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

Abstract

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)

Dissociation between changes in renal nerve activity and renal vascular resistance in conscious dogs.

“…Moreover, other studies have indicated that volume expansion increased renal blood flow and hemorrhage decreased renal blood flow (MANCIA et al, 1975;HENRICH et al, 1978). On the other hand, in conscious animals, acute volume expansion did not result in renal vasodilation (SIT et al, 1984), and hemorrhage did not result in renal vasoconstriction (VAINER, 1974). Our results in hemorrhage supported the study of GROSS and KIRCHHEIM (1980), who demonstrated that in conscious dogs, a 62% increase in renal nerve activity produced by bilateral carotid artery occlusion had no influence on renal blood flow, whereas a 500% increase in renal nerve activity elicited by acute excitement could induce a 40% decrease in renal blood flow.…”

“…Care was taken to prevent damage to the nerves along the vessels. This maneuver did not impair vasodilatory and vasoconstrictory reserve of the renal bed (SIT et al, 1984). Through a left thoracotomy, catheters were placed in the descending aorta, and in the right and left atria for measurement of the respective pressures.…”

“…For example, studies in conscious animals have indicated that acute volume expansion did not result in significant neurally mediated renal vasodilation (SIT et al, 1984), and that hemorrhage also did not result in renal vasoconstriction (VATNER, 1974). Since the responses of renal blood flow and vascular resistance to acute volume expansion and hemorrhage differ markedly in conscious and anesthetized animals (VATNER, 1974;SIT et al, 1984), it is considered important to determine the extent to which sympathetic efferent nerve activity to the kidney is altered in response to acute volume expansion and hemorrhage in conscious animals. To examine this, the renal vascular resistance and renal nerve activity in response to acute volume changes were investigated in chronically instrumented conscious dogs.…”

Saline‐induced natriuresis and renal blood flow in conscious dogs: effects of sodium infusion rate and concentration

“…The effects of volume expansion on renal blood flow have previously been investigated in experiments in conscious dogs (Sit et al. 1984, Morita & Vatner 1985).…”

“…≈770 μ mol kg −1 min −1 or 10–40 times the present rate) had no effect on renal blood flow whereas arterial blood pressure increased. However, when renal perfusion pressure was servo controlled, an increase in renal blood flow was observed (Sit et al. 1984), i.e.…”