“Redistribution” of Intrarenal Blood Flow: A Question of Microsphere Size?

Aukland, Knut

doi:10.1016/b978-0-08-026824-8.50027-8

Cited by 1 publication

(1 citation statement)

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“…The results from the present investigation, however, do not support this concept, i.e., there was no significant shift in the inrrarenal flow distribution during volume loading in the intact, conscious dogs. It is important to note that the radioactive microsphere technique to measure inrrarenal blood flow has been criticized on the basis of microsphere skimming (Aukland 1980(Aukland , 1981Ofjord and Clausen, 1983). Thus, although there were clear differences between our results in conscious dogs and prior work in anesthetized animals, the question of whether a significant shift in inrrarenal blood flow occurs with volume loading remains unanswered.…”

Section: Discussioncontrasting

confidence: 49%

Responses of renal hemodynamics and function to acute volume expansion in the conscious dog.

Sit¹,

Morita²,

Vatner³

1984

Circulation Research

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SUMMARY. The renal vascular and functional responses to acute volume expansion were determined in conscious dogs with all reflexes intact, sinoaortic arterial baroreceptor denervation, arterial baroreceptor denervation plus bilateral stellectomy, and arterial baroreceptor denervation plus bilateral vagotomy. In the intact dogs, when an isotonic saline infusion increased right atrial pressure by 6 mm Hg, arterial pressure increased by 15 ± 3 from 95 ± 3 mm Hg (P < 0.01) and heart rate rose from 87 ± 4 to 135 ± 6 beats/min (P < 0.01), while renal blood flow rose only slightly (4 ± 2%), and calculated renal resistance was not altered significantly. After arterial baroreceptor denervation, volume expansion with saline induced a greater rise in blood flow (16 ± 2 %), but did not alter arterial pressure, and calculated resistance fell by 19 ± 3% from 0.72 ± 0.05 mm Hg/ml per min (P < 0.01), while heart rate still increased. After arterial baroreceptor denervation and either bilateral stellectomy or vagotomy, volume expansion reduced renal vascular resistance by similar amounts. When intact animals were volume expanded by 20% of estimated blood volume with isooncotic, isotonic 3% dextran in saline solution, and with renal perfusion pressure held constant, central venous pressure increased by 4.5 ± 0.6 from 1.8 ± 0.4 mm Hg (P < 0.01), renal blood flow increased significantly by 16 ± 5 ml/min (P < 0.05) from 191 ± 30 ml/min, while calculated renal vascular resistance decreased significantly by 0.08 ± 0.02 from 0.62 ± 0.09 mm Hg/ml per min (P < 0.05). Average urine flow rate and sodium excretion 10-60 minutes after expansion increased markedly by 1.85 ± 0.27 ml/min and 9.84 ± 1.13 ^Eq/min per kg, respectively (P < 0.01). After arterial baroreceptor denervation, volume expansion induced a similar rise in central venous pressure and renal blood flow. The diuretic and natriuretic responses were not attenuated by arterial baroreceptor denervation. After arterial baroreceptor denervation plus bilateral vagotomy, there was a significant and similar rise in renal blood flow, whereas diuretic (urine flow rate rose by only 0.50 ± 0.10 from 0.35 ± 0.08 ml/min) and natriuretic (sodium excretion rose by only 4.83 ± 0.95 from 1.50 ± 0.48 ^Eq/min per kg) responses were significantly attenuated (P < 0.01). These data indicate that-in the intact conscious dog-vagal afferent mechanisms play an important role in mediating the diuretic and natriuretic responses to acute volume expansion, whereas the changes in renal hemodynamics that occur with volume expansion appear independent of reflex pathways. (Circ Res 54: 185-195, 1984)

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Section: Discussioncontrasting

confidence: 49%