Hypertension produced by constriction of the renal artery in sympathectomized dogs

Freeman, Norman E.; Page, Irvine H.

doi:10.1016/s0002-8703(37)90519-2

Cited by 61 publications

(12 citation statements)

References 14 publications

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“…They induced the experimental hypertension in the dog by the partial constriction of the renal artery using a silver clip. Their results were confirmed by several groups, 11 and the search for the mechanisms involved for the increase in blood pressure began. The section of the sympathetic nervous system that regulates the vasomotor mechanisms did not prevent or abolish the development of hypertension.…”

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confidence: 66%

History About the Discovery of the Renin-Angiotensin System

2001

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Abstract-The history of the discovery of the renin-angiotensin system began in 1898 with the studies made by Tigerstedt and Bergman, who reported the pressor effect of renal extracts; they named the renal substance renin based on its origin. In 1934, Harry Goldblatt induced experimental hypertension in dogs by clamping a renal artery. About 1936, simultaneously in the Medical School of the University of Buenos Aires, Argentina, and in the Eli-Lilly Laboratories in Indianapolis, 2 independent groups of researchers, using the Goldblatt technique to produce experimental hypertension, demonstrated renal secretion of a pressor agent similar to renin. In the following years, both teams described the presence of a new compound in the renal vein blood of ischemic kidneys. This agent was extracted from blood with 70% acetone and had a short pressor effect. The final conclusion was that renin acted enzymatically on a plasma protein to produce the new substance. He related hypertrophy to an increased resistance to blood flow in the small vessels due to the altered condition of the blood. In 1868, George Johnson, 2 reporting studies on nephritis, suggested that hyaline-fibroid alterations in the renal vessels were due to an impure condition of the blood, which was also responsible for left ventricular hypertrophy. F.A. Mahomed, 3 using a primitive sphygmograph for the first time, described high blood pressure in 1872. He also linked left ventricular hypertrophy to hypertension due to nephritis and reported the presence of high blood pressure in patients without renal disease. 4,5 Finally, Riva-Rocci, 6 in 1896, described the first indirect sphygmomanometer to measure arterial pressure in humans, and in 1905, Korotkoff 7 defined the sounds that are named after him.The relationship between pathological alterations in the kidney and the development of systemic arterial hypertension had been postulated for many years. In this sense, Franz Volhard 8 suggested the existence of a circulating vasopressor substance. He classified the hypertensive patients: those with slight vascular damage as reds, and those with important vascular lesions-mostly in the kidney, pale skin, and cerebral damage (malignant hypertension)-as white.On the other hand, by the end of the nineteenth century, Tigerstedt, a Finnish professor of physiology working at the Karolinska Institute, and his assistant Bergman 9 analyzed the effect of renal extracts on arterial pressure. They discovered the presence of a pressor compound in the renal tissue of the rabbit, and based on its origin, they named it renin. The pressor activity could be extracted with glycerin, did not dialyze, and was stable at 56°C and was destroyed by boiling. Moreover, they showed that the renal vein blood increased blood pressure when injected into nephrectomized animals. They also detected the potentiation and protraction of the pressor response to renin in the nephrectomized recipient. They explained that the association between renal disease and cardiac hypertrophy was due to the kidney ...

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confidence: 66%

History About the Discovery of the Renin-Angiotensin System

2001

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“…The literature covering the proposal and disposal of each substance is too vast to review here. However, the recent production -in animals of a persisting experimental hypertension due to renal ischemia (20) has once more directed attention to the kidney as a source of pressor material, particularly since this one form of experimental hypertension is not affected by sympathetic denervation either partial (21,22), or complete (23).…”

Section: Control Studiesmentioning

confidence: 99%

The Effects of Pressor Drugs and of Saline Kidney Extracts on Blood Pressure and Skin Temperature 1

Landis

Montgomery²,

Sparkman³

1938

J. Clin. Invest.

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Many pressor substances, including hormones, drugs, and variously prepared extracts of kidney tissue, have been studied intensively to determine their effects on blood pressure and their possible role in the pathogenesis of human hypertension. Many of these experiments were performed on anesthetized animals and observations usually dealt merely with changes of systemic blood pressure. According to recent studies, however, one of the remarkable features of human hypertension is the association of abnormally high arterial pressure with normal peripheral blood flow. When vasoconstrictor tone in the extremities is diminished by warming the body, blood flow in the forearm increases equally in hypertensive and normal subjects (1, 2). It seemed highly desirable therefore to determine whether the action of any of the known pressor substances simulated human hypertension to the extent of producing, in an experimental animal, a rise of blood pressure without reducing peripheral blood flow simultaneously.In order to study the action of pressor substances on peripheral blood vessels it was found necessary to develop a method which (1) did not require anesthesia, (2) excluded variations arising from spontaneous changes in vasoconstrictor tone of nervous origin, (3) avoided trauma of the vessels studied, and (4) the body of the rabbit. Changes of peripheral blood flow were detected by measuring skin temperature. The procedure required no anesthesia and observations could, if desired, be made on the same animal repeatedly on successive days. This paper compares the effects of epinephrine, tyramine, pituitrin, pitressin, ergot derivatives, guanidine and saline extracts of normal rabbit kidney on blood pressure, amplitude of arterial pulsation, and skin temperature of the rabbit's ear. Of the substances tested, a specially treated saline kidney extract was the only one which elevated peripheral blood pressure without simultaneously reducing skin temperature in the ear of the warmed rabbit. This property of raising blood pressure without measurably decreasing peripheral blood flow appears to depend upon a protein-like substance which remains in solution during heating to 560 C., but is precipitated or destroyed by heating to 650 C. METHODSUnanesthetized male rabbits, weighing usually between 2.0 and 2.7 kilos, were used throughout. The animals were fed either purina rabbit chow with miscellaneous greens or a composite food known to be adequate (3). Hair was removed from both ears with a barium sulphide mixture at least twenty-four hours before the animals were to be used. Under ordinary conditions the vessels of the rabbit's ear dilate and constrict intermittently in response to excitement and the need for radiation or conservation of heat. To abolish such variations of vasoconstrictor tone the animals were placed in a metal box with a double wall through which warm water could be pumped continuously from a reservoir. The temperature of the circulating water was controlled by a thermostat, so that the warmth of the box could be ...

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“…Calculated as the difference between the maximum heart rate after muscarinic blockade and the heart rate after ganglionic nicotinic receptor blockade (the intrinsic heart rate), one could wonder whether the maximum VCA activity is influenced by some sympathetic tone that remains after muscarinic blockade but is eliminated after nicotinic blockade. As the initial increase and subsequent decrease in heart rate has also been shown in reserpinized as well as in sympathectomized dogs ( Freeman & Page 1937, Brouha & Nowak 1939, Donald et al . 1967 , Brunsting et al .…”

Section: Discussionmentioning

confidence: 78%

The vagal cardiac accelerator system in the reflex control of heart rate in conscious dogs

Roossien

Brunsting

Zaagsma

et al. 2000

Acta Physiologica Scandinavica

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The reactions of the vagal cardioaccelerator (VCA) system to changes in mean arterial pressure (MAP) were studied in five beta-adrenoceptor blocked conscious dogs. An increase in MAP was obtained by administration of vasopressin or methoxamine, a decrease by doxazosin or nitroprusside. In the first series of experiments the MAP changes were induced after muscarinic receptor blockade, in a second series both before and after muscarinic blockade. Prior to these experiments, the maximum VCA activity, defined as the difference between maximum heart rate after muscarinic blockade and the rate after additional nicotinic blockade, was determined. We hypothesized that this quantity, as a measure of VCA activity, depends on the prevailing vagal tone. In the first series of experiments, a rise in MAP evoked an increase in heart rate, a fall in MAP indicated decrease. In the second series, when prior to muscarinic blockade the vagal tone was reflexly raised, the subsequent VCA reflex response to the rise in MAP was attenuated. Prior to the muscarinic blockade the vagal tone was reflexly lowered, the VCA reflex response was enhanced. Direct chronotropic effects of MAP-varying drugs were ruled out by the absence of a heart-rate response in experiments on vagotomized animals. We concluded that the vagal cardioaccelerator system is involved in the reflex control of heart rate. Both the VCA reflex response to changes in systemic blood pressure and the maximum VCA activity however, are determined by the prevailing vagal tone.

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Hypertension produced by constriction of the renal artery in sympathectomized dogs

Cited by 61 publications

References 14 publications

History About the Discovery of the Renin-Angiotensin System

History About the Discovery of the Renin-Angiotensin System

The Effects of Pressor Drugs and of Saline Kidney Extracts on Blood Pressure and Skin Temperature 1

The vagal cardiac accelerator system in the reflex control of heart rate in conscious dogs

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