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Cardiac Reflexes and Control of Renal Function in Primates
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Thus the available evidence indicates that neither vagal nor sympathetic afferent neural mechanisms play a mandatory role in eliciting the renal effects of immersion in anesthetized monkeys. Although this strongly suggests that cardiopulmonary receptors are not involved in mediating the renal responses, the question then arises as to what does cause the diuresis/natriuresis during this maneuver. This remains unanswered although it has been suggested that, since arterial pressure tends to increase consistently with immersion in anesthetized monkeys (Gilmore and Zucker, 1978a; Cornish and Gilmore, 1983; Peterson et al., 1987), this may have an effect, either directly on the kidney or through renal effects secondary to stimulation of sinoaortic baroreceptors (Echtenkamp et al., 1980; Abboud and Thames, 1983). Another possibility is atrial natriuretic factor (ANF) or atriopeptin (ANP) (deBold et al., 1981; Genest and Cantin, 1987; Baxter et al., 1988; Blaine, 1988; Goetz, 1988) since it has been shown that this cardiac hormone may be an important mediator of salt and water excretion during intravascular volume expansion (Benjamin et al., 1988a) or following acute oral intake of sodium in the monkey (Benjamin et al., 1988b). Whether it is also important during immersion is not known.
Gustatory Mechanisms of a Specific Appetite
Published in Robert H. Cagan, Neural Mechanisms in Taste, 2020
Sodium is the principal electrolyte of the extracellular fluid. The level of sodium in body fluids plays a crucial role in defining the electrochemical status of the intracellular and extracellular fluids. As such, sodium is essential for such processes as nerve cell function, blood volume and blood pressure maintenance, acid-base balance, and muscle contraction.3 Because of its importance to normal bodily processes, sodium levels are tightly regulated, primarily by the interplay of the kidneys and adrenal glands through hormonal signals. Physiochemical changes associated with sodium deficiency trigger activation of the renal-renin and blood-angiotensin system to promote the production and release of aldosterone from the adrenal gland. Aldosterone inhibits sodium loss through urination, perspiration, and salivation. Excess sodium, on the other hand, suppresses the renin-angiotensin system, thereby permitting sodium loss. In addition, a new hormonal factor was recently identified that may play an important role in promoting the excretion of excess sodium.4–6 In response to blood volume expansion, the atrial stretch receptors of the heart release atrial natriuretic factor, which, by its direct action on the kidney, promotes sodium excretion and inhibits aldosterone and renin secretion.
Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Although there may be other cardiac hormones, the atrial natriuretic factor (ANF) is the one most completely defined. The ANF is located in cells in both the right and left cardiac atria but chiefly in the right atrium. It is produced within the myocardial cells. The ANF, in contributing to blood volume control, acts as a set of stretch receptors in the atrial muscles.
The Potential Physiological Role of γ-Tocopherol in Human Health: A Qualitative Review
Published in Nutrition and Cancer, 2020
Mika D. Thompson, Robert V. Cooney
Although γ-tocopherol is the predominant form of tocopherol in the diet, α-tocopherol constitutes approximately 80% of the tocopherols normally found in the blood. In humans the relationship between α-, β-, γ-, and δ-tocopherol serum levels appear to be mediated, in part, by a tocopherol binding protein in the liver which differentially binds and maintains the four tocopherols in a ratio 1:0.01:0.15:0.1 for the four tocopherol species, respectively (89). This “typical” equilibrium can be altered by differential metabolism, oxidative stress, excessive intake of one particular form of tocopherol, and/or through undetermined mechanisms of physiological regulation. γ-Tocopherol, in particular, is metabolized via P450 to human natriuretic factor, which is responsible for regulating extracellular fluid volume (90). γ-Tocopherol levels are also observed to be higher in older adults (91), smokers (92), colon cancer patients (93), in individuals with vitamin D deficiency (94, 95), diabetics (85), and in those with poor dietary habits (96). The precise mechanisms regulating γ-tocopherol in the serum are unknown; however, levels do not appear to be related to dietary intake of γ-tocopherol (97). Supplementation with 400 mg/day and higher of α-tocopherol, however, can significantly depress serum levels of γ-tocopherol (98).
Clinicopathological features of clinically undiagnosed sporadic transthyretin cardiac amyloidosis: a forensic autopsy-based series
Published in Amyloid, 2021
Shojiro Ichimata, Yukiko Hata, Keiichi Hirono, Yoshiaki Yamaguchi, Naoki Nishida
Besides left heart failure (HF) that typically appears in advanced-phase patients, ATTR amyloidosis might be associated with atrial arrhythmia, especially atrial fibrillation (AF) [5–8]. Compared to patients with immunoglobulin light chain-derived amyloidosis and hereditary ATTR amyloidosis, more patients with sporadic ATTR amyloidosis present with AF at the first evaluation [9,10]. Thus, AF may be one of the major early symptoms of sporadic ATTR amyloidosis. In addition, sporadic ATTR amyloidosis may exhibit a characteristic atrial deposition pattern that is not observed in other types of amyloidosis at an early stage. Conversely, atrial natriuretic factor (AANF)-related amyloidosis is a type of isolated atrial amyloidosis, which is associated with localised amyloid deposition [11–14]. However, the frequency of AANF deposition increases with aging, and reports have indicated that it also causes disturbances for atrial conduction, thereby increasing the risk of AF [13,14]. Nonetheless, no studies have fully elucidated whether these two amyloid deposits are associated with atrial arrhythmia, possibly because direct amyloid infiltration in the specialised conduction tissue does not account for the majority of these disturbances [15], making it challenging to arrive at definite conclusions. Moreover, ‘senile’ amyloid deposits might be associated with other amyloid depositions when several conditions are favourable [16]. We hypothesised that both ATTR and AANF deposits are associated with the clinicopathological features of the same or related health condition because these deposits are age-related and they frequently affect the heart.
New and emerging cardiovascular and antihypertensive drugs
Published in Expert Opinion on Drug Safety, 2020
Steven G. Chrysant, George S. Chrysant
Sacubitril/valsartan is a single drug with dual action. It exerts its beneficial cardiovascular and BP lowering effects through its dual inhibition of RAS with valsartan and neprilysin with sacubitril. Neprilysin is an important catabolizing agent of the natriuretic peptides (NPs), which possess significant diuretic, natriuretic, and vasodilating effects [23–25]. The NPs are endogenous hormones released from the heart in response to wall stretching from pressure and volume overload and exert their beneficial cardiovascular and antihypertensive effects through plasma volume contraction and peripheral vasodilation. Since the original discovery of the atrial natriuretic factor by De Bold et al. [25], three natriuretic peptides have been discovered, the atrial natriuretic peptide (ANP), the beta natriuretic peptide (BNP), and the central natriuretic peptide (CNP). The ANP and BNP are circulatory peptides and help patients with HF and hypertension through their natriuretic, diuretic, and vasodilatory effects mediated by generation of (cGMP) cyclic guanosine monophoshate [23–25]. The CNP is not a circulatory peptide and is mainly localized in the central nervous system and not involved in the cardiovascular hemodynamics [26,27]. Unfortunately, the action of sacubitril/valsartan is associated with some desirable and some undesirable adverse effects [28]. Neprilysin is known to catabolize several peptide hormones, such as adrenomedulin, Ang II, bradykinin, endothelin, glucagon-like peptide-1 (GLP-1), NPs, neurotensin, oxytocin, substance P, and most importantly, amyloid β peptide. Therefore, the net effect of sacubitril/valsartan on its cardiovascular and BP effects will be a balance between the actions of valsartan on RAS and sacubitril on NEP.