Renal modulation of urinary catecholamine excretion during volume expansion in the dog.

Abstract

The role of the kidney in handling the biologically acthe, nnconjugated endogenous catecholamines epinephrine (E), noreptnephrine (NE), dopamlne (DA), and the O-methylated metabolite of NE, normetanephrine (NM), was studied in the anesthetized dog before and after Toloroe expansion with iaotonk saline by measuring renal arterial deUrery, urinary excretion rate, and renal Tenons return of these materials. Net turnover in the renal metabolic compartment was estimated by comparing arterial delivery to urinary excretion and renal Tenons return. The kidney extracted E and produced NE, DA, and NM before and after Tolume expansion. After Tolume expansion a significant decrease in the extraction of E, an Increase in the production of DA, and no change in the production of NE or NM was seen. Clearance of catecbolamlnes and NM through the kidneys appeared to increase with Tolume expansion. The clearance of DA exceeded the clearance of creatinine (Cr) after volume expansion, while the clearance of NM exceeded that of Cr before and after volume expansion, indicating that urinary DA and NM are derived, in part, from processes other than glomerular filtration. These observations suggest an important role for the kidney in the modulation of the excretion of catecholamines and metabolites. This role must be considered before the urinary excretion rate of N, E, DA, and NM can be related to generalized sympathetic function. The observed increases in renal DA production after saline infusion suggest a possible natriuretic function of intrarenal DA. (Hypertension 2: 383-389, 1980)

Is Dopamine a Physiological Natriuretic Hormone in the Dog?

“…During the hydropenic control period, the arterial concentration of dopamine and noradrendine ( Table 1) are in agreement with previous reports [6,18,19], bearing in mind that there is a large variation between animals [22] ; dopamine sulphate concentration was slightly higher than the results of Unger et al [19], but the biochemical techniques were not identical, making any comparison very difficult, especially for noradrenaline sulphate. As far as urinary excretion of free catecholamines is concerned, our data are in close agreement with those of Ball et al, which showed a urinary excretion of 3.2 ng/min for dopamine, and 7.2 ng/min for noradrenaline [19].…”

“…Catecholamines were measured as free and sulphate conjugates compounds by radioenzymatic methods, described by Johnson and colleagues [15,16] ; catechol-0-methyltranferase was prepared by either the method of Axelrod & Tomchick [17] or that of Boren et al [6]. All samples for a given animal were analysed at the same time by the same technical procedure, minimizing the effect of the interassay variation; with each method, a portion of pooled plasma was run as a quality control, giving an interassay coefficient of variation of 9.2% for dopamine, and 11.8% for noradrenaline (n = 36).…”

Central nervous system nitric oxide synthase activity regulates insulin secretion and insulin action.

“…Blood drawn for analysis of catecholamine levels was immediately transferred to heparin-treated tubes set on ice and spun for 1 min in a 0 Њ C centrifuge. The supernatant was pipetted into precooled capped tubes and stored at Ϫ 86 Њ C. All samples were analyzed within 3 wk of collection as previously described (19).…”

Metoclopramide Does Not Affect Renal Function and Atrial Natriuretic Peptide Release in Response to Acute Saline Loading in Conscious Rats

“…Acute ECFV expan sion with i.v. saline infusion, a condition in which the renal sympathetic tone is consider ably suppressed [22], was shown to be accom panied by increased urinary DA excretion [5][6][7][8][9][10], As the plasma levels of DA remain unde tectable [22] or decrease [10] under these con ditions, the production of endogenous DA within the kidney must have increased [23]. In PCT cells, L-amino acid decarboxylase converts L-DOPA to DA [24,25], This locally formed DA is thought to inhibit Na-KATPase activity [26,27] in PCT cells [28,29] by involving DA-1 and/or DA-2 receptors [30] and to participate in proximal tubular fluid and Na absorption [31].…”

“…a decrease in colloid oncotic and increase in hydrostatic pressures within peritubular cap illaries [2,3], as well as to the release of natri uretic substances [4], Exogenous dopamine (DA) raises renal blood flow and GFR as well as renal Na excre tion. Since the natriuresis during ECFV ex pansion is accompanied by a rise in urinary DA excretion [5][6][7][8][9], it is argued that renal DA acts as a natriuretic factor [10], possibly in a paracrine fashion [11], In fact, Pelayo et al [12] showed in the rat that m-flupenthixol, a predominant DA-1 receptor antagonist, blunts the natriuresis of acute Ringer infu sion, and Krishna et al [13] demonstrated in man that metoclopramide (MCP), a predomi nant DA-2 receptor antagonist, attenuates the natriuresis that follows head-out water im mersion. Moreover, it was claimed that in the rat DA mediates the renal effects of atrial natriuretic peptide (ANP) [14] released from the heart atria in response to an acute fluid load [15], Both, DA-1 and DA-2 receptor subtypes have been identified in the kidney [16,17] and may thus play a role in renal hemody namic and functional adaptations to changes in Na balance.…”