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The Renin-Angiotensin System
Published in Austin E. Doyle, Frederick A. O. Mendelsohn, Trefor O. Morgan, Pharmacological and Therapeutic Aspects of Hypertension, 2020
The most widely used agents are the nonapeptide converting-enzyme inhibitor, SQ 20881, and angiotensin-II-receptor blocker, [Sar1,Ala8]-angiotensin II (also known as saralasin or PI 13), or other angiotensin analogues with aliphatic residues at position 8 of the molecule. Neither of these two named agents are ideal for the evaluation of the role of angiotensin II in the maintenance of blood pressure. Converting enzyme inhibition may impair the degradation of the hypotensive peptide, bradykinin, as well as block the formation of angiotensin II as discussed under Section II.C.2.C. Either of these actions could lower blood pressure. The [Sar1,Ala8]-angiotensin-II analogue, hereafter called “Saralasin” for brevity, has some agonist action on vascular smooth muscle and adrenal zona glomerulosa cells, and its use as a blocking agent may, therefore, underestimate the effect of angiotensin II in maintenance of blood pressure.490,654
Kidney physiology and pathophysiology during heat stress and the modification by exercise, dehydration, heat acclimation and aging
Published in Temperature, 2021
Christopher L. Chapman, Blair D. Johnson, Mark D. Parker, David Hostler, Riana R. Pryor, Zachary Schlader
Activation of the sympathetic nervous system appears to be the primary mechanism by which heat stress causes vasoconstriction in the kidneys [272,274]. In support of this, heat stress-induced increases in RSNA have been reported in rats [275-280] and cats [281] across a wide range of core temperatures. Furthermore, increases in RSNA also occur with partial body heating, such as with the rat’s tail [282-285]. Importantly, there are additional redundant pathways (e.g., renin-angiotensin-aldosterone system, vasopressin, arterial baroreflex) that can induce renal vasoconstriction, but there is currently no direct evidence investigating the interdependent effects of all these systems on renal vasoconstriction during heat stress. That said, Eisman and Rowell [286] reported that renal vasoconstriction during whole body heating in baboons was largely attenuated with infusion of propranolol, which blocks the β-adrenergic release of renin, or with saralasin, which competes with angiotensin II for AT1R receptor-binding. This evidence suggests that angiotensin II also plays an important role in the renal vasoconstrictor response to heat stress. To our knowledge, despite evidence that vasopressin has vasoconstrictor actions in the kidneys [287], there has not been a study to further elucidate the mechanism by which vasopressin may induce renal vasoconstriction during heat stress. Indirect evidence suggests that this renal vasoconstriction to heat stress is not caused by the arterial baroreflex, due to evidence suggesting that vasomotor tone in other visceral vascular beds (e.g., the splanchnic circulation) are not modified by the arterial baroreflex in humans [288].
Cabergoline versus calcium infusion in the prevention of ovarian hyperstimulation syndrome: a randomised controlled study
Published in Journal of Obstetrics and Gynaecology, 2022
Usama M. Fouda, Hesham S. Elshaer, Gamal G. Youssef, Amal Hanafy, Waleed M. Mehrem, Mohamed A. Youssef, Mona Farouk, Hala Nabil
Morris et al. (1995) reported that the administration of oral enalapril in rabbits resulted in a 40% decrease in the incidence of OHSS. Şahin et al. (1997) reported that ACE inhibition (cilazapril) and AngII receptor blockage (saralasin) did not improve ascites in OHSS of rabbit.