By H. E. de Wardener, G. A. MacGregor (auth.), Franz H. Messerli MD (eds.)
The kidney, just like the guts, performs a three-fold function in crucial high blood pressure. First, it participates within the patho genesis of arterial high blood pressure. moment, it suffers as a aim organ of long-standing high blood pressure, and 3rd, it stories the consequences of antihypertensive treatment. might be so much contested this day is the involvement of the kidney within the patho genesis of crucial high blood pressure. greater than a century in the past, William Osler recommend 3 simple hypotheses concerning the "genuine reduced in size kidney. "l 1. "The hypertrophy could be considered as an impact to beat a kind of stop-cock motion of the vessels while less than the effect of an frustrating aspect within the blood vastly reduced in size and elevated the peripheral resistance. " essentially this speculation of an "irritating factor" could be the main convincing these days, and various makes an attempt were made to spot a selected vasoconstrictive agent within the blood in crucial high blood pressure. 2. "The obliteration of a big variety of capillary territories within the kidney materially raised the arterial strain. an extra issue of dimin ished excretion of water additionally heightened the strain in the blood vessel. " this present day we all know that fluid quantity overload within the presence of diminished renal mass appears to be like the main most likely mechanism accoun ting for renal parenchymal high blood pressure and, as proven by means of Guyton's team, for definite varieties of experimental high blood pressure. 3.
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Additional resources for Kidney in Essential Hypertension: Proceedings of the Course on the Kidney in Essential Hypertension held at New Orleans, Louisiana, March 18–19, 1983
11, p. 482, eds. B. Samuelsson, R. Paoletti and P. Ramwell, Raven Press, NY, 1983). 45 several minutes (5). defensive role. As noted, this mechanism serves a primary It is evoked when renal fUnction is threat- ened, as in response to excitation of renal nerves or activation of the renin-angiotensin system, and can be unmasked by inhibiting prostaglandin synthesis with indomethacin. For example, in the dog stressed by anesthesia and abdominal surgery, in contrast to the dog at rest, indomethacin caused a sharp decline in renal blood flow (6).
Proc Soc Exp BioI Med (161):508511, 1979. 9. Marie JP, Guillemot H, Hatt PY: Le degree de granulation des cardiocytes auriculaires. Etude planimetrique au cours des different apports d'eau et de sodium chez Ie rat. Pathol BioI (24):549, 1976. 1. 23 10. Sonnenberg H, Chong CK, Veress AT: Cardiac atrial factor -an endogenous diuretic? Can J Physiol Pharmacol (59):1278-1279, 1981. 11. Cupples WA, Veress AT, de Bold AJ, Sonnenberg H: Effect of cardiac atrial extract on segmental nephron transport in the rat kidney.
1984 Martinus Nijhoff Publishing, Boston/The HaguelDordrechtiLancaster. All rights reserved. 44 For example, PGE 2 was shown to inhibit the vasoconstrictor response to adrenergic nerve stimulation in the peptides (2). isolated kidney of the rabbit at a concentration two hundredfold less than that which dilates this vascular bed (3). This concentration of PGE 2 , 20 pg/ml, is likely to be realized intrarenally, as peak concentrations of PGE 2 in renal venous effluent and urine, which reflect tissue levels in the kidney, are well above this.
Kidney in Essential Hypertension: Proceedings of the Course on the Kidney in Essential Hypertension held at New Orleans, Louisiana, March 18–19, 1983 by H. E. de Wardener, G. A. MacGregor (auth.), Franz H. Messerli MD (eds.)