Bioactive Cardiac Substances: Potent Vasorelaxant Activity in Mammalian Atria

Currie, Mark G.; Geller, David M.; Cole, Barbara R.; Boylan, John G.; YuSheng, Wu; Holmberg, Sandra; Needleman, Philip

doi:10.1126/science.6857267

Cited by 694 publications

(188 citation statements)

References 14 publications

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“…De Bold et al (32) demonstrated the diuretic effect of atrial extracts and later determined the structure of ANP (33). The myorelaxing action of the atrial extracts on vascular muscle was demonstrated independently by different groups (34)(35)(36). These findings permitted the identification and characterization of hormones of the natriuretic peptide family, which are involved in the control of body fluid homeostasis (36,37).…”

Section: Neurohypophyseal Hormones and The Control Of Sodium And Watementioning

confidence: 99%

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Ventura

Gomes

Reis

et al. 2002

Braz J Med Biol Res

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The central nervous system plays an important role in the control of renal sodium excretion. We present here a brief review of physiologic regulation of hydromineral balance and discuss recent results from our laboratory that focus on the participation of nitrergic, vasopressinergic, and oxytocinergic systems in the regulation of water and sodium excretion under different salt intake and hypertonic blood volume expansion (BVE) conditions. High sodium intake induced a significant increase in nitric oxide synthase (NOS) activity in the medial basal hypothalamus and neural lobe, while a low sodium diet decreased NOS activity in the neural lobe, suggesting that central NOS is involved in the control of sodium balance. An increase in plasma concentrations in vasopressin (AVP), oxytocin (OT), atrial natriuretic peptide (ANP), and nitrate after hypertonic BVE was also demonstrated. The central inhibition of NOS by L-NAME caused a decrease in plasma AVP and no change in plasma OT or ANP levels after BVE. These data indicate that the increase in AVP release after hypertonic BVE depends on nitric oxide production. In contrast, the pattern of OT secretion was similar to that of ANP secretion, supporting the view that OT is a neuromodulator of ANP secretion during hypertonic BVE. Thus, neurohypophyseal hormones and ANP are secreted under hypertonic BVE in order to correct the changes induced in blood volume and osmolality, and the secretion of AVP in this particular situation depends on NOS activity. Central nervous system and hydromineral balancePrecise regulation of body fluid osmolality is essential. Osmolality is controlled by a finely tuned, intricate homeostatic mechanism that operates by adjusting both the rate of water intake and excretion. The central nervous system (CNS) plays an important role in the control of renal sodium excretion (1-7). Considerable evidence indicates that the median preoptic area (MnPO), anterior lateral hypothalamus, subfornical organ (SFO), anterior portion of the third ventricle (AV3V), supraoptic nucleus (SON), paraventricular nucleus (PVN), organum vasculosum laminae terminalis (OVLT), habenula, stria medullaris, and medial septal area are organized in a neural circuit involved in the regulation of water and sodium intake and excretion (1-3). Natriuresis accompanied by kaliuresis is induced by cholinergic or adrenergic stimulation of the medial septal area, MnPO, anterior lateral hypothalamus, SFO, and AV3V (1,4). Stimulation of AV3V with carbachol, a cholinergic drug, angiotensin II or hypertonic saline enhances natriuresis, which is blocked by the destruction of this brain area (1,4-7). Neurohypophyseal hormones and the control of sodium and water excretionAlthough the neuroendocrine control of sodium and water balance is not completely understood, alterations in volume and osmolality are responsible, at least in part, for changes in plasma vasopressin (AVP) concentration. Verney (8) originally demonstrated that AVP release into the blood is stimulated by the activation of os...

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Section: Neurohypophyseal Hormones and The Control Of Sodium And Watementioning

confidence: 99%

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Ventura

Gomes

Reis

et al. 2002

Braz J Med Biol Res

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“…Various sites of action of ANF have been documented, including arterial muscular tone [8,9], urinary sodium and water excretion [ 10,111, adrenal mineralocorticoid secretion [ 12,131 and pituitary vasopressin secretion [14]. The mode of action of ANF on kidney function is still debated [7].…”

Section: Introductionmentioning

confidence: 99%

Distribution of atrial natriuretic factor receptors in dog kidney fractions

1985

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Specific receptors for atria1 natriuretic factor were studied in purified glomeruli, proximal tubules, thick ascending limbs of Henle's loops and collecting ducts from dog kidney. Glomeruli contain the highest concentration of receptor sites (pK = 9.9, B,,,, = 200 fmol/mg protein), followed by collecting ducts (pK = 9.4, B mai = 150 fmol/mg). Low levels of receptor sites were also detectable in thick ascending limbs of Henle's loops (pK = 9.4, B,,, = 36 fmol/mg) while proximal tubules were completely devoid of specific binding sites. These results indicate that the glomeruli appear to be the primary site of interaction of artrial natriuretic factor in kidney cortex but that it might also act in the medulla on lower nephron tubular function. Atria1 natriuretic factor Vasoactive peptide Peptide receptor Glomerular function Tubular function (Dog kidney)

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“…Atrial natriuretic factor (ANF) has well-known vasorelaxant properties [1]. In particular, we have shown that atriopeptin III (APIII) inhibits angiotensin II (ANGII)-induced contraction of cultured rat glomerular mesangial cells while the shorter fragment atriopeptin I (API) has no such effect [2].…”

Section: Introductionmentioning

confidence: 99%

Effect of atrial natriuretic factor on cytosolic free calcium in rat glomerular mesangial cells

1987

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Since atrial natriuretic factor (ANF) inhibits angiotensin II (ANGII)-induced mesangial cell contraction, we studied its effect on cytosolic free calcium in fura-2-1oaded monolayers. ANF lowered basal calcium from 117 + 5 to 89 + 2 nM, and also reduced the ANGII-induced calcium transient. The absolute level of cytosolic calcium after ANGII was lower in cells preincubated with ANF compared to buffer. In a few cell lines, ANF had no effect on cytosolic calcium, while in all cell lines ANF had inhibited contraction. Thus, while ANF has effects on cytosolic calcium in mesangial cells, the vasorelaxant effects of ANF may require additional physiologic interactions.Atrial natriuretic factor; cytosolic free Ca2+; Tissue culture; Fura-2; (Mesangial cell)

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Bioactive Cardiac Substances: Potent Vasorelaxant Activity in Mammalian Atria

Cited by 694 publications

References 14 publications

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Distribution of atrial natriuretic factor receptors in dog kidney fractions

Effect of atrial natriuretic factor on cytosolic free calcium in rat glomerular mesangial cells

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