The steady-state relationship between mean arterial pressure (AP) and output of sodium and water was determined for one-kidney control (1KC), one-kidney Goldblatt (1KG), normotensive Wistar-Kyoto (WKY), and Okamoto spontaneously hypertensive rats (SHR). Control fluid intake (given by intravenous infusion) was set at approximately 30 ml/day Ringer solution. The infusion rate was then increased progressively to 2, 4, and 8 times control for 24- to 48-h periods each. Control AP averaged 115 Torr in 1KC, 152 Torr in 1KG, 120 Torr in WKY, and 158 Torr in SHR. The eightfold increase in salt and water intake was accompanied by almost equal increase in salt and water output and increases in AP to 157 Torr in 1KC, 190 Torr in 1KG, 126 Torr in WKY, and 166 Torr in SHR. The arterial pressure-urinary output relationship in 1KG is parallel to that of 1KC but shifted to higher AP levels. Similarly, this relationship in SHR is parallel to that of WKY but shifted to higher AP levels. This parallel shift is indicative of uniform renal vasoconstriction but normal functional renal mass in the SHR.
Approximately 70% of the total renal tissue was removed in 11 dogs. Control values were then established for mean arterial pressure, urine and plasma sodium concentrations, blood urea nitrogen, glomerular filtration rate, total body weight, and rate of urine formation for these dogs and for two dogs whose kidneys were left intact. Two of the partially nephrectomized dogs were allowed to drink water for the duration of the study while the other animals were required to drink 0.9% sodium chloride solution for various periods of time. The increased salt intake resulted in a 30% to 40% increase in arterial pressure within 48 to 72 hours; plasma sodium concentration increased concomitantly with the development of hypertension. The elevated pressure could be reduced to normal levels within 24 hours by simply allowing the dogs to drink tap water again. Similar results were obtained in a single dog in which renal function had fortuitously been reduced by chronic pyelonephritis.
Experimental hypertension was produced in dogs by increasing their dietary intake of sodium chloride after removing approximately 70% of their renal tissue. The changes in mean arterial pressure, interstitial fluid pressure, blood volume, and sodium space were observed during the development and maintenance of the hypertension. During the periods of increased salt intake, the arterial pressure increased from a mean of 114.6 mm Hg to a mean of 150.6 mm Hg, and there were concomitant increases of 19.8% in blood volume, 16% in sodium space, and 4 cm H2O in interstitial fluid pressure. However, the increases in all the paramteers studied except arterial pressure were transient. The blood volume remained elevated above control values for a longer period of time than the sodium space and interstitial fluid pressure, but it reapproached normal after approximately 16–20 days.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.