Combined effects of angiotensin converting enzyme inhibition and angiotensin II receptor antagonism in conscious pigs with congestive heart failure.

[1]  S. Prahalada,et al.  Lack of beneficial effects of growth hormone treatment in conscious dogs during development of heart failure. , 1998, American journal of physiology. Heart and circulatory physiology.

[2]  I. Zucker,et al.  Central gain of the cardiac sympathetic afferent reflex in dogs with heart failure. , 1997, The American journal of physiology.

[3]  M. Thames,et al.  Enalaprilat augments arterial and cardiopulmonary baroreflex control of sympathetic nerve activity in patients with heart failure. , 1996, Journal of the American College of Cardiology.

[4]  R. Walsh,et al.  Effects of angiotensin II generated by an angiotensin converting enzyme-independent pathway on left ventricular performance in the conscious baboon. , 1995, The Journal of clinical investigation.

[5]  T. Unger,et al.  Contribution of kinins to the cardiovascular actions of angiotensin-converting enzyme inhibitors. , 1995, Pharmacological reviews.

[6]  A. Katz The Cardiomyopathy of Overload: An Unnatural Growth Response in the Hypertrophied Heart , 1994, Annals of Internal Medicine.

[7]  S. Vatner,et al.  Factors involved in delaying the rise in peripheral resistance in developing heart failure. , 1994, The American journal of physiology.

[8]  M. Moroi,et al.  Endothelium-dependent relaxation by angiotensin-converting enzyme inhibitors in canine femoral arteries. , 1994, The American journal of physiology.

[9]  R. Busse,et al.  Angiotensin-converting enzyme inhibitors unmask endogenous kinin production by bovine coronary artery endothelium. , 1993, European heart journal.

[10]  K. Lally,et al.  Hormonal response of the premature primate to operative stress. , 1993, Journal of Pediatric Surgery.

[11]  Y. Miura,et al.  ENALAPRILAT RESTORES SENSITIVITY OF BAROREFLEX CONTROL OF RENAL AND TOTAL NORADRENALINE SPILLOVER IN HEART FAILURE RABBIT , 1993, Clinical and experimental pharmacology & physiology.

[12]  P. Hjemdahl,et al.  Converting enzyme inhibition modulates sympathetic neurotransmission in vivo via multiple mechanisms. , 1993, The American journal of physiology.

[13]  P. Vanhoutte,et al.  Endothelium-dependent effects of converting-enzyme inhibitors. , 1993, Journal of cardiovascular pharmacology.

[14]  W. Greenlee,et al.  In vitro pharmacology of L-158,809, a new highly potent and selective angiotensin II receptor antagonist. , 1992, The Journal of pharmacology and experimental therapeutics.

[15]  W. Greenlee,et al.  In vivo pharmacology of L-158,809, a new highly potent and selective nonpeptide angiotensin II receptor antagonist. , 1992, The Journal of pharmacology and experimental therapeutics.

[16]  P. Vanhoutte,et al.  Local production of kinins contributes to the endothelium dependent relaxations evoked by converting enzyme inhibitors in isolated arteries. , 1992, Agents and actions. Supplements.

[17]  D. Warltier,et al.  Mechanism of Coronary Vasodilation Produced by Bradykinin , 1991, Circulation.

[18]  G. Riegger,et al.  Systemic vasoconstriction induced by inhibition of nitric oxide synthesis is attenuated in conscious dogs with heart failure. , 1991, Cardiovascular research.

[19]  K. Misono,et al.  Identification of a highly specific chymase as the major angiotensin II-forming enzyme in the human heart. , 1990, The Journal of biological chemistry.

[20]  B. Healy,et al.  Angiotensin II-forming pathways in normal and failing human hearts. , 1990, Circulation research.

[21]  G. Bönner Kinin-related effects of angiotensin-converting enzyme inhibition. , 1990, Clinical physiology and biochemistry.

[22]  N. B. Olivier,et al.  Heart failure depresses endothelium-dependent responses in canine femoral artery. , 1989, The American journal of physiology.

[23]  M. Miyazaki,et al.  Different distribution of two types of angiotensin II-generating enzymes in the aortic wall. , 1987, Biochemical and biophysical research communications.

[24]  F. Tristani,et al.  Effect of Vasodilator Therapy on Mortality in Chronic Congestive Heart Failure. Results of a Veterans Administration Cooperative Study , 1987 .

[25]  F. Tristani,et al.  Effect of Vasodilator Therapy on Mortality in Chronic Congestive Heart Failure , 1986 .

[26]  H. B. Stoner,et al.  The relationship of plasma catecholamines to acute metabolic and hormonal responses to injury in man. , 1985, Circulatory shock.

[27]  M. Miyazaki,et al.  Evidence for a putatively new angiotensin II-generating enzyme in the vascular wall. , 1984, Journal of hypertension.

[28]  J. Cohn,et al.  Activity of the sympathetic nervous system and renin-angiotensin system assessed by plasma hormone levels and their relation to hemodynamic abnormalities in congestive heart failure. , 1982, The American journal of cardiology.

[29]  J. Halter,et al.  Mechanism of plasma catecholamine increases during surgical stress in man. , 1977, The Journal of clinical endocrinology and metabolism.

[30]  N. T. Smith,et al.  Effects of Halothane on Left Ventricular Function and Distribution of Regional Blood Flow in Dogs and Primates , 1974, Circulation research.

[31]  D. Garcia-Dorado,et al.  Cardiovascular Research , 1966 .