Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs

doi:10.1161/01.RES.27.5.799

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Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs

Journal Article•DOI•

Increased Cardiac Output as a Contributory Factor in Experimental Renal Hypertension in Dogs

Carlos M. Ferrario¹, Irvine H. Page¹, James W. Mccubbin¹•Institutions (1)

Cleveland Clinic¹

01 Nov 1970-Circulation Research (Lippincott Williams & Wilkins)-Vol. 27, Iss: 5, pp 799-810

TL;DR: Increased cardiac output probably has a contributory role in the development of renal hypertension, and absence of change in plasma volume and increase in mean circulatory pressure measured in a separate series of 7 dogs suggest that the initial increase in cardiac output preceding rise in pressure was due to enhanced venous return consequent to constriction of capacitance vessels.

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Abstract: It has been suggested, but not established, that renal hypertension is initiated by increase incardiac output. Recent refinements in electromagnetic flowmeter technology allowed a critical reevaluation of this possibility. Flowmeters were implanted around dogs' ascending aortas and arterial catheters inserted; measurements were made daily before and after production of hypertension by the cellophane perinephritis method. Eight to 15 days after wrapping one kidney in cellophane, with the opposite kidney untouched, group averages for both stroke volume and cardiac output rose significantly (P < 0.005) though there was no change in arterial pressure. Both heart rate and peripheral resistance decreased slightly. Following these measurements, the contralateral normal kidney was removed and measurements were recommenced 24 hours later. After 4 to 7 days, mean arterial pressure rose progressively in all dogs, reaching a plateau 77 ± 8 (SE) mm Hg above control after 14 to 25 days. Hypertension was associated init...

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Journal Article•DOI•

Circulation: Overall Regulation

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Arthur C. Guyton, Thomas G. Coleman, Harris J. Granger

01 Jan 1972-Annual Review of Physiology

832 citations

Journal Article•DOI•

Collagen remodeling of the pressure-overloaded, hypertrophied nonhuman primate myocardium.

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Karl T. Weber, J. S. Janicki, Sanjeev G. Shroff, Ruth Pick, R M Chen, R I Bashey - Show less +2 more

01 Apr 1988-Circulation Research

TL;DR: Early in left ventricular hypertrophy, reactive fibrosis and collagen remodeling occur in the absence of necrosis while, later on, reparative fibrosis is present; in this study, the remodeled collagen matrix appeared responsible for variations in force generation observed during various phases ofleft ventricularhypertrophy.

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Abstract: Cardiac muscle is tethered within a fibrillar collagen matrix that serves to maximize force generation. In the human pressure-overloaded, hypertrophied left ventricle, collagen concentration is known to be increased; however, the structural and biochemical remodeling of collagen and its relation to cell necrosis and myocardial mechanics is less clear. Accordingly, this study was undertaken in a nonhuman primate model of left ventricular hypertrophy caused by gradual onset experimental hypertension. The amount of collagen, its light microscopic features, and proportions of collagen types I, III, and V were determined together with diastolic and systolic mechanics of the intact ventricle during the evolutionary, early, and late phases of established left ventricular hypertrophy (4, 35, and 88 weeks, respectively). In comparison to controls, we found 1) increased collagen at 4 weeks, as well as a greater proportion of type III, in the absence of myocyte necrosis; 2) collagen septae were thick and dense at 35 weeks, while the proportion of types I and III had converted to control; 3) necrosis was evident at 88 weeks, and the structural remodeling and proportion of collagen types I and III reflected the extent of scar formation; and 4) unlike diastolic myocardial stiffness, which was unchanged at 4, 35, or 88 weeks, the systolic stress-strain relation of the myocardium was altered in either a beneficial or detrimental manner in accordance with structural remodeling of collagen and scar formation. Thus, early in left ventricular hypertrophy, reactive fibrosis and collagen remodeling occur in the absence of necrosis while, later on, reparative fibrosis is present.(ABSTRACT TRUNCATED AT 250 WORDS)

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574 citations

Journal Article•DOI•

Beta adrenergic blockade in hypertension. Practical and theoretical implications of long-term hemodynamic variations.

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Robert C. Tarazi¹, Harriet P. Dustan¹•Institutions (1)

Cleveland Clinic¹

01 May 1972-American Journal of Cardiology

TL;DR: The hypertensive effect of propranolol seemed to imply a long-term adaptation of peripheral resistance to chronic reduction of output, which nearly always controlled any tachycardia due to or persisting despite the other drugs and often improved the response of blood pressure.

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Abstract: The effectiveness of propranolol, used alone, in reducing arterial pressure was reevaluated in 52 hypertensive patients (42 with essential and 10 with renovascular hypertension) with special regard to the hemodynamic basis for patient selection and the relation of variations in cardiac output to control of blood pressure. Repeated hemodynamic studies were performed before and during chronic treatment with propranolol, and in all the efficacy of beta adrenergic blockade was demonstrated by inhibition of chronotropic response to infusion of isoproterenol. Four patients discontinued propranolol because of side effects; among the rest, arterial pressure was reduced in 26 and unchanged in 22. There was no difference in responsiveness between subjects with essential and renovascular hypertension. Arterial pressure responses could not be predicted from hemodynamic values before treatment; although increased cardiac output was more frequent among responders than among nonresponders (59 vs. 37 percent), group averages were not significantly different. Treatment reduced cardiac output in both groups, so that effect on arterial pressure was related to changes in total peripheral resistance (r = 0.737, P <0.001) not to changes in output (r = 0.067). Thus, the hypertensive effect of propranolol seemed to imply a long-term adaptation of peripheral resistance to chronic reduction of output. The prolonged follow-up and repeat studies allowed a hemodynamic characterization of the occasional hypertensive responses to office visits and investigative procedures. These transient responses were not prevented during treatment although their hemodynamic basis was altered so that they were always related to increased peripheral resistance. Used in combination with other antihypertensive agents (12 patients), administration of propranolol nearly always controlled any tachycardia due to or persisting despite the other drugs and often improved the response of blood pressure.

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416 citations

Journal Article•DOI•

The role of humoral agents in volume expanded hypertension.

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Francis J. Haddy¹, Henry W. Overbeck¹•Institutions (1)

Michigan State University¹

01 Oct 1976-Life Sciences

TL;DR: Evidence suggests that some humoral agent or agents, operating through the Na+−K+ pump in cardiovascular muscle, participate in the genesis of the volume expanded hypertensions.

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406 citations

Journal Article•DOI•

Hypertension in chronic renal failure: An abnormal relation between sodium and the renin-angiotensin system

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M.A. Schalekamp, D.G. Beevers, J. D. Briggs, J. J. Brown, D.L. Davies, Fraser R, M. Lebel, Anthony F. Lever, A. Medina, James J. Morton, J.I.S. Robertson - Show less +7 more

01 Sep 1973-The American Journal of Medicine

TL;DR: In this article, it was suggested that the rise in arterial pressure in this group results from a failure of renin to suppress normally with sodium retention, which may perpetuate the hypertension.

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184 citations

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References

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Journal Article•DOI•

On the local reactions of the arterial wall to changes of internal pressure.

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W. M. Bayliss

28 May 1902-The Journal of Physiology

TL;DR: My attention was first directed to these phenomena by the occurrence of curves like that reproduced in Fig. 11, which showed the effect of a fall of arterial pressure produced by exI citing the central end of the depressor nerve on the volume of the hind leg of the rabbit, the sciatic and the nerves accompanying the femoral artery having been cut.

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Abstract: MY attention was first directed to these phenomena by the occurrence of curves like that reproduced in Fig. 11. In the course of experiments on vaso-dilator reflexes I sometimes observed what looked like a reflex of this kind, in a limb of which the nerves had been divided; the figure _ reproduced shows the effect of a fall of arterial pressure produced by exI citing the central end of the depressor nerve on the volume of the hind leg of the rabbit, the sciatic and the nerves accompanying the femoral artery having been cut. It will be noticed that as long as the fall of blood-pressure lasts there is a passive diminution of volume in the limb, but that as soon as the previous height of blood-pressure is attained, on cessation of the excitation, there is a considerable expansion of the limb lasting for some time. Such a curve would usually be explained by stating that Fig. 1. Effect of depressor excitation on there was present all through the volume of enervated leg. Upper curve blood-pressure, next below it volume of excitation a relaxration of the vessels, leg, upper of two chronographs-period but that it was prevented from showof excitation of depressor nerve, lower ing itself in an actual expansion of one-time in 10 sec. intervals. the limb by the simultaneous fall of blood-pressure; although it was

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1,466 citations

"Increased Cardiac Output as a Contr..." refers background in this paper

...They propose that any increase in total peripheral resistance is due to the Bayliss From the Research Division, Cleveland Clinic Foundation, Cleveland, Ohio 44108....
[...]
...Forty-two days after nephrectomy, only one dog (2) continued to show increases in both cardiac output and peripheral resistance....
[...]
...Although it has been suggested that longterm, whole body "autoregulation" can occur and be the basis for gradual increase in peripheral resistance (2, 5, 20), it is not yet established experimentally that it occurs over a period of days or months....
[...]
...We suggest the following sequence of events: increased venous return due to increased venous tone increases the filling pressure of the heart and causes both larger end-diastolic ventricular and stroke volume; this in turn increases cardiac output, and cardiac slowing may also contribute by lengthening the ventricular filling time; arterial pressure does not increase at this time, probably because decrease in peripheral resistance accommodates the excess circulating flow; after the normal kidney is removed (with the associated loss of the undefined "antihypertensive function" of the kidney), further increase in cardiac output causes increase in both arterial pressure and peripheral resistance; increase in peripheral resistance may depend, at least in part, on existence of an "autoregulatory" mechanism as suggested by Bayliss (2)....
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Journal Article•DOI•

The production of persistent arterial hypertension by cellophane perinephritis

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Irvine H. Page

02 Dec 1939-JAMA

TL;DR: During the course of experiments designed to prevent the development of renal cortical collateral circulation, cellophane was tried because it was believed that it would cause little damage to the tissues, but it was soon apparent that arterial hypertension had developed in the animals in whichcellophane had been wrapped around the kidneys.

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Abstract: Perinephritis apparently has not been recognized as a possible cause of arterial hypertension. Occasionally hypertension has been recorded for patients whose renal parenchyma from one cause or another has been chronically compressed. Any genetic relationship seems, however, to have been ignored. During the course of experiments designed to prevent the development of renal cortical collateral circulation, cellophane was tried because it was believed that it would cause little damage to the tissues. It was soon apparent that arterial hypertension had developed in the animals in which cellophane had been wrapped around the kidneys. Examination showed them to be enclosed within a fibrocollagenous hull from 3 to 4 mm. thick. The cellophane had been fragmented and taken up, chiefly by the omentum. The kidney bulged from the hull when it was cut, indicating that the parenchyma was held fast under tension. The reaction of tissue to cellophane is extraordinary. Contact for relatively short periods (three to thirty days) is enough to evoke a proliferative reaction which continues for a time, at least, after the cellophane has been dispersed by the omentum.

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406 citations

"Increased Cardiac Output as a Contr..." refers background or methods in this paper

...At the conclusion of this control period, each dog's left kidney was wrapped in cellophane using the technique described by Page (6, 8)....
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...Olmsted and Page (4) implanted electromagnetic flowmeters in dogs and found that both heart rate and cardiac output decreased during the first 4 days after renal artery constriction and contralateral nephrectomy; rise in arterial pressure was due entirely to increased peripheral resistance....
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...On the other hand, Olmsted and Page (4) found in dogs that onset of experimental renal hypertension due to renal artery constriction and contralateral nephrectomy was accompanied by decrease in cardiac output and heart rate, while there was an abrupt rise in peripheral resistance....
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...Cardiac output returned to the control level in one dog (6) during the fourth week, in two other dogs (3 and 5) during the fifth week and in two others (1 and 7) during the sixth week (Tables 2 and 3)....
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...The cellophane perinephritis method of producing hypertension in dogs (6) was chosen, in part because the hemodynamic changes accompanying this type of hypertension have not been measured previously....
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Journal Article•DOI•

Hemodynamics of Hypertension

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Edward D. Freis

01 Jan 1960-Physiological Reviews

TL;DR: In such a broad coverage, material presented in previous reviews of cardiovascular function must be discussed, and it is hoped that these excursions will not be considered a reiteration of the obvious.

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Abstract: HE HEMODYNAMICS OF HYPERTENSION have not been a popular subject for review. In 1938 Wiggers (246) summarized primarily the excellent work of his own group on this subject. It is fitting that a fresh attempt be made to correlate the hemodynamic features of hypertension, particularly as it is evidenced in man, with current physioIogica1 concepts. In such a broad coverage, material presented in previous reviews of cardiovascular function must be discussed. It is hoped that these excursions will not be considered a reiteration of the obvious. To provide an organizationa framework the hemodynamic features are considered in relation to the various functional subdivisions of the cardiovascular system. Certain aspects not readily covered on this basis are discussed in separate sections.

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345 citations

Journal Article•DOI•

Hypertension explained by starling's theory of circulatory homœostasis

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J.G.G. Borst¹, Alida Borst-de Geus¹•Institutions (1)

University of Amsterdam¹

30 Mar 1963-The Lancet

264 citations

Journal Article•DOI•

Hypertension Caused by Salt Loading in the Dog

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Thomas G. Coleman¹, Arthur C. Guyton¹•Institutions (1)

University of Mississippi¹

01 Aug 1969-Circulation Research

TL;DR: It is concluded that salt loading in a partially nephrectomized dog causes elevated arterial pressure that is initially induced by increased cardiac output but that is eventually sustained by increased peripheral resistance.

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Abstract: Experimental hypertension was produced in dogs by salt loading after renal mass had been surgically reduced to an estimated one-third normal. Salt loading was accomplished in one group of five dogs by administering isotonic saline in lieu of drinking water and in another group of six dogs by continuously infusing isotonic saline. Arterial pressure, cardiac output, heart rate, stroke volume, and total peripheral resistance were determined at frequent intervals during a 1-week control period and a 2-week salt-loading period in both groups. In addition, right atrial pressure, blood urea nitrogen, serum sodium, and serum potassium were determined in the group that was continuously infused. Both groups demonstrated an increase in mean arterial pressure to hypertensive levels, transiently increased cardiac output and stroke volume, initially depressed then subsequently increased total peripheral resistance, and initially depressed and variable heart rate. It is concluded that salt loading in a partially nephrectomized dog causes elevated arterial pressure that is initially induced by increased cardiac output but that is eventually sustained by increased peripheral resistance. Possible mechanisms are discussed.

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263 citations

"Increased Cardiac Output as a Contr..." refers background in this paper

...Although it has been suggested that longterm, whole body "autoregulation" can occur and be the basis for gradual increase in peripheral resistance (2, 5, 20), it is not yet established experimentally that it occurs over a period of days or months....
[...]
...Mean circulatory pressures were estimated by the method described by Guyton et al. (14) within an average of 6 seconds after stopping the heart (range 4 to 8 seconds)....
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...While others have suggested that an increase in cardiac output may accompany experimental renal hypertension (1, 5, 19, 20) we were nonetheless surprised that the increase, though modest, occurred with regularity....
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...Coleman and Guyton (20) administered large amounts of fluid to dogs with diminished renal mass and produced hypertension accompanied by increase in plasma and extracellular fluid volumes....
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