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Cellular and Molecular Basis of Human Biology
Published in Lawrence S. Chan, William C. Tang, Engineering-Medicine, 2019
Even though it is generally recognized as a system of waste disposal, the urinary system also has important regulatory functions for the human body. The system is consisted of kidney, urinary duct (ureter), urinary bladder, and urinary outlet (urethra). Besides the function of removing metabolites and breakdown products out of the human body, the kidney also performs its osmoregulation by titrating the salt concentration through selectively close or open the “salt gate” or “water gate” to maintain a normal level of salt concentration in the human body. The urinary system is also dependent on the cardiovascular system to deliver the “waste” to it for filtering and disposal. In addition, the endocrine system also influences the urinary system in that mineralocorticoids of the adrenal gland promotes reabsorption of Na+ and excretion of K+ (Reece et al. 2014). The proper function of urinary system also requires the intact nervous function. Neurological diseases could lead to urinary dysfunction, such as neurogenic bladder, which could result in renal failure, upper urinary tract dilatation and infections (Amarenco et al. 2017).
An Overview on the Beneficial Effects of Hydration
Published in Datta Sourya, Debasis Bagchi, Extreme and Rare Sports, 2019
Osmoregulation is considered a vital part of thirst regulation. The osmotic pressure of the fluid (plasma osmolality) typically lies between 280–295 mosmol/kg/H2O. Losses as small as 1–2% of body weight stimulate thirst. Increased thirst is directly proportional to the osmotic gradient. Changes in NaCl and/or glucose induce this response by not crossing cell membranes so easily. The osmotic differences between the intracellular and extracellular spaces are what dictate the flow of fluids (higher to lower concentration occurring typically by osmosis). Osmosis is partially regulated by osmoreceptors (relative to vasopressin) in the brain and in the liver. The hypothalamus, an integral component of the brain, initiates thirst regulation and control.
ENTRIES A–Z
Published in Philip Winn, Dictionary of Biological Psychology, 2003
Osmoregulation is the term given to the control of WATER BALANCE in the body. It is a complex process involving the integrated actions of a variety of tissues, chemical processes, and of course behaviour. Animal bodies contain four fluid compartments: about two thirds of body water is contained within cells (INTRACELLULAR FLUID), the remaining one-third being outside cells (EXTRACELLULAR FLUID). There are three types of extracellular fluid: CEREBROSPINAL FLUID (which has relatively little to do with osmoregulation, forming only about 1% of the total body fluid volume); INTRAVASCULAR FLUIDS (that is, blood plasma; see BLOOD) which forms about 7.5% of the body fluid volume); and, making up the bulk of the extracellular fluids, INTERSTITIAL FLUID (the fluid found in the spaces between cells—about 25% of total body fluid volume). Intracellular, interstitial and intravascular fluids are separated by a SEMIPERMEABLE MEMBRANE: cell walls divide intracellular from interstitial fluids, and the walls of blood vessels separate intravascular fluids from all others. Interstitial fluids normally are ISOTONIC with the others so water remains in whatever compartment it is already in: if the interstitial fluids lose water (that is, become HYPERTONIC), fluid will be drawn out of cells (by a process of OSMOSIS). If the interstitial fluids become too diluted (that is, become HYPOTONIC), cells will gain water (again, by osmosis). The maintenance of an appropriate amount of water in the various body compartments uses two systems: osmometric thirst (the production of physiological changes and DRINKING following cellular dehydration) and VOLUMETRIC THIRST (which involves the production of physiological change and drinking following intravascular fluid maintenance).
The anti-hypertensive effects of sodium-glucose cotransporter-2 inhibitors
Published in Expert Review of Cardiovascular Therapy, 2023
Luxcia Kugathasan, Lisa Dubrofsky, Andrew Advani, David Z.I. Cherney
Under normal physiological conditions, blocking sodium transport in the proximal tubule increases distal tubular load and promotes a compensatory enhancement of sodium, chloride, and potassium reabsorption at the loop of Henle primarily by Na-K-2Cl (NKCC2) cotransporters. However, owing to the natriuretic-diuretic coupling effect of SGLT2 inhibition at the proximal tubule, it has been postulated that a diluted load with a low chloride concentration is delivered to the distal nephron and renders tubular reabsorption at the loop of Henle ineffective (Figure 3) [96]. Specifically, since the proximal tubule is highly permeable to water and SGLT2 inhibition renders glucose non-resorbable, isotonicity between the tubular fluid and blood is maintained by osmoregulation. The resulting diuresis is thought to decrease the chloride ion concentration in the proximal tubular filtrate [92]. Therefore, it is speculated that the requirement of two chloride ions for each cotransport at the thick ascending limb subsequently reduces NKCC2 cotransporter activity in a diluted chloride environment [92,96]. The off-target impact of SGLT2 inhibitors at the thick ascending limb may indicate similar activity to that of a loop diuretic to promote plasma volume contraction, although this effect has yet to be proven [96].
The pharmacotherapeutic options in patients with catecholamine-resistant vasodilatory shock
Published in Expert Review of Clinical Pharmacology, 2022
Timothy E. Albertson, James A. Chenoweth, Justin C. Lewis, Janelle V. Pugashetti, Christian E. Sandrock, Brian M. Morrissey
The endogenous hormone vasopressin circulates in the blood after it is released from the posterior pituitary gland. VP mainly ensures osmoregulation by its effect on the arginine vasopressin receptor 2 (AVPR2) located primarily in the distal convoluted tubules promoting water retention. The antidiuretic hormone effect is normally the major effect of VP, but in shock conditions, even higher circulatory levels of VP are naturally released. These higher levels also stimulate arginine vasopressin receptor 1a (AVPR1a) generating powerful vasoconstriction. Potentially when VP is given exogenously, it maintains better kidney perfusion than exogenous NE because there are more AVPR1a receptors in the glomerular efferent than afferent arterioles [21]. In addition, the stimulation of arginine vasopressin receptor 1b (AVPR1b) by VP generates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary resulting in release of cortisol from the adrenal gland. The higher levels of ACTH generated by VP release generate increased natural levels of endogenous cortical steroids in shock patients.
Taurine and GABA neurotransmitter receptors, a relationship with therapeutic potential?
Published in Expert Review of Neurotherapeutics, 2019
Lenin Ochoa-de la Paz, Edgar Zenteno, Rosario Gulias-Cañizo, Hugo Quiroz-Mercado
Taurine is a β-amino acid present in high concentrations in different tissues of mammals including all areas of the CNS. A deficiency of taurine during fetal life or lactation manifests itself as an embryonic and postnatal growth deficit and as several defects during development, and many of them related to the visual and nervous system. It participates in physiological processes such as osmoregulation and neurotransmission, among others. Initially, taurine was proposed as an inhibitory neurotransmitter; however, it is not considered a classic neurotransmitter because to date a specific receptor has not been identified, and its release is independent of Ca2+. Taurine exerts its neuronal inhibitory effect through the activation of GABAA receptors (GABAAR) but with less affinity than the specific agonists of each receptor [1]. Taurine has been used in different clinical trials as antiepileptic drug; in these protocols, one-third of the patients have shown a significant reduction of seizures by taurine medication. However, this effect is limited by the capacity to internalize the taurine into the brain under pathological conditions and the mechanism of taurine excretion by urine [2].