Changes in renal salt and water excretion secondary to alterations in blood volume represent appropriate responses for maintaining body fluid homeostasis. In spite of the simplicity of the concept, the mechanisms linking blood volume and renal excretion are not clearly understood. This is particularly true for the nonhuman primate since little investigative work has been done using this species, especially experiments on conscious animals. The primary objective of the research proposed in this application is to clarify and better define the functional impartance of some of these blood volume control mechanisms in the conscious monkey. The factors to be investigated include renal nerves, cardiac nerves and atrial natriuretic factor (ANF). Thus the objective encompasses both neural and humoral mechanisms.
The specific aims are: (1) to determine if the renal nerves exert tonic or basal effects on renal excretion, including assessments of the effect of unilateral renal denervation on contralateral innervated kidney function and potential importance of denervation hypersensitivity to norepinephrine as a factor which may complicate the interpretation of chronic renal denervation protocols, (2) to determine the necessity of the renal nerves and/or increases in ANF for eliciting postprandial increases in urinary excretion, (3) to determine the necessity of the renal nerves and/or increases in ANF for eliciting the renal excretory responses to chronic changes in dietary sodium intake, (4) to determine if the level of sodium intake affects the magnitude of and renal nerve and ANF contribution to the renal responses to volume expansion, (5) to determine the sensitivity of the renal and humoral responses to increases and decreases in blood volume and necessity of the renal nerves for eliciting the excretory effects and (6) to determine the role of cardiac receptors in eliciting changes in plasma vasopressin, ANF and norepinephrine levels and plasma renin activity during graded changes in central blood volume (lower body positive and negative pressure). The results from these experiments may suggest possible mechanisms which may be involved in the pathogenesis of congestive heart failure and hypertension, conditions often characterized by body fluid imbalance.
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