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The renin-angiotensin-aldosterone system: a personal perspective and Festschrift for John H. Laragh, MD.

John Laragh has been a great inspiration to me and many others in the field of hypertension research. His inquisitive mind, deep knowledge of physiology and medicine, and keen clinical insights led him to discoveries and innovation that were critical to our current understanding of the renin– angiotensin–aldosterone system (RAAS) and to the development of effective therapies for hypertension. I first met John in the 1970s during one of his visits to Mississippi, along with his research group, to meet with our Department of Physiology, led at that time by Arthur Guyton. My lab was engaged in basic research studies on the intrarenal actions of angiotensin II (Ang II) in regulating glomerular filtration rate, tubular reabsorption, and longterm control of blood pressure, and I was deeply impressed by the work of John and his colleagues at Cornell. Teprotide (SQ-20881), the peptide inhibitor of angiotensin-converting enzyme (ACE), and peptide antagonists of the ANG II type 1 receptor were just becoming available, and I was eager to use these compounds to investigate the intrarenal role of Ang II in long-term blood pressure regulation. One major reason for my interest was John’s previous studies that showed that low-dose Ang II infusions in humans had powerful effects on blood pressure that were not only sustained but also actually amplified during several days of infusion. 1 The progressive hypertensive effect of Ang II was related to sodium balance and was even more impressive than that of aldosterone. The effects of Ang II contrasted with those of norepinephrine, which had progressively weaker blood pressure effects during several days of infusion and caused either natriuresis or no change in sodium balance. 1 In a seminal series of studies in humans, John and his colleagues found that Ang II controls sodium balance and blood pressure not only through stimulation of aldosterone but also by direct actions on the kidneys. A paragraph in his 1965 paper in the Journal of Clinical Investigation 1 was especially enlightening: