Carotid-aortic and renal baroreceptors mediate the atrial natriuretic peptide release induced by blood volume expansion.

Abstract

Our previous studies have shown that stimulation of the anteroventral third ventricle (AV3V) region of the brain increases atrial natriuretic peptide (ANP) release, whereas lesions of the AV3V region or median eminence of the tuber cinereum block the release of ANP caused by blood volume expansion. These results suggest that participation of the central nervous system is critical to this response. The role of baroreceptors in the response was evaluated in the current research by studying the response of plasma ANP to blood volume expansion induced by intravenous injection of hypertonic saline solution (0.3 M NaCl, 2 ml/100 g of body weight, over 1 min) in conscious, freely moving male rats. Plasma samples were assayed for ANP by radioimmunoassay. In sham-operated rats, blood volume expansion induced a rapid increase in plasma ANP: the concentration peaked at 5min and remained elevated at 15 min after saline injection. One week after deafferentation of the carotid-aortic baroreceptors, basal plasma ANP concentrations were highly significantly decreased on comparison with values of sham-operated rats; plasma ANP levels S min after blood volume expansion in the deafferented rats were greatly reduced. Unilateral right vagotomy reduced resting levels of plasma ANP but not the response to blood volume expansion; resting concentrations of plasma ANP and responses to expansion were normal in bilaterally vagotomized rats. In rats that had undergone renal deafferentation, resting levels of ANP were normal but the response to blood volume expansion was significantly suppressed. The evidence indicates that afferent impulses via the right vagus nerve may be important under basal conditions, but they are not required for the ANP release induced by blood volume expansion. In contrast, baroreceptor impulses from the carotid-aortic sinus regions and the kidney are important pathways involved in the neuroendocrine control of ANP release. The evidence from these experiments and our previous stimulation and lesion studies indicates that the ANP release in response to volume expansion is mediated by afferent baroreceptor input to the AV3V region, which mediates the increased ANP release via activation of the hypothalamic ANP neuronal system. Atrial natriuretic peptide (ANP), which is primarily localized to the atrial myocytes, plays an important role in control of body fluid homeostasis by decreasing salt and water intake and increasing salt and water excretion (1-7). When the blood volume is expanded-for example, by intravenous injection of saline solution-ANP is released into the circulation and induces natriuresis, in part by direct action on the kidneys (8, 9). Natriuresis is also promoted by direct suppression of the release of aldosterone from the adrenal glomerulosa by ANP (1). ANP also inhibits the release of renin from the juxtaglomerular apparatus of the kidneys (10, 11), which decreases the release of angiotensin II, further decreasing the release of aldosterone. Since angiotensin II is an important mediator of sa...

Serotonergic mechanisms of the lateral parabrachial nucleus in renal and hormonal responses to isotonic blood volume expansion

“…These responses depend on the activation of sinoaortic baroreceptors and/or cardiopulmonary receptor afferents located in the atria, lungs, great veins, and ventricles that project to the nucleus of the solitary tract (NTS) (1,12,22). The NTS neurons convey blood volume expansion signals and project to and excite different areas within the forebrain and hindbrain to produce neuroendocrine responses.…”

“…The present results suggest the involvement of LPBN serotonergic mechanisms in the regulation of urinary sodium, potassium and water excretion, and hormonal responses to acute isotonic blood volume expansion. serotonin; natriuresis; atrial natriuretic peptide; oxytocin; vasopressin ISOTONIC BLOOD VOLUME expansion, by reflex mechanisms, induces a series of regulatory responses, including the inhibition of the sympathetic outflow to the kidney, heart, and blood vessels, reduction of renin and vasopressin (VP) secretion, and increase in the levels of circulating atrial natriuretic peptide (ANP) and oxytocin (OT) that leads to diuresis and natriuresis (1,2,12,14,20,24,45,53).…”

“…The present results suggest the involvement of LPBN serotonergic mechanisms in the regulation of urinary sodium, potassium and water excretion, and hormonal responses to acute isotonic blood volume expansion. serotonin; natriuresis; atrial natriuretic peptide; oxytocin; vasopressin ISOTONIC BLOOD VOLUME expansion, by reflex mechanisms, induces a series of regulatory responses, including the inhibition of the sympathetic outflow to the kidney, heart, and blood vessels, reduction of renin and vasopressin (VP) secretion, and increase in the levels of circulating atrial natriuretic peptide (ANP) and oxytocin (OT) that leads to diuresis and natriuresis (1,2,12,14,20,24,45,53).There are several reports demonstrating the correlation between natriuresis and diuresis and plasma ANP levels in response to systemic volume expansion, e.g., atrial balloon inflation, blood volume expansion, salt load, and water immersion (4,7,17,32,50,59). These responses depend on the activation of sinoaortic baroreceptors and/or cardiopulmonary receptor afferents located in the atria, lungs, great veins, and ventricles that project to the nucleus of the solitary tract (NTS) (1, 12, 22).…”

Neuroendocrine control of body fluid homeostasis

“…We considered the possibility that the baroreceptors, when stretched by volume expansion, would activate the brain ANP neurons, which would then produce the release of ANP and the ensuing natriuresis. Therefore, we determined the role of the baroreceptors in affecting the increase in plasma ANP from volume expansion induced by intravenous injection of hypertonic saline solution (0.3 M NaCl, 2 ml/100 g body weight, over 1 min) into conscious, freely moving male rats (44). In sham-operated rats, BVE induced a rapid increase in plasma ANP as before.…”

Role of the Acid-Sensing Ion Channel 3 in Blood Volume Control

“…Stretch-activated receptors are also found in the aortic arch and carotid sinus (aortic and carotid baroreceptors), where the volume expansion triggers an autonomic response. 5 As well, renal baroreceptors are involved in blood volume control by increasing the plasma ANP concentration, 5 which induces natriuresis and diuresis in the kidney to return blood volume and pressure back to normal. 1 Although ANP is released in response to volume receptor stretch, the mechano-sensing molecules underlying the mechanotransduction are largely unknown.…”