Persistent Hypertension in the Dog Following Disruption of the Carotid Sinus Nerves and Subsequent Unilateral Renal Artery Constriction

Kezdi, Paul

doi:10.1161/01.res.8.5.934

Cited by 12 publications

(6 citation statements)

References 15 publications

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“…" 17 In the present study of neurogenic hypertensive rats no positive correlation was observed between increases in pressure and increases in heart rate. The facts that these rats had intact all the efferent vagal fibers to the heart and that the heart rate in the rat is normally under almost maximal sympathetic tonus, 28 -M may partially explain why the unrestrained quiet denervated rats exhibited hypertension accompanied by normal heart rate.…”

contrasting

confidence: 62%

“…" 17 In the rats of the present study no appreciable changes of pressure were observed after pure sinus denervation, but the elimination of only the aortic depressor fibers produced a transitory hypertension. Further work is necessary to assess whether there is really a predominance of the aortic over the sinus depressor fibers in the regulation of blood pressure in the rat.…”

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confidence: 43%

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Neurogenic Hypertension in the Rat

Krieger

1964

Circulation Research

493

228

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Several techniques of radical denervation of the sino-aortic depressor areas were tried in order to produce a permanent neurogenic hypertension in the rat. The aortic depressor fibers were interrupted at the neck level by resecting the nerves which usually exhibit baroreceptor activity, namely, isolated aortic nerve, sympathetic, and laryngeal nerves. The carotid sinus was denervated by stripping the carotid bifurcation and painting with phenol. When the carotid bifurcation was resected bilaterally, in a one-stage operation, all rats showed symptoms of cerebral ischemia, dying shortly thereafter. Isolated denervation of the aortic baroreceptors was followed by a transitory hypertension. No changes in preasure were observed when only the carotid sinuses were denervated. A few rats in which the usual baroreceptor pathways were interrupted, except the superior laryngeal nerve, developed chronic hypertension. Yet, to obtain consistently permanent hypertension it was necessary to include in the denervation every baroreceptor route. A simple one-stage operation for complete sino-aortic baroreceptor denervation is described. This procedure was used in 140 rats that were then studied for periods up to one year. All the operated animals presented some degree of hypertension. Blood pressure measurements made during the first week showed even then that the rats were hypertensive. This observation suggests that in the rat no latent period for the appearance of neurogenic hypertension is present. Hypertension was permanent in 75% of the rats observed up to one year; blood pressure returned to normal values in the remaining 25%, usually after the third month. Extirpation of the adrenal medulla had no effect on the evolution of the hypertension in the denervated rats. Blood pressure was measured repeatedly in unanesthetized rats by tail plethysmography. Pressure values determined by this method, though 10 to 20 mm Hg lower, approximated the mean arterial pressure recorded directly from the femoral artery in normotensive and hypertensive rats. The hypertension in denervated rats included an increase of systolic as well as diastolic pressure. The heart rates of quiet hypertensive rats were within the normal range and, in general, no close correlation was observed between increases in blood pressure and elevations in heart rate. Normal rats have marked fluctuations in both pressure and heart rate when walking or when stimulated; these fluctuations were much greater in the neurogenic hypertensive animals. Moreover, the hypertensive rats showed large oscillations of blood pressure synchronous with respiratory movements particularly when the latter were slower and deeper than normal. The rats seemed to tolerate both the denervation and the hypertension very well. Histological examination of tissues from hypertensive rats showed myocardial hypertrophy and a thickening of the basement membrane of the glomerular capsule. The severity of the latter abnormality was closely associated with the duration of the hypertension.

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contrasting

confidence: 62%

contrasting

confidence: 43%

Neurogenic Hypertension in the Rat

Krieger

1964

Circulation Research

493

228

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“…Other investigators have measured an increase in the magnitude of renal hypertension following partial or total sinoaortic deafferentiation (24)(25)(26)(27).…”

Section: Discussionmentioning

confidence: 99%

Renin, Aldosterone, Body Fluid Volumes, and the Baroreceptor Reflex in the Development and Reversal of Goldblatt Hypertension in Conscious Dogs

Liard

Cowley

McCaa

et al. 1974

Circulation Research

139

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The renal artery to a sole remaining kidney was constricted in unanesthetized dogs while renal arterial pressure was recorded distal to the occluder. Following the constriction, mean arterial blood pressure, which was continuously monitored 24 hours a day for 1 week, exhibited a biphasic increase. The first peak in pressure correlated with a large increase in plasma renin activity; the second peak correlated with an increase in plasma volume brought about by positive sodium and water balances. Renin activity was returning to normal when the second peak occurred. Increased drinking played a major role in the positive water balance. Plasma aldosterone concentration was moderately and transiently increased for only a few hours following the constriction. The experiment was repeated in sinoaortic baroreceptor-denervated dogs; apparently, the baroreceptor reflex significantly slows the time course of the arterial blood pressure increase during the first few days of constriction but does not alter the magnitude of the pressure increase after 1 week. After release of renal artery constriction, mean arterial blood pressure decreased progressively over a 3-day period, during which time significant negative sodium and fluid balance occurred. The slow return of the pressure back to normal correlated highly with a decrease in plasma volume. In the baroreceptor-denervated dogs, the initial fall in arterial blood pressure apparently also resulted at least partly from a decrease in plasma renin activity, but this effect was not observed in the intact dogs because the renin activities in these dogs had already decreased to normal prior to constrictor release. The effects of the baroreceptor reflex on the time course of the pressure decrease did not seem to be as significant as those on the time course of the pressure increase. KEY WORDSarterial blood pressure heart rate sodium space sodium potassium continuous data collection fluid balance studies plasma volume• The magnitude and the time course of the increase in mean arterial blood pressure following constriction of the renal artery to a sole remaining kidney (Goldblatt hypertension) depend on the interaction of a number of mechanisms: the release of renin by the kidney (1, 2), the retention of sodium and water, the expansion of fluid volumes (1, 3-6), the buffering action of the baroreceptor reflexes, and still other arterial blood pressure control systems are all involved. However, few studies

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“…They could not incriminate the depressed baroreflex sensitivity as a cause of hypertension in patients with chronic renal failure. Thus although baroreceptor dysfunction does not by itself appear to cause persistent hypertension in chronic renal failure, denervation of baroreceptors has been found by some workers (Kezdi, 1960; Lawrence & Dickinson, 1964) to augment renal hypertension or at least to accelerate the rise of pressure (Liard, Cowley, McCaa, McCaa & Guyton, 1974;Cowley & Guyton, 1975).…”

Section: Osamu Tomiyarna Et Almentioning

confidence: 98%

“…Motor nerve conduction velocity was measured on the ulnar nerve (Kitaoka, 1976). Its normal range is more than 49 m/s.…”

Section: Serum Creatinine Concentrations Were Measured With An Autoanmentioning

confidence: 99%

Baroreflex Sensitivity in Renal Failure

et al. 1980

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1. Baroreflex sensitivity was evaluated in 22 non-dialysed patients with chronic renal failure secondary to chronic glomerulonephritis. Baroreflex sensitivity was judged by the slope of the linear regression of the pulse interval on the rise in systolic blood pressure with injection of phenylephrine or reduction by amyl nitrite inhalation. 2. Baroreflex sensitivity was reduced in these patients as compared with normal controls. Reduction of baroreflex sensitivity was significantly greater in nine hypertensive than 13 normotensive patients with chronic renal failure. 3. A significant positive correlation was found between baroreflex sensitivity and motor nerve conduction velocity measured on ulnar nerve in 13 patients examined. 4. Saline was given with high dietary salt intake to seven normotensive patients with chronic renal failure for 2 or 5 days in order to determine whether the severe depression of baroreflex sensitivity can be an initiating factor for hypertension. Blood pressure was raised to hypertensive levels within 5 days in two patients in whom baroreflex sensitivity was nearly as low as that of hypertensive patients, but not in five cases whose baroreflex sensitivity was normal or only mildly depressed. Plasma volume increased to the same degree in both groups. Baroreflex sensitivity did not change in the former two cases despite blood pressure elevation. 5. It is concluded that reduced baroreflex sensitivity in chronic renal failure correlated with the prescence ofhypertension, as well as uraemic neuropathy, and may be one of the pathogenetic mechanisms of hypertension in end-stage chronic glomerulonephritis.

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Persistent Hypertension in the Dog Following Disruption of the Carotid Sinus Nerves and Subsequent Unilateral Renal Artery Constriction

Cited by 12 publications

References 15 publications

Neurogenic Hypertension in the Rat

Neurogenic Hypertension in the Rat

Renin, Aldosterone, Body Fluid Volumes, and the Baroreceptor Reflex in the Development and Reversal of Goldblatt Hypertension in Conscious Dogs

Baroreflex Sensitivity in Renal Failure

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