Abstract
Renal sodium metabolism, an important determinant of blood pressure, is regulated with great precision by a variety of endocrine, autocrine, and neuronal factors. Although these factors regulate sodium metabolism by affecting the rate of tubular sodium reabsorption, the molecular mechanisms by which they act are poorly understood. It has been proposed that the antidiuretic agents angiotensin II and norepinephrine and the diuretic agents dopamine and atrial natriuretic peptide (ANP) may achieve their effects through a common pathway that involves a bidirectionally regulated intracellular protein phosphorylation cascade. This in turn modulates the activity of renal tubular Na+/K+-ATPase [1]. An exaggerated natriuretic response to acute volume expansion by intravenous saline has been demonstrated in essential [2] as well as borderline hypertension [3]. The overall response to acute volume expansion by intravenous saline has been characterized by a complex humoral pattern which includes the acute suppression of the renin-angiotensin-aldosterone system [4]. Recent studies by Bullivant et al. [5] demonstrate that plasma levels of angiotensin II, prostaglandins, kinins, dopamine, ANP, adrenal hormones, or factors released by the renal nerves are unchanged by renal arterial saline infusion. Thus none of these is directly responsible for the saline induced natriuresis.
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Benaksas, E.J., Murray, E.D., Wechter, W.J. (1995). Natriuretic hormones II. In: Jucker, E. (eds) Progress in Drug Research / Fortschritte der Arzneimittelforschung / Progrès des Recherches Pharmaceutiques. Progress in Drug Research / Fortschritte der Arzneimittelforschung / Progrès des recherches pharmaceutiques, vol 45. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7164-8_7
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