced contractions involve degradation of kinins by kininase. We conclude that TAME-esterase induced contractions can be prevented by the use of ACE inhibitors. However the role of TAME-esterase in hypertension remains to be established. Acknowledgement We are grateful to the Tertiary Education Commission of Mauritius and the University of Mauritius for financial support. References Bhoola DK, Figueroa CD and Worthy K. Bioregulation of Kinins, Kallikrein Kininoges and Kinases. Pharmacol. Rev. 44: 1-80, 1992. Andreas DA, Wolfrum S and Dominiak A. Pharmaocology and cardiovascular Implications of the Kinin-Kallikrein System. Jpn. J.Pharmacol. 79: 403-426, 1999. DeMery JG, Vanhoutte PM. The Endothelium: Modulator of cardiovascular Function. Boca Raton: CRC Inc, 1990. Figuera CD, Gonzales CB, Muller-Esterl W and Bhoola KD. Cellular Localization of Human Kininogens. Agents Actions. 38(1): 617-626, 1992. Furchgott RF and Zawadzki JV. The Obligatory Role of Endothelial Cells in the relaxations of the arterial Smooth Muscle by Acetylcholine. Nature. 286: 373-376, 1980. Hashimoto K, Hamamoto H, Honda Y, Hirose M, Furukawa S and Kimura E. Changes in Components of Kinin System and Hemodynamics in Acute Myocardial Infarction. Am. Heart J. 95: 619-626, 1978. Linz W and Scholkens B. Role of Bradykinin in the Cardiac Effects of Angiotensin- Converting enzyme Inhibitors. J. Cardiovasc. Pharmacol. 20(9): S 83-90, 1992. Scholkens BA. Kinins in the cardiovascular system. Immunopharmacol. 33: 209-216, 1996. Schmaier AH, Kuo A, Lundberg D, Murray S and Clines DB. The Expression of High Molecular Weight Kininogen in Human Umbilical Vein Endothelial Cells. J. Biol. Chem. 263: 16327-16333, 1988. Subratty AH and Hossany R. Does TAME induced contraction involve an endothelium nitric oxide-cyclic GMP mediated pathway? Indian. J. Exp. Biol. 37: 406-
408, 1999. Subratty AH, Lee Kwai Yan MY and Kok Shun LH. TAME–esterase activity during a prolonged attack of asthma. Inter. Clin. Pharmacol Ther. 32(11): 598-599, 1999. Subratty AH and Moonsamy J. Is TAME a potent constrictor of non-airway smooth muscles? Indian. J. Exp. Biol. 36: 618-621, 1994. Vanhoutte PM, Boulanger CM, Vidal MJ and Mombouli JV. Endothelium-Derived Mediators and the Renin Angiotensin System. In The Renin- Angiotensin System. Edited by Robertson JIS, Nicholls MG, London. 71: 291, 1993. Captopril effects on contractions 29
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