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Medical evaluation and management of pregnant patients undergoing non-obstetrical surgery
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
The cardiovascular system undergoes significant alteration under the influence of the altered hormonal milieu of pregnancy. Progesterone inhibits distal tubular sodium reabsorption leading to natriuresis. The juxtaglomerular cells of the kidney in response to this secrete renin to stimulate aldosterone release from the adrenals, maintaining sodium homeostasis (1–3). Renin is converted into angiotensin and catecholamines are released from the adrenal gland. Pregnancy is a state of maternal hyper-catecholaminism from its early stages. These catecholamines stimulate both inotropic and chronotropic effects on the heart, leading to an increase in cardiac output. Cardiac output begins to rise in the first trimester and continues on a steady increase to peak at 30% to 50% of the preexisting levels by approximately 32 weeks of gestation (3–7). Both heart rate and stroke volume increase. Peripheral systemic vascular resistance is reduced secondary to progesterone, exerting a direct effect to relax the intimal smooth muscle in the precapillary resistance vessels (2,3). The resulting vasodilatation leads to a decreased vascular resistance. There is a slight decrease in mean arterial pressure in the second trimester of a normal pregnancy due to the reduction in peripheral resistance. Blood volume increases with pregnancy, peaking at approximately 50% of prepregnancy levels at around 32 weeks of gestation. As the pregnant woman approaches term, mean arterial pressure normalizes as the increase in blood volume compensates for the decreased resistance and fills the capacitance of the vasculature (8,9).
Tubular Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The secretion of renin by juxtaglomerular cells is controlled by renal sympathetic nerves, intrarenal baroreceptors, macula densa and angiotensin II. The renal sympathetic nerves and circulating catecholamines each increase renin secretion via β1 receptors. Baroreceptor reflexes, which detect low systemic cardiovascular pressures, increase renin secretion.
Renal Pathophysiology
Published in Manit Arya, Taimur T. Shah, Jas S. Kalsi, Herman S. Fernando, Iqbal S. Shergill, Asif Muneer, Hashim U. Ahmed, MCQs for the FRCS(Urol) and Postgraduate Urology Examinations, 2020
Herman S. Fernando, Mohamed Yehia Abdallah, Iqbal S. Shergill
The glomerulus, which is about 200 μm in diameter, is formed by the invagination of a tuft of capillaries into the dilated, blind end of the nephron. In the distal convoluted tubule, while the predominant principle cells (P) are involved in Na+ reabsorption and vasopressin-stimulated water reabsorption, the intercalated cells (I) are associated with acid secretion and HCO3− transport. It is the wall of the afferent arteriole that contains renin-secreting juxtaglomerular cells. At this point the wall of the tubular epithelium is modified histologically to become the macula densa. The juxtaglomerular cells, the macula densa and the lacis cells near them are collectively known as juxtaglomerular apparatus. The kidney receives 25% of cardiac output.
The roles of hydrogen sulfide in renal physiology and disease states
Published in Renal Failure, 2022
Jianan Feng, Xiangxue Lu, Han Li, Shixiang Wang
H2S attenuates pathological signaling of the renin–angiotensin–aldosterone system (RAAS) to preserve kidney function. The RAAS is a humoral regulatory system composed of hormones and corresponding enzymes that regulates the excretion of water and sodium. The release of renin from juxtaglomerular cells determines the onset and development of renovascular hypertension, a procedure adjusted by intracellular 3′–5′–cyclic adenosine monophosphate (cAMP). H2S has been reported to downregulate cAMP by inhibiting adenylate cyclase activity, thereby regulating renin release and controlling BP [29,30]. In primary cultures of renin–rich kidney cells, NaHS significantly reduces the levels of intracellular cAMP and reduces renin activity. In a Dahl rat model of high–salt–induced hypertension, treatment with H2S has been found to inhibit RAAS system activation in the kidneys and to regulate BP [31]. H2S also regulates BP via angiotensin–converting enzyme, which belongs to the RAAS system. In human endothelial cells, H2S can directly interfere with zinc in the active center of angiotensin–converting enzyme [32].
Acute restraint stress increases blood pressure and oxidative stress in the cardiorenal system of rats: a role for AT1 receptors
Published in Stress, 2020
Gabriel T. do Vale, Drieli Leoni, Arthur H. Sousa, Natália A. Gonzaga, Daniela L. Uliana, Davi C. La Gata, Leonardo B. Resstel, Cláudia M. Padovan, Carlos R. Tirapelli
Our results are in line with previous findings showing that acute restraint stress increased both MAP and HR (Busnardo et al., 2010, 2013; Crestani et al., 2010; Dos Reis et al., 2014). Additionally, we found that blockade of AT1 receptors with losartan reduced acute restraint stress-induced MAP increase. This observation corroborates previous findings showing that angiotensin II plays a role in acute stress-induced cardiovascular changes (Busnardo et al., 2014; Erdos et al., 2010; Jezova et al., 2008; Kubo et al., 2001; Saiki et al., 1997). On the other hand, losartan did not prevent the increase in HR induced by acute restraint stress, suggesting that AT1 receptors do not play a role in such response. Moreover, our findings suggested that acute restraint stress activated the RAS. In fact, circulating levels of angiotensin II are described to be increased after acute stress (Gonzaga et al., 2015; Yang, Lu, Yu, & Raizada, 1996). The sympathetic nervous system modulates RAS activation. Renal juxtaglomerular cells are in contact with sympathetic nerve varicosities that express post-junctional β1-adrenergic receptors and activation of these receptors increases renin release with further activation of the RAS (Montezano & Touyz, 2014). Thus, activation of the RAS during acute restraint stress could be mediated by the sympathetic system, whose activity is increased in such condition (Dos Reis et al., 2014; Crestani, 2016).
Atorvastatin protects against contrast-induced acute kidney injury via upregulation of endogenous hydrogen sulfide
Published in Renal Failure, 2020
Lin Yan, Lin Jiaqiong, Guo Yue, Li Xiaoyong, Tan Xuexian, Long Ming, Li Yinglan, Liao Xinxue, Huang Zena
In kidney, H2S is produced through four pathways, while CSE and CBS are the two dominated enzymes for its generation [38]. In physiological conditions, H2S was found to inhibit sodium transporters on renal tubular cells, and thus regulate the excretory function of the kidney [39]. Likewise, it also influences the release of renin from juxtaglomerular cells and thereby modulates blood pressure [40]. What’s more, H2S modulates urine concentration by upregulating renal AQP-2 protein expression [41]. Liu et al. [42] recently showed that both CSE and CBS levels were severely decreased in a cisplatin-treated rats. Moreover, in renal ischemia/reperfusion models, supplement of H2S exerted protective effect likely through anti-inflammatory, anti-apoptotic, and anti-oxidative responses [43,44]. In our study, serum level of H2S, as well as renal expression of CSE and CBS, were significantly reduced in the CM-treated rats, paralleling to the renal injury. This indicated a decrease of systemic and localized generation of H2S in CIAKI model. Furthermore, when a H2S donor, NaHS, was employed in NRK-52E cells, CM-induced apoptosis and inflammation were both ameliorated remarkably. Therefore, our data prompted that H2S may also exhibited protection against CIAKI by anti-inflammatory, antiapoptotic, and antioxidative mechanism.