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Effects of Adrenergic Nervous System and Catecholamines on Systemic and Renal Hemodynamics, Sodium and Water Excretion and Renin Secretion

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Effects of Adrenergic Nervous System and Catecholamines on Systemic and Renal Hemodynamics, Sodium and Water Excretion and Renin Secretion View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Elsevier - Publisher Connector Kidney International, Vol. 6 (1974), p. 291—306 Effects of adrenergic nervous system and catecholamines on systemic and renal hemodynamics, sodium and water excretion and renin secretion ROBERT W. SCHRIER Department of Medicine, University of Colorado Medical Center, Denver, Colorado The influences of the adrenergic nervous system on tion to the direct cardiac effect, in the increase in various organ systems in the body are protean. No cardiac output during i.v. administration of isopro- attempt will be made in this review to survey these terenol. On the other hand, if the rise in cardiac output many effects; but rather the focus will be on the specific during infusion of isoproterenol increases arterial influences that adrenergic tone and catecholamines blood pressure, then the fall in peripheral vascular re- exert on systemic and renal hemodynamics, the excre- sistance may be mediated both by the direct peripheral tion of sodium and water excretion and the secretion of vascular effect of the agonist and the baroreceptor- renin. Where possible, emphasis will be placed on the mediated reflex vasodilatation. Thus, several inter- integration of these functions intoa teleologically orien- related influences occur as a result of systemic ted system of control of systemic hemodynamics and of beta-adrenergic stimulation and the summation of body fluid volume and composition, including the im- these influences may result in different effects on mean plications for the pathogenesis of disease states. arterial blood pressure. In some instances isoproterenol Effect of adrenergic nervous system and catecho- administration may increase mean arterial pressure lamines on systemic and renal hemodynamics. The as a result of the predominant effect of the drug to endogenous catecholamines, norepinephrine and epine- increase cardiac output. In other circumstances the phrine, each exert a combination of alpha- and beta- peripheral vasodilatation associated with i.v. ad- adrenergic effects and the use of specific receptor ministration of isoproterenol may predominate and blocking agents has allowed pharmacological separa- cause a diminution in mean arterial pressure. In still tion of these two properties. When appropriate, there- other situations, the relative effect of beta-adrenergic fore, the separate effects of alpha- and beta-adrenergic stimulation to increase cardiac output and decrease stimulation will be discussed. peripheral vascular resistance may be such that arterial The primary cardiovascular effect of beta-adrener- pressure is unchanged. The extent to which either of gic stimulation relates to its inotropic and chrono- these effects of beta-adrenergic stimulation on syste- tropic action on the heart [1]. The increase in cardiac mic arterial pressure predominate appears to be related, output associated with the beta-adrenergic agonist, at least in part, to the amount of the stimulating agent isoproterenol, therefore is due to a rise in both heart administered. Because of these extrarenal effects of rate and stroke volume. An increase in 3'5'-adenosine beta-adrenergic stimulation on cardiac output and monophosphate (cyclic AMP) appears to be the intra- peripheral vascular resistance, it is difficult to isolate cellular hormonal mediator (secondary messenger) of the intrarenal effects of beta-adrenergic stimulation the increase in stroke volume produced by isopro- during the i.v. administration of these agonists. For terenol [2]. Beta-adrenergic stimulation has also been example, although i.v. administered isoproterenol demonstrated to exert a vasodilatory effect on the decreases total peripheral resistance, renal vascular peripheral vasculature [1]. This decrease in total peri- resistance may be unchanged or even increased if the pheral resistance may be a determining factor, in addi- net effect of the drug is to lower arterial pressure [3]. In this circumstance, the baroreceptor-mediated in- © 1974, by the International Society of Nephrology. crease in renal sympathetic tone may obscure any 292 Schrier direct intrarenal effect that isoproterenol may have to long t.4 value of this agent so that its accumulation may decrease renal vascular resistance. Since none of the lead to extrarenal hemodynamic alterations which known adrenergic agents exerts selective effects on the could obscure any intrarenal effects of beta blockade. kidney, neither the systemic administration of the In contrast to beta-adrenergic stimulation, changes agents nor the systemic blockade of their action per- in alpha-adrenergic tone definitely appear to exert mits delineation of any direct effects on the kidney. major physiological effects on renal hemodynamics. Moreover, due to the prolonged action of most beta- Norepinephrine, the adrenergic neurohumoral trans- and aipha-adrenergic blocking agents, systemic effects mitter, is primarily an alpha-adrenergic agonist; there- are observed even when these blocking agents are ad- fore, increases in renal sympathetic tone produce ministered into a renal artery. A selective intrarenal vasoconstriction of the renal vasculature. It appears adrenergic blockade, therefore, has been difficult to that several renal vascular sites for alpha-adrenergic obtain; thus, the intrarenal infusion of beta- and stimulation exist including the afferent and efferent alpha-adrenergic agonists has been the primary mode arterioles as well as the venules. With marked adren- of delineating the intrarenal effects of adrenergic ergic stimulation, an increase in renal vascular resist- stimulation. ance no doubt occurs as a result of vasoconstriction at In contrast to the effects of beta-adrenergic stimula- all of these locations and the result is a decrease in both tion, the primary cardiovascular effect of alpha- glomerular filtration rate and renal blood flow. Intra- adrenergic stimulation is vasoconstriction of the peri- renally administered norepinephrine and renal nerve pheral arterioles and venules [1]. This increase in stimulation, however, may exert a preferential vaso- peripheral vascular resistance results in an increase in constrictor effect on the efferent arteriole so that the arterial pressure which also may be secondarily modi- fall in glomerular filtration rate is less than the decrease fied by reflex changes in arterial baroreceptor tone. As in renal blood flow; thus, filtration fraction increases. with beta-adrenergic agonists, the intrarenal effect of With modest doses of norepinephrine, either infused alpha-adrenergic stimulation is best defined by direct i.v. or into the renal artery, mild constriction of the infusion of the agonist into the renal artery. Norepine- afferent arteriole may be counterbalanced by sufficient phrine possesses both alpha- and beta-adrenergic constriction of the efferent arteriole so that glomerular stimulating properties; therefore, the intrarenal alpha- filtration rate is maintained constant although renal adrenergic effect of the substance is best observed in blood flow decreases [12]. The counterpart of this the presence of beta-adrenergic blockade. Since the effect may occur during beta-adrenergic stimulation kidney has been demonstrated to be an effective site of with isoproterenol in which preferential vasodilatation inactivation of catecholamines, including isoproterenol of the efferent arteriole leads to a rise in renal blood [4] and norepinephrine [5], intrarenal effects of these flow as glomerular filtration rate remains constant agents can be produced in the absence of either syste- [6]. mic effects or effects in the contralateral kidney. The effect of alpha-adrenergic stimulation to con- Evidence has been obtained that the kidney possesses strict renal venules is another component of the in- both alpha- and beta-adrenergic receptors. The intra- crease in renal vascular resistance and, in the presence renal infusion of the beta-adrenergic agonist, isoprote- of drug-induced renal vasodilatation, may be primarily renol, has been demonstrated to produce vasodilata- responsible for the observed increase in deep renal tion of the kidney [6]. In quantitative terms this effect venous pressure with a norepinephrine infusion [13]. of isoproterenol appears to be less potent than other In addition to these renal vasoconstrictor effects of renal vasodilators such as acetylcholine [7, 8], brady- alpha-adrenergic stimulation, there have been reports kinin [7, 8] and prostaglandin E1 [9]. In the presence of that aipha-adrenergic stimulation may not produce the beta-adrenergic blocker, propranolol, large doses homogeneous vasoconstriction throughout all of the of isoproterenol can be associated with renal vasocon- nephrons. Using the 85krypton washout method, striction, an alpha-adrenergic effect [6]. Whether Pomeranz, Birtch and Barger [14] suggested that renal either the intrarenal beta- or aipha-adrenergic effect of nerve stimulation induced either by bilateral carotid isoproterenol is of physiological importance remains ligation or splanchnic nerve stimulation decreased to be determined. In this regard, the intrarenal infusion outer cortical and increased medullary blood flow. In of the beta-blocking agent, propranolol, has not been contrast to these results, estimation of renal blood dis- found to produce any detectable unilateral alterations tribution by investigators using radioactive micro- in renal hemodynamics in anesthetized dogs which are spheres has failed to demonstrate
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