bluuebunny/crossref_metadata_2025_split huggingface dataset:
DECREASED NOREPINEPHRINE CONTENT IN THE MEDULLA OBLONGATA IN SEVERELY HYPERTENSIVE RATS
Authors: Takami Takeshi , Ito Hiroyuki , Suzuki Tsuneyuki 
Published: June 2007

SUMMARY1. To clarify possible abnormalities in catecholamines in the medulla oblongata in relation to severe hypertension, the authors measured changes in catecholamine levels in the medulla oblongata of malignant stroke‐prone spontaneously hypertensive rats (M‐SHRSP). Effects of the adrenal medullae and peripheral nerves were ruled out by adrenal demedullation and chemical sym‐pathectomy.2. The level of norepinephrine in the medulla oblongata was significantly lower in untreated M‐SHRSP than in untreated WKY (control) rats at 10 weeks of age. Further, it was significantly lower in treated M‐SHRSP than in the treated WKY group at both 6 and 10 weeks of age. The level of epinephrine in 6 week old treated M‐SHRSP was significantly higher than that in age‐matched treated WKY, but no other differences were observed in terms of epinephrine content. There were no age‐ or treatment‐related differences in dopamine levels in the medulla oblongata.3. Since norepinephrine has an inhibitory effect on blood pressure elevation in the nucleus tractus solitarii (NTS) in the medulla oblongata, the suppression of negative feedback due to a decrease in the activity of inhibitory neurons in the medulla oblongata appears to be involved in the development and progression of severe hypertension in M‐SHRSP.
THE NOVEL MARINE NATURAL PRODUCT PLOCAMADIENE A CAUSES HISTAMINE RELEASE FROM MAST CELLS OF THE GUINEA‐PIG AND RAT IN VITRO
Authors: Thomas Steven G. , Beveridge Andrew A. 
Published: June 2007

SUMMARY1. Plocamadiene A is a polyhalogenated monoterpene, (1R, 2S, 4S, 1′E)‐2‐bromo‐l‐chloro‐4‐(2′‐chloroethenyl)‐I‐methyl‐5‐methylenecyclohexane, isolated from red marine algae of the Plocamium genus.2. This study examined the activity of plocamadiene A on guinea‐pig isolated ileum (GPI) and subsequently on rat isolated peritoneal mast cells.3. Plocamadiene A (1 μg/mL) produced a slow onset, sustained contraction of the GPI. This was insensitive to atropine (1 μmol/ L) and tetrodotoxin (1 μmol/ L), but was significantly reduced by H1‐histamine receptor antagonists including mepyramine (10 nmol/L), chlorcyclizine (10 nmol/L) and diphenhydramine (0.1 μmol/L). The H2‐histamine receptor antagonists cimetidine (0.1 μmol/L) and ranitidine (10 nmol/L) potentiated the response to plocamadiene A (1 μg/mL).4. The amplitude of contraction caused by plocamadiene A (1 μg/mL) gradually decreased when the compound was applied repeatedly to the GPI for 5 min every 10 min for 150 min.5. Contractions to plocamadiene A (1 μg/mL) were reduced to approximately 66% of the time control in ovalbumin‐sensitized GPI challenged with ovalbumin to release endogenous contractile agents.6. Cromolyn (0.1 mmol/ L) inhibited (by 40%) the response in the GPI caused by plocamadiene A (1 μg/mL) as compared with time controls.7. Spectrofluorometric assay suggested that both plocamadiene A (10 μg/mL) and compound 48/80 (10 μg/mL) caused histamine release from rat peritoneal mast cells in vitro. This release of histamine was reduced by cromolyn (100 μg/mL).8. This study concluded that plocamadiene A releases histamine from mast cells of the GPI and peritoneal mast cells in the rat.
RELAXANT EFFECTS OF BRAIN NATRIURETIC PEPTIDE ON GUINEA‐PIG TRACHEAL SMOOTH MUSCLE
Authors: Takagi Kenzo , Araki Nobuyasu 
Published: June 2007

SUMMARY1. The relaxant effects of brain natriuretic peptide (BNP) were investigated on guinea‐pig tracheal smooth muscle.2. Various amounts of BNP (10−9– 10−6 mol/L) showed concentration‐dependent relaxant effects on resting tone, leukotriene D4 (LTD4; 10−8 mol/L) and endothelin‐1 (ET‐1; 10−8 mol/L) induced contraction of tracheal smooth muscle with EC50 values of 3.1± 0.7 ± 10−8, 3.9 ± 1.0 ± 10−8 and 3.5 ± 1.0 ± 10−8 mol/L, respectively.3. BNP increased tissue cyclic GMP levels in tracheal smooth muscle concentration dependently (187 ± 26 fmol/mg protein in control, 334 ± 77 fmol/mg protein at 10−8 mol/L, 680 ± 54 fmol/mg protein at 10−7 mol/L, 2162 ± 133 fmol/mg protein at 10−6 mol/L).4. With the addition of BNP, tissue cyclic GMP levels reached a maximum at 1–3 min. The relaxation of tracheal smooth muscle began at 1 min and reached a maximum level at 5 min after the superfusion of BNP (10−6 mol/L). The elevation of cyclic GMP preceded the relaxation of tracheal smooth muscle.5. These results suggest that BNP may have a potent relaxant effect on tracheal smooth muscle and this effect may be mediated by cyclic GMP level.
ANGIOTENSIN CONVERTING ENZYME INHIBITOR, CAPTOPRIL, INHIBITS CARDIAC HYPERTROPHY WITHOUT CHANGING COLLAGEN TYPES AND CONCENTRATION IN SPONTANEOUSLY HYPERTENSIVE RATS
Authors: Kuzuo Hiroshi , Honda Masaaki , Ishinaga Yuji , Morioka Shigefumi , Tanaka Koichi , Kuramochi Takehiko , Mansoor Abdul M. , Yamori Yukio , Moriyama Katsutoshi 
Published: June 2007

SUMMARY1. The effects of the ACE inhibitor, captopril, on collagen metabolism in spontaneously hypertensive rats (SHR) with cardiac hypertrophy was examined. Captopril (100 mg/kg per day) was administered in drinking water to 20 week old male SHR for 12 weeks. Collagen concentration was calculated from hydroxyproline content, and relative proportions of types I, III and V collagen were determined by non‐interrupted SDS‐polyacrylamide gel electrophoresis (SDS‐PAGE). These parameters were examined in age and sex matched Wistar‐Kyoto (WKY) rats, as well as in non‐treated SHR, and compared with those of captopril‐treated SHR.2. Captopril significantly reduced both blood pressure (191 ± 12.1 vs 146 ± 11.2 mmHg, P < 0.01), and the ratio of left ventricular (LV) weight to bodyweight (BW; 2.38 ± 0.17 vs 2.05 ± 0.12 mg/g, P < 0.01). There were no significant differences in collagen concentration among WKY rats, captopril‐treated SHR and non‐treated 32 week old SHR. However, total collagen content in captopril‐treated SHR reduced significantly compared with non‐treated 32 week old SHR (16.8 ± 2.0 vs 21.3 ± 0.8 mg, P < 0.01). The relative proportion of type V collagen was significantly higher in both captopril‐treated (58.6 ± 3.4 vs 46.8 ± 1.3%, P < 0.01) and non‐treated 32 week old SHR (59.9 ± 3.1 vs 46.8 ± 1.3%, P < 0.01) compared with WKY rats. However, there were no significant differences between captopril‐treated SHR and non‐treated 32 week old SHR.3. The data from this study showed that captopril reduced cardiac hypertrophy, as reported previously, but did not change collagen types and concentration of the hypertrophied myocardium in SHR.
OXYGEN‐HAEMOGLOBIN DISSOCIATION CURVE IN HYPOXIC RATS OF FIRST OR SECOND GENERATION
Authors: Quatrini U. , Licciardi A. , Morici G. 
Published: June 2007

SUMMARY1. Albino Wistar rats were raised in a normobaric hypoxic environment (10% O2 in N2). Two generations of hypoxic rats were observed for changes in their haemoglobin‐oxygen (Hb‐O2) dissociation curves (ODC), 2,3‐diphosphoglycerate (2,3‐DPG), haemoglobin (Hb), and Hill coefficients at P50 (n50). The first generation were called (H1) and the second generation (H2). The control group (N) had a normoxic environment.2. Thirty‐five rats (13 N rats, 12 H1 rats and 10 H2 rats) were used. The 2,3‐DPG was significantly higher in both hypoxic groups when compared with N rats (2.02 ± 0.51 mmol/L) but 2,3‐DPG of H2 rats was significantly lower than that of H1 rats (H1 = 3.48±0.58 mmol/L and H2 = 2.76±0.54 mmol/L). The haemoglobin values were N = 2.00±0.26, H1 = 2.65±0.32and H2 = 2.36±0.30 mmol/L, respectively.3. We observed considerable differences in Hb‐O2 affinity between the three groups of rats. In standard conditions (pH = 7.400; pCO2= 40 mmHg at 37°C) the H1 rats showed a significantly decreased Hb‐O2 affinity (P50, st= 37.0 ± 1.3 mmHg) when compared with both H2 and N rats; the H2 rats showed a significantly increased Hb‐02 affinity (P50, st 1 31.1 ± 1.5 mmHg) when compared with controls N (P50, st= 34.7±2.1 mmHg). There were no significant differences in n50 values: N = 2.88 ± 0.44; H1 = 2.88 ± 0.77; and H2 = 2.94 ± 0.67.4. Therefore, the H1 rats’ ODC was located well to the right of that of N rats; and the H2 rats had an ODC located to the left when compared with both HI and N rats. It is likely that in H2 rats the adaptive processes to the new environment are more advanced; therefore, the magnitude of the compensatory mechanisms required to maintain a sufficient tissue oxygenation may be reduced.
TRANSMEMBRANEIN VITRO AND IN VIVO SODIUM‐LITHIUM COUNTERTRANSPORT IN NEW ZEALAND MAORI
Authors: Maling T. J. B. , van Wissen K. , Siebers R. W. L. 
Published: June 2007

SUMMARY1. Erythrocytic sodium‐lithium (Na‐Li) countertransport (CT) was measured in normotensive Maori and non‐Maori by in vitro and in vivo methods to determine its relationship to erythrocytic hypernatraemia previously identified in Maori.2. In vivo and in vitro CT rates were correlated within race and were similar between races. Countertransport rate was correlated with erythrocytic sodium concentration only in Maori.3. The findings suggest the possibility of a genetically determined alteration in CT stoichiometry in Maori.
EVIDENCE THAT PRIMARY ALDOSTERONISM MAY NOT BE UNCOMMON: 12% INCIDENCE AMONG ANTIHYPERTENSIVE DRUG TRIAL VOLUNTEERS
Authors: Gordon Richard D. , Ziesak Mary D. , Tunny Terry J. , Stowasser Michael , Klemm Shelley A. 
Published: June 2007

SUMMARY1. Six (12%) out of 52 respondents to newspaper advertisements for antihypertensive drug trials had elevated aldosterone to renin ratio, confirmed by repeated measurement.2. Failure to suppress aldosterone with fludrocortisone acetate administration and oral salt loading confirmed the presence of primary aldosteronism in all six patients.3. Two of the six patients have already had aldosterone‐producing adenomas removed, one has commenced spironolactone, and one has an adrenal mass on computerized tomography but investigation is incomplete.4. None of the six patients with primary aldosteronism had unprovoked hypokalaemia.5. Plasma aldosterone levels did not distinguish those patients with subsequently proven primary aldosteronism from the others. Plasma renin activity (PRA) was a better discriminator, but not as good as the aldosterone to renin ratio.6. The incidence of primary aldosteronism is probably much higher than the 1% currently quoted in texts, with earlier, normokalaemic forms accounting for the majority of cases.
HUMORAL DETERMINANTS OF Na+ EXCRETION AFTER INTRAVENOUS NaCl LOADING IN NORMAL VOLUNTEERS
Authors: Stokes G. S. , Johnston H. J. , Monaghan J. C. 
Published: June 2007

SUMMARY1. Twelve healthy volunteers maintained on a 100 mmol/day Na+ diet, were given an intravenous infusion of 2L saline (0.9%) between 10.00 and 13.00h on 2 study days at least 1 week apart. Urine collections (90 min) were made from 08.30 to 16.00 h. Either carbidopa 100 mg or indomethacin 50 mg was given orally at 07.45 h on one study day and placebo was given on the other (in random order).2. On the placebo day, saline infusion caused significant decreases in plasma albumin concentration, plasma renin activity (PRA), plasma aldosterone concentration and urinary aldosterone excretion, with 2 to 3‐fold increases in plasma atrial natriuretic peptide (ANP) concentration and urinary dopamine: noradrenaline ratio (DA:NA), whereas mean urinary kallikrein and prostaglandin E2 (PGEI) excretion rates were unchanged. Carbidopa decreased urinary DA:NA and indomethacin decreased urinary PGE2 excretion, compared with the placebo day. Excretion of sodium (Na+) decreased below baseline in two out of six carbidopa‐treated subjects and in three out of six indomethacin‐treated subjects, but showed little or no change in the remainder.3. These preliminary observations suggest that some subjects in the early phase of natriuresis after an intravenous Na+ load can be identified as having prostaglandin‐dependent or dopamine‐dependent mechanisms for Na+ excretion.
DISSOCIATION OF BLOOD PRESSURE AND ALBUMINURIA IN NORMAL SUBJECTS INFUSED WITH ANGIOTENSIN II AND NORADRENALINE
Authors: Cohen Neale , Phillips Paddy , Gilbert Richard , Jerums George 
Published: June 2007

SUMMARY1. Albuminuria is a predictor of diabetic renal disease and atherosclerosis. Changes in blood pressure (BP) may influence albuminuria.2. The effect of acute BP elevation on albumin excretion rates (AER) using noradrenaline (NA) and angiotensin II (AII) infusions in six normal subjects was examined.3. The average rise in BP during a 120 min infusion was 23 mmHg for AII and 16 mmHg for NA.4. There was a marked dissociation between AER and BP levels in both AII and NA infusions.5. Previously described correlations between BP and AER in ambulatory BP studies may be explained by other factors such as exercise and postural changes.
ANGIOTENSIN‐CONVERTING ENZYME AND REGULATION OF BLOOD PRESSURE IN A LARGE AUSTRALIAN FAMILY
Authors: Summers K. M. , West J. A. , Huggard P. R. , West M. J. 
Published: June 2007

SUMMARY1. Animal studies have implicated the angiotensin‐converting enzyme (ACE) gene as an inherited risk factor contributing towards elevation of blood pressure.2. A polymorphism of the ACE gene, involving the presence or absence of a 287 base pair (bp) segment within the gene region, was assessed for association with high blood pressure in a large, multigeneration Australian family. The association of these alleles with hypertension in unrelated individuals was also examined.3. There was no evidence to link the ACE gene and high blood pressure in the large family. Similarly, there was no significant association between this gene and high blood pressure in the population tested. As has been reported previously, plasma levels of the enzyme were associated with genotype. These results suggest that this gene is unlikely to be a major risk factor for hypertension in this group.
AGE‐DEPENDENT ALTERATIONS IN VASCULAR SMOOTH MUSCLE CELL RESPONSIVENESS TO PLATELET‐DERIVED GROWTH FACTOR IN GENETIC HYPERTENSION
Authors: Saltis John , Agrotis Alex , Bobik Alex 
Published: June 2007

SUMMARY1. This study examined and compared the growth characteristics of vascular smooth muscle cells (VSMC) isolated from 4 and 12 week old spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) rats following stimulation with platelet‐derived growth factor‐BB (PDGF‐BB).2. Vascular smooth muscle cells from 4 week old SHR proliferated at a slower rate than VSMC isolated from 12 week old SHR (1.08±0.06/day vs 1.89±0.13/day respectively, P < 0.05). In contrast, there was no difference in the proliferation of VSMC from 4 and 12 week WKY rats (0.62±0.06/day vs 0.82±0.13/day, respectively, P>0.05).3. The cell density at which VSMC from 4 and 12 week old SHR become refractory to the mitogenic effects of PDGF‐BB was similar and approximately two‐fold greater than VSMC from age‐matched WKY rats.4. This study concludes that there is an age‐dependent, differential and specific upregulation of growth rate mechanisms in VSMC from SHR which enhance proliferation in response to PDGF‐BB.
VASCULAR SMOOTH MUSCLE CELL PROLIFERATION IN SHR AND WKY RATS: EVIDENCE FOR SPECIFIC DIFFERENCES IN GROWTH INHIBITORY REGULATORY MECHANISMS
Authors: Agrotis Alex , Bray Paula J. , Saltis John , Bobik Alex 
Published: June 2007

SUMMARY1. This study examined and compared the actions of transforming growth factor‐β1 (TGF‐β1), heparin, dexamethasone and interferon‐γ on platelet‐derived growth factor‐BB (PDGF‐BB)‐stimulated proliferation of vascular smooth muscle cells (VSMC) from normotensive, Wistar‐Kyoto (WKY) rats and spontaneously hypertensive rats (SHR).2. Heparin, dexamethasone and interferon‐γ all inhibited VSMC proliferation stimulated by PDGF‐BB in both SHR and WKY rats. There was no difference (P>0.05) in their inhibitory effects, which varied between 40 and 85% for the different agents.3. Similarly, TGF‐β1 inhibited PDGF‐BB‐stimulated VSMC proliferation in WKY rats by approximately 50%. In contrast, TGF‐β1 potentiated growth factor action on cell proliferation in the SHR by approximately 40%.4. Specific TGF‐β1‐stimulated regulatory mechanisms involved in the inhibition of proliferation are absent in SHR and this defect may contribute to the vascular hypertrophy which is apparent in genetic hypertension.
ACCURATE DETERMINATION OF THE SIZE OF THE FIRST INTRON DELETION IN THE RENIN GENE OF SHR FROM AN AUSTRALIAN COLONY
Authors: Wang D. Z‐M. , Gregorio‐King C. , Aykut L. , Wilks A. , Morgan T. O. , Nicolantonio R. Di 
Published: June 2007

SUMMARY1. It has been reported that the first intron of the renin gene of the spontaneously hypertensive rat (SHR) is shorter than that of the Wistar‐Kyoto (WKY) rat, suggesting a role for this difference in the development of hypertension.2. The genealogy of some Australian SHR colonies has raised doubts about its similarity to the Japanese, American and European colonies.3. The polymerase chain reaction (PCR) technique has been used with primers identical to the flanking region of the first intron of the renin gene to determine its length in SHR, WKY and Sprague‐Dawley (SD) from an Australian colony.4. The size of the first intron of the renin gene in SHR, WKY and SD was found to be approximately 3870, 4550 and 5000 base pairs, respectively, results which agree with those previously published.5. It was concluded that the first intron deletion, and its size, has been conserved in an Australian SHR colony.
ABNORMALITY OF THE GLOMERULAR ANGIOTENSIN II RECEPTOR IN EXPERIMENTAL DIABETIC NEPHROPATHY
Authors: Makarious M. , Duggan K. , Charlesworth J. A. , Macdonald G. J. 
Published: June 2007

SUMMARY1. The combined effect of diabetes and hypertension on the plasma angiotensin II (AII)/glomerular AII receptor (AII‐R) relationship in streptozotocin‐induced diabetes was investigated as well as the effect of glycaemic control on this relationship.2. Diabetes was induced in spontaneously hypertensive rats (SHR) and Wistar‐Kyoto (WKY) rats with streptozotocin 60 mg/kg and blood sugars maintained between 18–21 mmol/L (uncontrolled diabetes) and 4–8 mmol/L (controlled diabetes). Rats were killed on days 1 and 7. Angiotensin II receptor was estimated by saturation analysis and plasma AII by radio‐immunoassay.3. Angiotensin II receptors were significantly higher in non‐diabetic SHR than WKY rats (708 ± 62 and 388 ± 36 fmol/mg protein, respectively, P = 0.0008). Plasma AII were comparable in both groups (47 ± 2.7, 38 ± 3.5 pg/mL, respectively) and a significant inverse relationship between AII/AII‐R was observed (WKY P = 0.02 and SHR P = 0.004).4. On day 7, plasma AII and AII‐R levels in diabetic groups were comparable with those of their non‐diabetic controls. Diabetic WKY rats maintained an inverse correlation between AII and AII‐R (controlled P= 0.04 and uncontrolled P= 0.015), but this did not occur in the SHR.5. Absence of receptor response to varying ligand concentrations in the diabetic SHR may contribute to the development of nephropathy. Glycaemic control does not appear to reverse this abnormality in the SHR, so that co‐existent hypertension may have a more direct influence on renal function.
NEUROGENIC VASODILATATION IN ISOLATED PERFUSED SEGMENTS OF RABBIT JEJUNAL ARTERY
Authors: La M. , Rand M. J. 
Published: June 2007

SUMMARY1. Vasodilator responses were elicited by field stimulation in isolated perfused segments of rabbit jejunal arteries when noradrenergic and purinergic vasoconstrictor responses had been abolished and the smooth muscle partly contracted by endothelin.2. The stimulation‐induced vasodilator responses were abolished by tetrodotoxin, but were not affected by atropine, propranolol or a nitric oxide synthase inhibitor.3. After recovery from the vasodilator action of capsaicin, the stimulation‐induced vasodilator responses were greatly reduced or abolished.4. A competitive antagonist of calcitonin gene‐related peptide (CGRP) blocked vasodilator responses elicited by field stimulation and exogenously administered CGRP.5. The findings indicated that the mediator of the stimulation‐induced vasodilator responses is neurogenic in origin, and it is not acetylcholine, noradrenaline acting on P‐adrenoceptors, nitric oxide or an endothelium‐dependent vasodilator. It appears to be CGRP, presumably released from sensory nerves in the periarterial plexus.
EFFECTS OF CILAZAPRIL ON THE STRUCTURE OF MESENTERIC RESISTANCE ARTERIES OF NEW ZEALAND GENETICALLY HYPERTENSIVE AND NORMOTENSIVE CONTROL RATS
Authors: Ledingham J. M. , Phelan E. L. , Millar J. A. 
Published: June 2007

SUMMARY1. New Zealand genetically hypertensive (GH) rats and their normotensive controls (N) rats between the ages of 10 and 16 weeks were treated with cilazapril in the diet for 6 weeks.2. Systolic blood pressure (SBP; tail‐cuff) was measured weekly and intra‐arterial blood pressure (BP) was measured at the end of the treatment period.3. The effect of cilazapril on the structure of mesenteric resistance arteries (MRA) was evaluated by both stereological and myographic techniques.4. Cilazapril lowered SBP significantly throughout the treatment period (16 weeks; GH with cilazapril 135 ± 5 vs GH 216 ± 9 mmHg, P < 0.001; N cilazapril 91 ± 6 vs N 137 ± 3 mmHg, P < 0.001); intra‐arterial BP was also significantly lowered.5. Bodyweight (BW) of treated GH rats was significantly lower than that of untreated GH at 16 weeks (P < 0.01; t‐test); however, the weight of treated N rats was not significantly affected. Ventricular mass was reduced by cilazapril in GH and N rats (GH 259 ± 10 vs 306 ± 11, P < 0.001; N 171 ± 3 vs 195 ± 4 mg/100g BW, P < 0.001).6. Lumen volume of MRA was not significantly affected by cilazapril in either strain; media volume was reduced by 14% in both strains and the media/lumen ratio was significantly reduced. Vascular smooth muscle cell density significantly increased in cilazapril‐treated GH rats.
THE DOPAMINE PRODRUG, GLUDOPA, DECREASES BOTH RENAL AND EXTRARENAL NORADRENALINE SPILLOVER IN CONSCIOUS RABBITS
Authors: Wang Zhi‐Qin , Shimizu Kazumasa , Way Diana , Secombe John , McGrath Barry P. 
Published: June 2007

SUMMARY1. Renal and total noradrenaline (NA) spillover rates were examined under control conditions and during graded infusions of gludopa (γ‐l‐glutamyl‐l‐dopa) in conscious rabbits.2. Gludopa infusion at 25 and 100 μg/kg per min did not alter mean arterial pressure (MAP) and heart rate (HR), but had significant dose‐related effects on the renal dopamine (DA) system. At the high dose there were pronounced increases in urinary DA excretion (>6000‐fold) and renal DA content (> 100‐fold); renal NA content doubled.3. Renal venous DA increased after gludopa infusion, but arterial plasma DA concentrations were not significantly changed. Mean arterial plasma gludopa and l‐dopa concentrations reached 890, 3190 ng/mL and 3, 10 ng/mL at low and high doses, respectively.4. Gludopa resulted in a pronounced dose‐dependent fall in renal NA spillover, which at 100 μg/kg per min accounted for almost half of the reduction in overall NA spillover rate.5. The significant falls in renal and extrarenal NA spillover rate during gludopa infusion are consistent with suppression of renal and overall sympathetic activity. Gludopa‐induced inhibition of renal NA spillover is likely to be due to the actions of DA generated in the kidney on presynaptic DA‐2 and α‐2 receptors. A central sympathoinhibitory mechanism may explain the reduced total NA spillover.