AJP - Regulatory, Integrative and Comparative Physiology, Vol 264, Issue 2 281-R289, Copyright © 1993 by American Physiological Society
Evaluation of renal hormones in natriuresis induced by renal arterial saline infusion
E. M. Bullivant and D. J. Munoz
Department of Physiology, School of Medicine, University of Auckland, New Zealand.
Low rates of unilateral renal arterial infusion with isotonic saline (154
mM NaCl) produce a natriuresis in both kidneys in anesthetized rats, with
the involvement of a blood-borne factor. We investigated whether this
response was modulated by known renal or adrenal hormones. The response to
saline infusion at 0.05 ml/min was tested after acute adrenalectomy (n =
7), in the presence of various blocking agents [captopril (3 mg.kg-1.h-1, n
= 7), indomethacin (5 mg/kg, n = 8), aprotinin (25 KIU/min, n = 8),
propranolol (1 micrograms/min, n = 6), or benserazide (15 micrograms/min, n
= 6)], and after lignocaine infusion around the renal artery (12.5
micrograms/min, n = 5). In all cases, the overall increase in sodium
excretion by both kidneys was not significantly less (alpha < or = 0.01)
than that in untreated rats; it was increased by aprotinin, renal nerve
blockade, and propranolol. Plasma levels of angiotensin II, aldosterone,
and atrial natriuretic peptide were unchanged by renal arterial saline
infusion. We conclude that the saline-induced natriuresis is not reduced by
inhibition of the production of angiotensin II, prostaglandins, kinins,
dopamine, or adrenal hormones, or by factors released by the renal nerves,
indicating that none of these is directly responsible for the
saline-induced natriuresis.
