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      Effects of anesthesia on plasma and kidney ANG II levels in normotensive and ANG II-dependent hypertensive rats.

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          Abstract

          Previous studies have implicated that normotensive rats with normal renal renin activity respond to anesthesia and surgery with greater increases in plasma and kidney angiotensin II (ANG II) concentrations than ANG II-dependent hypertensive rats with intrarenal renin depletion. In the present study, we therefore compared plasma and kidney ANG II levels in anesthetized and conscious normotensive and ANG II-dependent hypertensive rats.

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          Interactions between the sympathetic nervous system and the kidneys in arterial hypertension.

          Rainer Rettig, Olaf Grisk (2004)
          Elevated sympathetic activity changes renal function and accelerates the development of hypertension. Principles of sympatho-renal interactions in chronic hypertension are reviewed. Alterations in the ontogeny of the sympathetic nervous system and the kidney, inherited abnormalities in sensory receptor function and exaggerated responsiveness to mental stress contribute to inappropriately high sympathetic activity in primary or essential hypertension. Careful characterization of clinical study populations shows that elevated sympathetic activity and "essential" hypertension are not unequivocally associated. Prospective clinical studies which investigate a broader array of physiological functions and experiments in recombinant inbred rodents with less traumatic nerve recording techniques than currently available will help to define under which conditions elevated sympathetic activity is indeed a cause of primary hypertension. Signals arising from the kidney which activate the renin-angiotensin system and afferent renal nerves increase sympathetic activity. These mechanisms importantly contribute to the pathogenesis of hypertension secondary to renal artery stenosis and end-stage renal disease.
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            Effects of angiotensin-(1-7) blockade on renal function in rats with enhanced intrarenal Ang II activity.

            Marcela Bürgelova, Monika Thumová, Vladimir Teplan … (2005)
            Increasing evidence suggests that angiotensin-(1-7) [Ang-(1-7)] acts as an endogenous antagonist of Ang II when the renin-angiotensin system (RAS) is activated. In the present study, we therefore compared the effects of acute intrarenal (i.r.) Ang-(1-7) receptor blockade on renal function under conditions of normal and increased intrarenal Ang II concentration. Salt-replete Hannover-Sprague Dawley rats (HanSD) served as control animals. As models with enhanced action of Ang II we first used transgenic rats harboring the Ren-2 renin gene (TGR), second, Ang II-infused rats, third, 2-kidney, 1-clip (2K1C) hypertensive rats on normal salt intake, and fourth, salt-depleted TGR and HanSD. I.r. Ang-(1-7) receptor blockade elicited significant decreases in glomerular filtration rate (GFR), renal plasma flow (RPF), and sodium excretion in 2K1C rats, and in salt-depleted TGR and HanSD. In contrast, i.r. Ang-(1-7) receptor blockade did not significantly change GFR, RPF, and sodium excretion in salt-replete TGR and HanSD, or in Ang II-infused rats. These findings suggest that under conditions of normal intrarenal RAS activity and increased intrarenal Ang II action by infusion of Ang II or by insertion of a renin gene in salt-replete conditions, Ang-(1-7) is not an important factor in the regulation of renal function. In contrast, under conditions of endogenous RAS activation due to clipping of the renal artery or to sodium restriction, Ang-(1-7) serves as opponent of the vasoconstrictor actions of Ang II.
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              Effects of diethyl ether, halothane, ketamine and urethane on sympathetic activity in the rat.

              Michele Carruba, GianPietro Bondiolotti, Giovanni B. Picotti … (1987)
              The present paper describes the effects of different general anaesthetics on plasma catecholamine (CA) concentrations taken as biochemical index of peripheral sympathetic activity. In chronically catheterized rats, diethyl ether, ketamine and urethane increased plasma adrenaline (A) and noradrenaline (NA) concentrations, indicating that these drugs stimulate both neurosympathetic and adrenomedullary functions. These effects appear to be centrally mediated, since ganglionic blockade or spinal transection completely counteracted the diethyl ether- and ketamine-induced increases in plasma CA levels. Halothane induced a transient decrease in circulating A and an increase in NA. These results support the concept that general anaesthetics may have different effects on sympathetic function. Arterial blood pressure and heart rate were also measured to look for possible correlations with peripheral sympathetic activity. The enhanced release of peripheral CAs seemed to be the determining factor for increasing blood pressure and heart rate with ketamine only. In the other instances the activation of the peripheral sympathetic system appeared to maintain homeostasis by counterbalancing the various depressive effects of anaesthetics on the cardiovascular system.
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                Author and article information

                Journal
                Journal ID (iso-abbrev): Kidney Blood Press. Res.
                Title: Kidney & blood pressure research
                Publisher: S. Karger AG
                ISSN: 1420-4096
                ISSN (Print): 1420-4096
                Publication date (Electronic): 2006
                Volume: 29
                Issue: 2
                Affiliations
                [1 ] Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
                Article
                Publisher Item ID: 92981
                DOI: 10.1159/000092981
                PubMed ID: 16651849
                SO-VID: e4681258-fc34-4a1c-949c-ebcce0271932
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