It's called the ANF hormone and is produced by the right atrium. JV has mentioned it in classes in the past but unfortunately none of the few resources I've checked so far mention any direct influence on the brain.
Hi Andrew, Try a search for "Cardiac hormones",you should be able to find lots of interesting information. I'll include some info found at http://www.rcpsych.ac.uk
Communication via hormones: the heart as a hormonal gland.
Another component of the heart-brain communication system was provided by researchers studying the hormonal system. The heart was reclassified as an endocrine gland when, in 1983, a hormone produced and released by the heart called atrial natriuretic factor (ANF) was isolated. This hormone exerts its effect on the blood vessels, on the kidneys, the adrenal glands, and on a large number of regulatory regions in the brain. It was also found that the heart contains a cell type known as 'intrinsic cardiac adrenergic'' (ICA) cells. Theses cells release noradrenaline and dopamine neurotransmitters, once thought to be produced only by neurons in the CNS. More recently, it was discovered that the heart also secretes oxytocin, commonly referred to as the 'love' or bonding hormone. In addition to its functions in childbirth and lactation, recent evidence indicates that this hormone is also involved in cognition, tolerance, adaptation, complex sexual and maternal behaviours, learning social cues and the establishment of enduring pair bonds. Concentrations of oxytocin in the heart were found to be as high as those found in the brain.
(New Endocrine Systems)
Recent advances in physiology, during the last two decades, have established an endocrine role of the heart in addition to its normal function as a pump. It is now well known that both atria and ventricles are capable of producing natriuretic peptides. Since the discovery of atrial natriuretic factor by DeBold and his coworkers in 1981, a vast amount of research has been performed on cardiac natriuretic peptides concerning their synthesis , release and physiological activities. These natriuretic factors are of special interest both physiologically and clinically, because they participate in the regulation of cadiovascular and renal homeostatic mechanisms. They are thought to be involved in the regulation of body fluid volume and electrolyte balance.
The principal actions of these endogenous natriuretic factors are natriuresis,diuresis and hypotension. They exert these effects by altering renal haemodynamics, inhibition of tubular reabsorption of Na+ and water indirectly through inhibition of vasopressin release and antagonizing the effects of renin - angiotensin - aldosterone system. Their direct vasorelaxant properties contribute mainly to the hypotensive effect.
The release of cardiac natriuretic peptides is enhanced mainly by expansion of the extracellular fluid volume and atrial distension. Their release is increased manyfold in oedematous disorders such as
congestive heart failure and chronic renal failure.
Morphologic observations showed that the atrial myocytes contain structures resembling secretory granules , located at the nuclear pole near the mitochondria and Golgi apparatus . Their endocrine function was not demonstrated until De Bold and his colleagues in 1978, described the structural similarities between atrial granules and the secretory granules that exist or seen in other endocrine tissues, and speculated that atrial granules could contain a hormone. De Bold's initial experiments demonstrated a change in the number and density of these granules with alteration in salt and water intake. Thus, it seemed likely that these granules were intimately involved in the control of ECF volume. These investigators did further work and they prepared an extract of rat cardiac atria and injected that intravenously into bioassay rats.
The atrial extract produced dramatic natriuresis and diuresis (DeBold et al. 1981). At the beginning, the term atrial natriuretic factor has been commonly used to describe the active substance in the extract, until its chemical structure was identified, thereafter it was known as atrial natriuretic peptide (ANP).
Another physiologically important natriuretic factor named brain natriuretic peptide (BNP), was first discovered in porcine brain by Sudoh et al. in 1988. New reports have shown that significant amount of this natriuretic peptide is also synthesized in and released into the circulation from the heart. It exerts physiological and pharmacological actions very similar to that of ANP, such as natriuresis, diuresis and hvpotension. Recent evidences suggest that BNP and ANP act in a dual natriuretic peptide system involved in circulatory homeostasis.
Storage and release of ANP and BNP:
ANP is primarily formed, stored and secreted from atrial myocytes. However, a larger amount of ANP prohormone has been identified in atrial tissue and it is therefore, the most likely storage form. It has been reported that ANP is stored in atrial cardiocytes as ANP precursor and cleavage of this precursor occursduring the process of secretion to yield the active ANP. Whereas, BNP was first isolated form brain, but it is also found in the circulation and in highest amounts in the heart ventricles, especially in pathophysiologic states. BNP is formed by cleavage of human BNP (hBNP) precursor before secretion and stored in cardiocytes and regarded as a major storage form both in atria and ventricles.
Atrial Reflexes That Activate the Kidneys—The “Volume Reflex.”
Stretch of the atria also causes significant reflex dilation of the afferent arterioles in the kidneys. And still other signals are transmitted simultaneously from the atria to the hypothalamus to decrease secretion of antidiuretic hormone. The decreased afferent arteriolar resistance in the kidneys causes the glomerular capillary pressure to rise, with resultant increase in filtration of fluid into the kidney tubules.
The diminution of antidiuretic hormone diminishes the reabsorption of water from the tubules. Combination of these two effects — increase in glomerular filtration and decrease in reabsorption of the fluid - increases fluid loss by the kidneys and reduces an increased blood volume back toward normal. Atrial stretch caused by increased blood volume also elicits a hormonal effect on the kidneys — release of ANP that adds still further to the excretion of fluid in the urine and return of blood volume toward normal.
Physiological actions of ANP and BNP: Both ANP and BNP exert similar physiological actions such as natriuretic, diuretic and hypotensive effects.
Renal effects: The renal actions of cardiac natriuretic peptides include, effects on therenal 16 vasculature, the glomerular mesangial cells, renin secretion and tubular sodium reabsorption. It has been demonstrated that intrarenal administration of synthetic ANP markedly increases the urine volume and sodium excretion with associated increase in GFR and decreased tubular reabsorption of sodium. Injection of the atrial extract into bioassay rats was associated with significant increases in urine flow rate, Na+ excretion (20 folds)and K+ excretion.
Micropuncture studies on euvolemic Munich-wistar rats demonstrated that ANP infusion decreases the arterial resistance in the glomerular afferent arteriole in a dose dependant manner, while leaving the resistance of the efferent arteriole unchanged or increased. This effect of ANP, makes the ANP system as unique and different
from classic renal vasodilators such as bradykinins and acetylcholine. Thus an increased GFR is likely to occur by the selective effect of 17 ANP on glomerular microcirculation. An increase in GFR occurs as a result of a rise in glomerular capillary hydrostatic pressure from afferent arteriolar vasodilation and efferent arteriolar vasoconstriction.
Moreover, small changes or increase in GFR (such as 5%), which certainly may escape detection, can reduce a significant increase in urine output and alteration in sodium excretion, independent of changes in tubular sodium handling. The natriuretic effect of ANP may also be mediated in part, by renal specific tubular mechanisms rather than purely by effects on the intrarenal haemodynamics. There is no clear understanding mechanism showing the direct effect of ANP on proximal tubules and loops of Henle. In spite of the presence of natriuretic peptide receptors on proximal tubular cells, it has been found that atrial natriuretic peptides, modulate the 18 proximal tubular transport of sodium and water only in the presence of angiotensin II. Moreover, there is no demonstrable direct ANP effect on isolated proximal tubular cells. Atrial natriuretic peptides do not appear to affect the proximal tubular transport directly, but act via specific receptors on the basolateral and luminal membranes to raise the intracellular cGMP levels and inhibit the angiotensin 11 stimulated transport. Regarding the effects of ANP on the loops of Henle and renal medullary washout, animal experiments have shown the loss of medullary solute gradient after ANP infusion. Moreover, all human studies have demonstrated a marked fall in urinary osmolality by administration of ANP, which indicates an increase in medullary washout that can dissipate the medullary hyperosmolality and contribute to the diuresis. Although, the mechanism of 19 action of ANP on the distal tubules and cortical collecting ducts is not clear, it has been reported that ANP is capable of inhibiting the action of vasopressin in this segment of the nephron.
In inner medullary collecting ducts (IMCD), receptors for ANP have been characterized, and cGMP was identified as an intracellular second messenger. The sodium transport across IMCD cells occurs through amiloride-sensitive Na+ channels in the apical membrane. It has been suggested that cGMP may directly inhibit these channels by phosphorylation independent mechanism and also by a cGMP- dependant protein kinase phosphorylation step. Thus the reduced entry of Na will indirectly inhibit the Na+-K+ ATPase pump on the basolateral surface of these cells. These actions of ANP clearly favour natriuresis and diuresis effects of aldosterone and angiotensin II.
Moreover, ANP decreases the responsiveness of zona glomerulosa cells to stimuli that normally increase the aldosterone secretion. It has been reported that ANP is capable of inhibiting the action of vasopressin on distal tubules and cortical collecting ducts. Meanwhile, it has been shown that synthetic ANP can inhibit dehydration and haemorrhage-induced ADH release in vivo. Also, it has been suggested that ANP directly acts on the posterior pituitary to inhibit ADH secretion and the effect is partly mediated by the increased production of cGMP and decreased production of cAMP. On other hand,the production of ANP within the brain is thought to be involved locally in the control of ADH release. 23 ANP, was observed to have a significant effect on AVP-induced decrease in urine output and sodium excretion in patients with congestive heart failure (CHF). Co-infusion of ANP with AVP in patients with CHF ,enhanced both the urine flow rate and Na+ excretion without change in the systemic arterial blood pressure.
Cardiovascular effects of ANP and BNP: Cardiac natriuretic peptides proved to be potent vasorelaxant agents. ANP has a vasorelaxant effect on renal vasculature, and on large arteries and vascular beds and also on non-vascular smooth muscles. There is some evidence to indicate that renal arteries are more sensitive than other arterial tissues to the vasodilator effect of ANP. Although, ANP opposes the vasoconstriction induced by all hormonal and pharmacologic agents, but its antagonism is greater to 24 angiotensin II than to norepinephrine - induced contraction of rabbit aorta. Direct negative inotropic effect, of the peptide on the cardiac myocytes has not been reported, and its hypotensive action is partly attributed to the stimulation of parasympathetic and inhibition of sympathetic discharges into the heart.
Moreover, the hypotensive effect of ANP is reduced markedly after vagatomy. In spite of the inhibitory effect of ANP on the sympathetic activity, it has been shown that intense activation of the sympathetic system resulted in a significant reduction in the level of the circulating ANP.
The antagonistic relationship between ANP and the renin - angiotensin system in the central nervous system as well as in the periphery, affects the modulation of the body fluids, blood pressure and baroreflex responses. Hence, the 25 cardiovascular effects ANP can be summarized in the following points:
1. Reduction in the peripheral resistance (afterload).
2. Reduction in the venous return and atrial filling pressure (preload).
3. Stimulation of the parasympathetic activity (vagi).
4. Reduction in the cardiac output.
All or most of these effects are secondary to inhibition or stimulation of the mechanisms regulating the cardiovascular system.
Effects on the brain: The distribution of ANP and its receptors in the brain are localized in the regions identified to be intimately involved in the ECF volume and pressure homeostasis such as the supraoptic,
paraventricular nuclei, nucleus of tractus solitareus, the area postrema and chnoroid plexus. It has been reported that intracerebroventricular injection of both ANP and BNP antagonize the central effects of angiotensin II. Moreover, they bind to the supraoptic and paraventricular nuclei and directly inhibit the AVP release.
The regional distribution or BNP in procine brain, and highest concentrations of immunoreactive BNP (irBNP) were found in the hypothalamus, medulla, pons and spinal cord.