• The use of systems analysis as an experimental tool for solving complex physiological problems is not new. Actually, systems analysis is merely the logical analysis of how systems perform. However, modern usage of the term implies a more formalized type of logic, especially a type of logic that includes quantification at each step in the analysis. Several of the figures in this paper illustrate systems analysis flow diagrams that show interrelationships between the different parts of simple or complex mechanisms for the control of arterial blood pressure. One can readily see that each part of each systems analysis diagram is only a symbolic way in which a composite of individual physiological phenomena fit together in a complete system.The principal advantage of the formalized systems analysis approach to understanding any physiological mechanism is that it often allows greater depth of thought than our minds can perform using simple logical procedures. The mind has the capability of holding and analyzing perhaps five to ten different sequential phenomena, each occurring at different rates and each interrelated with the other phenomena by various cross-linkages. However, beyond this size of system it is almost impossible to think through all the complex relationships simultaneously. On the other hand, the modern computer can handle literally thousands of such crosslinking interrelationships at the same time and can develop answers that the mind alone cannot achieve. Now setting aside this philosophizing about systems analysis per se, we will attempt to show how the systems analysis approach has been useful in the study of long-range arterial blood pressure control and the understanding of hypertensive
SUMMARY We studied the combined effect of subpressor amounts of angiotensin and long-term sodium chloride infusion on arterial pressure in 16 dogs for periods of 2-8 weeks. In dogs receiving 3.5 liters of isotonic NaCl daily, but no angiotensin, the arterial pressure increased an average of only 3 mm Hg. When angiotensin was infused continuously at a rate of 5 ng/kg per min (a rate too small to cause an observable immediate increase in pressure), subsequent infusion of 3.5 liters of saline daily then increased the pressure by 39 mm Hg. The urinary output of sodium increased to the same extent in both instances, that is, there was no extra sodium loss because of the elevated pressure. This suggests that the angiotensin significantly blocked the normal "pressure natriuresis" usually seen with such large increases in pressure. However, the plasma aldosterone levels during angiotensin infusion were not found to be different from those in the absence of angiotensin. Therefore, we have suggested that the tendency of the kidneys to retain sodium under the influence of angiotensin was probably caused mainly by a direct effect of angiotensin on the kidney itself. Such a direct renal sodium-retaining effect also could be a contributing factor in the marked hypertension that results from salt administration in the presence of small amounts of angiotensin.
SUMMARY The mean arterial pressure (MAP) of nine sinoaortic denervated (SAD) and eight control rats housed in standard-sized metabolic cages was determined continuously via aortic cannuiae and computerized data collection over 24 hours. These continuous measurements were compared with direct, mean aortic pressure measurements and indirect, tail-cuff systolic pressure determinations made while these rats were resting in a Luclte restralner. Denerrated rats were studied 1 month after debuffering. Both types of measurements made during restraint indicated that the SAD rats were hypertensive; the MAP averaged 145 ± 3.4 mm Hg (mean ± SEM) in SAD rats compared with 119 ± 2.8 mm Hg in the control group (p < 0.001), and the tailcuff pressure in SAD rats was 156 ± 5.4 vs 121 ± 2.7 mm Hg in control rats (p < 0.001). In contrast, continuous monitoring showed that the SAD rats were normotensive; the MAP averaged 119 ± 4. determined that the MAP of baroreceptor-denervated dogs was only 11 mm Hg greater than that of control animals if the pressure was monitored 24 hours per day. A recent report 5 indicates that these investigators have now recorded the MAP throughout the day in over 40 control and baroreceptor-denervated dogs, and the MAP in the denervated group averaged just 1 mm Hg greater than in the control. These SAD dogs had a much broader range of arterial pressure over a 24-hour period, but the MAP dropped to hypotensive levels as often as it rose to hypertensive levels. There are other reports, though, that baroreceptor denervation in dogs causes at least a mild hypertension.' 17The effect of baroreceptor denervation on the arterial pressure level of rats has been much less controversial, and in general the SAD rat has been Received February 12, 1980; revision accepted July 7, 1980. 119 accepted as a model for "neurogenic hypertension."" Studies of SAD rats have focused on determining the mechanism of this "neurogenic hypertension." Krieger 9 reported that cardiac output is normal in SAD rats, and that the hypertension is due to increased total peripheral resistance. Alexander et al. 10 demonstrated that plasma dopamine beta-hydroxylase is elevated in these denervated rats, and that plasma volume is decreased during the first few days following denervation but is normal thereafter.11 Chalmers et al. 12 reported that altered activity of central adrenergic and noradrenergic neurons may be important in initiating and maintaining hypertension in the SAD rat. However, the controversy about whether baroreceptor denervation of dogs produces hypertension suggested that the techniques used to measure pressure in SAD rats might be crucial in interpretation of these results.This study was designed to quantitate the effect of sinoaortic denervation on the blood pressure of rats during nominal restraint and during residence in a normal laboratory environment. The MAP was monitored 24 hours per day in conscious rats maintained in standard-sized metabolic cages. These continuous MAP data were then compared with pressures...
Renal denervation has been reported to delay development of hypertension in Okamoto spontaneously hypertensive rats (SHR) but to have no effect on the final hypertensive state. However, functional reinnervation begins to occur about 1 mo after renal denervation. The arterial pressure of SHR undergoing repeated bilateral renal denervations at the age of 4, 7, 10, 13, and 16 wk was compared with that in sham-operated SHR. In addition, the effect of successive renal denervations at 4, 7, and 10 wk of age in Wistar-Kyoto (WKY) control rats was determined. Both indirect measurement of pressure by the tail-cuff technique and mean arterial pressure (MAP) measurement indicated that renal denervation prevents full expression of hypertension in SHR. MAP in 19-wk-old renal-denervation SHR averaged 159 +/- 5.1 mmHg (SE) vs. 178 +/-0 4.2 mmHg in sham-operated SHR. Renal denervation had no effect on arterial pressure of WKY rats. Renal norepinephrine content in the renal-denervated WKY rats and SHR was less than 20% of that in the sham-operated groups. Successive bilateral renal denervations every 3 wk blocks 30-40% of the expected progressive elevation of arterial pressure in aging SHR.
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.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.