Loss of the Renal Vasoconstrictor Activity of Angiotensin II during Renal Ischemia*

McGiff, John C.; Itskovitz, Harold D.

doi:10.1172/jci105110

Cited by 36 publications

(12 citation statements)

References 23 publications

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“…While examining the role of the nervous system in the production of this effect, renal denervation was observed to produce a loss of the renal vasoconstrictor activity of angiotensin II, similar to that produced by renal ischemia (9). The present study reports on the role of the nervous system in determining the renal vascular reactivity to angiotensin II.…”

mentioning

confidence: 71%

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The relationship of the renal vascular activity of angiotensin II to the autonomic nervous system.

McGiff¹,

Fasy²

1965

J. Clin. Invest.

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confidence: 71%

“…BP = blood pressure. mined by earlier work as an appropriate interval (9). c) The observations were confined to the first 90 minutes after having set up the preparation, during which no appreciable time trend was observed (9, 11).…”

mentioning

confidence: 88%

The relationship of the renal vascular activity of angiotensin II to the autonomic nervous system.

McGiff¹,

Fasy²

1965

J. Clin. Invest.

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“…It is interesting to speculate on the possible role of renin in producing the observed changes, since plasma volume depletion is a potent stimulus for renin release (48). Since the renin-angiotension axis is said to have a profound effect upon renal vascular tone (49)(50)(51)(52), an interrelationship between these mechanisms in the development of oliguric acute renal failure may quite properly be suspected.…”

Section: Resultsmentioning

confidence: 99%

Glycerol-induced hemoglobinuric acute renal failure in the rat. I. Micropuncture study of the development of oliguria.

Oken¹,

Arce²,

Wilson³

1966

J. Clin. Invest.

217

126

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The oliguria of acute renal failure has been attributed to tubular obstruction (1-12), "leakage" of the glomerular filtrate through rents in the tubular wall (13)(14)(15)(16)(17)(18)(19), and vascular mechanisms of various types (20)(21)(22)(23)(24)(25). In a previous paper, it was shown that the oliguria of mercury-induced acute renal failure in the rat reflects a primary decrease in glomerular filtration rate and cannot be attributed to tubular mechanisms (26). The applicability of these findings to most types of acute renal failure occurring in humans may be questioned, however, because of the very dissimilar etiologies and the known effect of large doses of mercury on the renal circulation (27). The present study concerns hours before glycerol injection. They lost an average of 8% of body weight in the period of dehydration, during which time their food intake was one-third less than that of nondehydrated animals. Blood samples were obtained by cardiac puncture from a number of glycerolinjected animals and dehydrated control rats that were exempted from micropuncture studies to determine the change in their blood urea nitrogen (BUN) occurring over a 48-hour period. BUN was measured on 0.2-ml samples by a modification of the urease method of Gentzkow (28). Urinary osmolalities were determined with an Advanced osmometer.Acute renal failure was induced by injecting 50%o glycerol in water into the muscle of both hind limbs at a total dose of 10 ml per kg of body weight. Within 2 hours after this injection, the urine was found to be burgundy red in color due to the presence of heme pigments.The animals were subjected to micropuncture experiments at times ranging from 30 minutes to 26 hours after glycerol injection. They were anesthetized with sodium pentobarbital given intraperitoneally at a dose of 40 to 50 mg per kg body weight. Their blood pressure was monitored as described earlier (26) either by a tail cuff microphone method or intra-arterial manometry. Although hypotension typically did not occur, animals whose mean arterial blood pressure was less than 85 mm Hg were excluded from micropuncture study. The left kidney was exposed through an abdominal incision and carefully dissected free of the perirenal fat. The renal hilus was disturbed as little as possible, and the renal capsule was left intact. The kidney was placed in a Lucite holder to minimize its displacement with respiration. Its surface was covered with warm mineral oil to prevent drying and to aid in visualization of the renal structures.Micropuncture methods were those described in an earlier paper (26). In short, proximal tubular hydrostatic pressure was measured by a modification of the manometric method of Wirz (29), using a water manometer to obtain maximal definition of the end point. The manometer was calibrated at zero pressure before each measurement. Glomerular filtration rate and fractional water absorption were determined at least 30 minutes after the injection of 40 ,uc of "C-labeled inulin 1 in 0.3 to 0.5 ml of 140 mM NaCl. Labele...

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“…The alternate hypothesis of primary dilation of the afferent arteriole (and accompanying constriction of the efferent arteriole) by angiotensin II within the ischemic kidney challenges a large body of work demonstrating that a vasoconstrictor action, presumably of physiologic significance, is a fundamental property of this polypeptide (18). Attenuation of the vasoconstrictor action of angiotensin II during renal ischemia was described, but a direct renal vasodilator action has not been demonstrated (6). The suggested locus of action of angiotensin II under these experi-mental conditions does not exclude a dominant preglomerular action under other conditions.…”

Section: Discussionmentioning

confidence: 95%

“…The observation of the attenuation or loss of the renal vasoconstrictor action of angiotensin II during renal ischemia (6) suggested to us that the effect of angiotensin II on GFR may be altered in a similar manner. This consideration may be relevant to the proposals that angiotensin participates in the regulation of GFR.…”

Section: Introductionmentioning

confidence: 93%

Some determinants of the effects of VAL-5-angiotensin II amide on glomerular filtration rate and sodium excretion in dogs

McGiff¹,

Lynch²,

Leinicke³

et al. 1969

J. Clin. Invest.

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A B S T RA C T In 12 dogs anesthetized with chloralose, angiotensin (angiotensin II amide) given intravenously increased the glomerular filtration rate (GFR) of an ischemic kidney while simultaneously having little effect on the GFR of the contralateral kidney. In the ischemic kidney, in 14 of 30 observations, increments of GFR greater than 100% of mean control GFR (9 ml/min) occurred in response to angiotensin. The magnitude of the increase in GFR produced by angiotensin was independent of dose (range 0.005-0.050 jug/kg per min), the degree of accompanying pressor response, and alterations in renal blood flow (RBF) (electromagnetic flowmeter). In the ischemic kidney, increments of GFR could be produced by sub-pressor doses of angiotensin.Dissociations between increments of GFR and sodium excretion occurred. Equivalent increments of GFR in the ischemic kidney in dogs receiving either 5% glucose in water or 10% mannitol in 0.3% saline were associated with natriuresis only in the latter group: a) as an initial response of the contralateral kidney to renal arterial constriction (RAC) in spite of a concomitant reduction in RBF and an unchanged GFR; b) in the ischemic kidney on giving angiotensin. The natriuresis produced by angiotensin was independent of the magnitude of elevations in blood pressure, altered filtration fraction, and was associated with a further reduction in RBF. After release of RAC in the dogs receiving mannitol, an antinatriuresis was again observed in response to angiotensin.

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Loss of the Renal Vasoconstrictor Activity of Angiotensin II during Renal Ischemia*

Cited by 36 publications

References 23 publications

The relationship of the renal vascular activity of angiotensin II to the autonomic nervous system.

The relationship of the renal vascular activity of angiotensin II to the autonomic nervous system.

Glycerol-induced hemoglobinuric acute renal failure in the rat. I. Micropuncture study of the development of oliguria.

Some determinants of the effects of VAL-5-angiotensin II amide on glomerular filtration rate and sodium excretion in dogs

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