Why the study?
Does low-frequency renal nerve stimulation affect renal function and renin release in cats, and what is the role of angiotensin?
Does low-frequency renal nerve stimulation affect renal function and renin release in cats, and what is the role of angiotensin?
The maintenance of glomerular filtration rate during renal nerve stimulation may be mediated by local angiotensin generation, which does not appear to play a major role in the associated sodium retention.
Answers are grounded in this paper and cite their sources.
Suggests local angiotensin preserves GFR during renal nerve stimulation without driving sodium retention; leaves open translation to human cardiorenal physiology.
The effect of low-frequency stimulation of the renal nerves on renal function and renin release has been investigated. The experiments were performed in unilaterally nephrectomized, anaesthetized cats in which the nerves to the remaining kidney were sectioned. 2. When stimulation frequency was adjusted to reduce renal blood flow by approximately 15% for 15 min, glomerular filtration rate was hardly affected. The ratio sodium clearance/glomerular filtration rate was significantly reduced and plasma renin activity was significantly increased. 3. When the renal nerves were similarly stimulated in the presence of the beta-adrenergic receptor blocking agent, propranolol, the glomerular filtration rate was significantly reduced and the rise in plasma renin activity was significantly inhibited. The reduction of sodium clearance/glomerular filtration rate was as great as in the control animals. 4. The results are consistent with the view that the maintenance of glomerular filtration rate, during renal nerve stimulation which reduced renal blood flow, may be mediated by the local generation of angiotensin. The results also suggest that angiotensin does not play an important role in the sodium retention associated with increased renal nerve activity.
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Johns et al. (1976) studied this question.
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