ANP as a neuroendocrine modulator of body fluid homeostasis

The role played by the central nervous system (CNS) in the control of body fluid homeostasis has been demonstrated by several authors. The AV3V plays a key role in central control of sodium excretion since its cholinergic, adrenergic, angiotensinergic and osmotic stimulation enhances and its destruction blocks sodium excretion in rats and goats. Cholinergic stimulation of the AV3V induced an increase in plasma ANP as well as a marked elevation in content of the peptide in medial basal hypothalamus, neuro and adenohypophysis. On the other hand, a decline in plasma ANP after AV3V lesions was accompanied by dramatic declines in content of ANP in these same structures. Our previous work has also indicated the essential role of the AV3V region and its ANPergic neurons in the control of ANP release in response to volume expansion (BVE) and indicated that alpha-adrenergic and muscarinic receptors are critical in mediating these responses. Lesions of the AV3V region, or of the median eminence or posterior lobe of pituitary gland blocked the increase in plasma ANP concentration in response to BVE. That this effect is related to blockage of the activity of the brain ANPergic neurons is supported by fyndings in sheep and in rats that the injection of the antiserum directed against ANP into the AV3V region at least partially blocked the BVE-induced release of ANP. We and others have also previously shown that denervation of baroreceptors inhibits ANP release induced by BVE. Activation of the ANP neurons also cause release of ANP from the anterior and neural lobe of pituitary gland. ANP neurons may activate oxytocinergic neurons in the supraoptic and paraventricular, which projects to neural lobe. Oxytocin would circulate to the atria and may directly activate release of ANP from the atrial myocytes, since i.v. or i.p. injection of oxytocin increases sodium excretion as well as elevates plasma ANP. Oxytoxin is present in the neural lobe in large quantity, which could reach the atria myocytes in high concentration and release ANP that circulate to the kidneys and evokes natriuresis to return circulating blood volume to normal.

Angiotensin II antiserum decreases luteinizing hormone-releasing hormone in the median eminence and preoptic aea of the rat

Ovariectomized female rats were sacrificed 3 h after intracerebroventricular microijnjection of normal rabbit serum (NRS), specific antiserum against angiotensin II (AB-AII) or atrial natriuretic factor (AB-ANF). AB-AII decreased plasma LH by 50% and LH-RH content by 70% in the median eminence and medial preoptic area, respectively, but did not change plasma FSH when compared to animals which receivede NRS. There was no difference in these parameters when the animals were injected with AB-ANF or NRS.These results indicate that endogenous AII plays a physiological role in LH release acting directly or indirectly through LH-RH neurons of the median eminence and medial peroptic area