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1986. Magnocellular axons in passage through the median eminence release vasopressin. Nature 319: 326-329. S. H. Chan. 1985. Inhibition of central angiotensin II induced drinking by GABA in the rat. Clin. Exp. Hypertens. A6: 1777-1780. , and D. Felix. 1980. Angiotensin II-sensitive neurons in septal areas of the rat. Brain Res. 195: 187-195. R. Miselis. 1984. Area postrema and adjacent nucleus of the solitary tract in water and sodium balance. Am. J. Physiol. 247: R173-R182. M. Correa, M. M. Saavedra.

In contrast to catecholamines, the peptide does not shorten the time to peak systolic tension or the contraction cycle duration. 48 Michael J. , 1982). There is no evidence that IP 3 plays any role in the cardiac response to Ang II. , 1976). , 1965). In part, these responses are due to a decrease in coronary blood flow. Other possible mechanisms for a negative inotropic action will be discussed in Section IV,D, which concerns cardiac receptors and regulatory proteins. C. Cardiac Hypertrophy In 1971, Robertson and Khairallah reported autoradiographic evidence for perinuclear localization of 3 H in cardiocytes following the administration of [3H]Ang II to rats.

1966. Interrelationship between angiotensin II and the sympathetic nervous system. Pharmacol. Exp. Ther. 153: 530-537. , J. S. D. Connor. 1970. A central effect of angiotensin: release of pituitary pressor material. / . Pharmacol. Exp. Ther. 174:27-34. , J. Summy-Long, A. D. Connor. 971a. Influence of andrenergic blocking drugs on central angiotensin effects. Pharmacology 5: 205-214. , A. Daniels-Severs, J. J. Radio. 1971b. Effects of centrally administered angiotensin II on salt and water excretion.

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