IN RESPONSE:
We thank the Goldblatts for their letter and appreciate their interest, and we would like to respond to their comments.
Harry Goldblatt did not mention that the conclusions of his own work presented in 1934 had been reported previously. For this reason, we believe that John Loesch did not receive due recognition until he was recalled by us.
The Goldblatts cited Fahr using their father's article. Indirect quotation may result in changes, as in the case of P.J. Goldblatt's statement on the lecture of 1932 (1). Loesch's article is actually in 3 parts. Loesch was familiar with Volhard's vasospasm hypothesis, but he did not test it (2, 3). Goldblatt and Loesch both realized that they could generate persistent hypertension by means of ischemia, and both of them rightly received recognition for this. Loesch stated very clearly that he did not occlude the ureter. To prevent uremia, he successfully varied the occlusion intervals and, thus, the extent of ischemia. He was, therefore, able to extend the animals' lives, and this fact should be acknowledged. Goldblatt also had to deal with the problem of animals dying due to uremia. Goldblatt, in contrast to Loesch, did not examine the urine sediment.
At least 2 different "Goldblatt models" are known. We believe it would be appropriate to call them "LoeschGoldblatt models," because Goldblatt had not yet fully realized the difference between the 2 models in 1934. The "one kidneyone clip model" in a rabbit, for example, does not exhibit "the characteristics of benign human essential hypertension" because these animals die of malignant hypertension after a few weeks (4).
The LoeschGoldblatt models still puzzle us, but a solution to one of the greatest puzzles is now imminent: The structures of the lipid antihypertensive hormones, the "medullipins" and "angiolysins," which are released by the kidney into the bloodstream after "unclipping" or when perfusion pressure is increased (4), will be elucidated shortly. These are among the most potent antihypertensive agents and vasodilators known (5, 6). The means of achieving this are now available (5, 6). The paradigm will shift once more, and then we will again remember 2 great researchers: Harry Goldblatt and John Loesch.
1. Goldblatt PJ. The Goldblatt experiment: a conceptual paradigm. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis, and Management. 2nd ed. New York: Raven Pr: 1995;23-35.
2. Loesch J. Ein Beitrag zur experimentellen Nephritis und zum arteriellen Hochdruck. I. Die Veränderungen im Blutdruck. II. Die Veränderungen in der Blutchemie. Zentralblatt für Innere Medizin. 1933;7:144-169.
3. Loesch J. Ein Beitrag zur experimentellen Nephritis und zum arteriellen Hochdruck. III. Die Veränderungen in den Geweben. Zentralblatt für Innere Medizin. 1933;8:177-85.
4. Muirhead EE. Renomedullary vasodepressor lipid: medullipin. In: Swales ED, ed. Textbook of Hypertension. Oxford: Blackwell Scientific Publications; 1994:341-59.
5. Glodny B, Pauli GF. The vasodepressor function of the kidney: prostaglandin E2 is not the principal vasodepressor lipid of the renal medulla. Acta Physiol (Oxf). 2006;187:419-30. [PMID: 16776667].[Medline]
6. Glodny B, Pauli GF. The vasodepressor function of the kidney: further characterization of medullipin and a second hormone designated angiolysin. Hypertens Res. 2006;29:533-44. [PMID: 17044666].[Medline]