Thirst and Body Fluid Regulation

Body fluid regulation is pivotal to human health and is served by extensive clinical and pre-clinical science. By combining modern advances with previous findings in the field, this book presents a comprehensive treatment of major experiments, theories, and new advances in the field of body fluid regulation, thirst, and drinking. It features the main integrative brain mechanisms for fluid regulation, the development of such systems, fluid balance during heat and exercise, aging and clinical disorders, and comparative aspects of fluid regulation. The volume focuses on mammalian thirst or drinking behaviour alongside relevant aspects of the physiology of fluid balance. The principal fluid compartments and their regulation by both intakes and losses are highlighted, using both human and animal studies to illustrate the main concepts.

A new paradigm of sodium regulation in inflammation and hypertension

Dysregulation of sodium (Na+) balance is a major cause of hypertensive cardiovascular disease. The current dogma is that interstitial Na+ readily equilibrates with plasma and that renal excretion and reabsorption is sufficient to regulate extracellular fluid volume and control blood pressure. These ideas have been recently challenged by the discovery that Na+ accumulates in tissues without commensurate volume retention and activates immune cells, leading to hypertension and autoimmune disease. However, objections have been raised to this new paradigm, with some investigators concerned about where and how salt is stored in tissues. Further concerns also include how Na+ is mobilized from tissue stores and how it interacts with various organ systems to cause hypertension and end-organ damage. This review assesses these two paradigms of Na+ regulation in the context of inflammation-mediated hypertension and cardiovascular disease pathogenesis. Also highlighted are future perspectives and important gaps in our understanding of how Na+ is linked to inflammation and hypertension. Understanding mechanisms of salt and body fluid regulation is the sine qua non of research efforts to identify therapeutic targets for hypertension and cardiovascular disease.

Diverse mechanisms for body fluid regulation in teleost fishes

Teleost fishes are the major group of ray-finned fishes and represent more than one-half of the total number of vertebrate species. They have experienced in their evolution an additional third-round whole genome duplication just after the divergence of their lineage, which endowed them with an extra adaptability to invade various aquatic habitats. Thus their physiology is also extremely diverse compared with other vertebrate groups as exemplified by the many patterns of body fluid regulation or osmoregulation. The key osmoregulatory organ for teleosts, whose body fluid composition is similar to mammals, is the gill, where ions are absorbed from or excreted into surrounding waters of various salinities against concentration gradients. It has been shown that the underlying molecular physiology of gill ionocytes responsible for ion regulation is highly variable among species. This variability is also seen in the endocrine control of osmoregulation where some hormones have distinct effects on body fluid regulation in different teleost species. A typical example is atrial natriuretic peptide (ANP); ANP is secreted in response to increased blood volume and acts on various osmoregulatory organs to restore volume in rainbow trout as it does in mammals, but it is secreted in response to increased plasma osmolality, and specifically decreases NaCl, and not water, in the body of eels. The distinct actions of other osmoregulatory hormones such as growth hormone, prolactin, angiotensin II, and vasotocin among teleost species are also evident. We hypothesized that such diversity of ionocytes and hormone actions among species stems from their intrinsic differences in body fluid regulation that originated from their native habitats, either fresh water or seawater. In this review, we summarized remarkable differences in body fluid regulation and its endocrine control among teleost species, although the number of species is still limited to substantiate the hypothesis.

Effect ofPoria cocoson Puromycin Aminonucleoside-Induced Nephrotic Syndrome in Rats

Nephrotic syndrome is associated with altered renal handling of water and sodium and changes in the levels of aquaporins (AQPs) and epithelial Na channels (ENaCs). The dried sclerotia ofPoria cocosWolf (WPC) have been used for treating chronic edema and nephrosis. We evaluated the effects of WPC on puromycin aminonucleoside- (PAN-) induced renal functional derangement and altered renal AQP2 and ENaC expression. In the nephrotic syndrome rat model, animals were injected with 75 mg/kg PAN and then treated with Losartan (30 mg·kg−1·day−1) or WPC (200 mg·kg−1·day−1) for 7 days. In the WPC group, proteinuria and ascites improved significantly. Plasma levels of triglyceride, total cholesterol, and low-density lipoprotein- (LDL-) cholesterol reduced significantly in the WPC group. In addition, the WPC group exhibited attenuation of the PAN-induced increase in AQP2 and ENaCα/βsubunit protein and mRNA levels. WPC suppressed significantly PAN-induced organic osmolyte regulators, reducing serum- and glucocorticoid-inducible protein kinase (Sgk1) and sodium-myo-inositol cotransporter (SMIT) mRNA expression. Our results show that WPC improves nephrotic syndrome, including proteinuria and ascites, through inhibition of AQP2 and ENaC expression. Therefore, WPC influences body-fluid regulation via inhibition of water and sodium channels, thereby, improving renal disorders such as edema or nephrosis.

Central neural control of sympathetic nerve activity in heart failure following exercise training

Typical characteristics of chronic congestive heart failure (HF) are increased sympathetic drive, altered autonomic reflexes, and altered body fluid regulation. These abnormalities lead to an increased risk of mortality, particularly in the late stage of chronic HF. Recent evidence suggests that central nervous system (CNS) mechanisms may be important in these abnormalities during HF. Exercise training (ExT) has emerged as a nonpharmacological therapeutic strategy substitute with significant benefit to patients with HF. Regular ExT improves functional capacity as well as quality of life and perhaps prognosis in chronic HF patients. The mechanism(s) by which ExT improves the clinical status of HF patients is not fully known. Recent studies have provided convincing evidence that ExT significantly alleviates the increased sympathetic drive, altered autonomic reflexes, and altered body fluid regulation in HF. This review describes and highlights the studies that examine various central pathways involved in autonomic outflow that are altered in HF and are improved following ExT. The increased sympathoexcitation is due to an imbalance between inhibitory and excitatory mechanisms within specific areas in the CNS such as the paraventricular nucleus (PVN) of the hypothalamus. Studies summarized here have revealed that ExT improves the altered inhibitory pathway utilizing nitric oxide and GABA mechanisms within the PVN in HF. ExT alleviates elevated sympathetic outflow in HF through normalization of excitatory glutamatergic and angiotensinergic mechanisms within the PVN. ExT also improves volume reflex function and thus fluid balance in HF. Preliminary observations also suggest that ExT induces structural neuroplasticity in the brain of rats with HF. We conclude that improvement of the enhanced CNS-mediated increase in sympathetic outflow, specifically to the kidneys related to fluid balance, contributes to the beneficial effects of ExT in HF.