Effect of dietary sodium intake on the pressor reactivity to angiotensin II in rats with experimental cirrhosis of the liver

1989 ◽  
Vol 67 (12) ◽  
pp. 1506-1511 ◽  
Author(s):  
L. M. Villamediana ◽  
Angel L. García-Villalón ◽  
Carlos Caramelo ◽  
José M. López-Novoa
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Vascular Reactivity ◽  
Sodium Intake ◽  
Pressor Response ◽  
Experimental Cirrhosis ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet

The present experiments were designed to evaluate vascular reactivity to angiotensin II in rats with experimental cirrhosis of the liver (induced with CCl4 and phenobarbital) before ascites appearance. The systemic pressor response to angiotensin II in conscious animals and the contractile effect of angiotensin II in isolated femoral arteries were studied. In addition, the effect of high sodium intake on these parameters was also analyzed. Both renin and aldosterone plasma concentrations were similar in control and cirrhotic rats on the normal or on the high sodium diet. Basal mean arterial pressure was higher in control rats than in cirrhotic rats on the normal sodium (116 ± 4 vs. 101 ± 4 mmHg (1 mmHg = 133.3 Pa),p < 0.05) or on the high sodium diet (118 ± 7 vs. 98 ± 6 mmHg). No differences in plasma renin activity or plasma aldosterone were found between control and cirrhotic rats. Upon injection of angiotensin II, control rats show a dose-dependent increase in mean arterial pressure which is higher in high sodium than in normal sodium rats. Cirrhotic rats showed a lower hypertensive response to angiotensin II than their corresponding control rats. In addition, no difference between pressor responses to angiotensin II was observed when normal sodium and high sodium cirrhotic rats were compared. On application of angiotensin II, femoral arteries of control and cirrhotic rats exhibited a dose-dependent contraction. However, maximal contraction was higher in high sodium control rats (145 ± 12 mg) than in normal sodium control rats (99 ± 6 mg, p < 0.05). No significant differences between control and cirrhotic rats on either sodium diet were observed. In conclusion, cirrhotic, nonascitic rats showed an impaired pressor response to angiotensin II that is more marked after a high sodium diet. These differences are not due to changes in the contractility of peripheral arteries to angiotensin II.Key words: angiotensin II, liver cirrhosis, sodium intake, mean arterial pressure, vascular reactivity.

Comparison of systemic and direct intrarenal angiotensin II blockade on sodium excretion in rats

1995 ◽  
Vol 269 (1) ◽  
pp. F40-F46 ◽  
Author(s):  
Y. Peng ◽  
F. G. Knox
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Sodium Excretion ◽  
Systemic Effects ◽  
Ang Ii ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet ◽  
Interstitial Infusion

To dissociate the renal effects from the systemic effects of angiotensin II blockade, the present study was designed to determine the effects of systemic and renal interstitial infusion of the specific angiotensin II (ANG II) receptor antagonist, losartan, on blood pressure and sodium excretion in rats fed a low-, normal, or high-sodium diet. Fractional sodium excretion (FENa) and mean arterial pressure (MAP) were measured in rats before and during systemic infusion of losartan (10 mg/kg) or renal interstitial infusion of losartan (3 mg/kg) by means of a chronically implanted matrix. In rats fed a low- or normal sodium diet, systemic infusion of losartan markedly decreased MAP (delta -21 +/- 2, delta -10 +/- 2 mmHg, respectively; P < 0.05) with an accompanying fall in FENa (delta -0.10 +/- 0.05, delta -0.91 +/- 0.40%, respectively; P < 0.05). In contrast, preferential blockade of renal ANG II with renal interstitial losartan infusion resulted in an increase in FENa (delta 0.13 +/- 0.04, delta 0.95 +/- 0.45%, respectively; P < 0.05) and no significant change in MAP. In rats fed a high-sodium diet, both systemic and renal interstitial infusion of losartan increased FENa (delta 1.90 +/- 0.26, delta 1.40 +/- 0.56%, respectively; P < 0.05). Although systemic infusion of losartan decreased MAP (delta -4.4 +/- 0.6 mmHg, P < 0.05) in rats fed a high-sodium diet, the reduction in MAP was much less than that in rats fed a low- and normal sodium diet.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Sodium Intake and Heart Failure

2020 ◽  
Vol 21 (24) ◽  
pp. 9474
Author(s):  
Yash Patel ◽  
Jacob Joseph
Keyword(s):  
Heart Failure ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Mechanical Performance ◽  
Sodium Intake ◽  
Heart Association ◽  
Dietary Practices ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet

Sodium is an essential mineral and nutrient used in dietary practices across the world and is important to maintain proper blood volume and blood pressure. A high sodium diet is associated with increased expression of β—myosin heavy chain, decreased expression of α/β—myosin heavy chain, increased myocyte enhancer factor 2/nuclear factor of activated T cell transcriptional activity, and increased salt-inducible kinase 1 expression, which leads to alteration in myocardial mechanical performance. A high sodium diet is also associated with alterations in various proteins responsible for calcium homeostasis and myocardial contractility. Excessive sodium intake is associated with the development of a variety of comorbidities including hypertension, chronic kidney disease, stroke, and cardiovascular diseases. While the American College of Cardiology/American Heart Association/Heart Failure Society of America guidelines recommend limiting sodium intake to both prevent and manage heart failure, the evidence behind such recommendations is unclear. Our review article highlights evidence and underlying mechanisms favoring and contradicting limiting sodium intake in heart failure.

The Influence of Sodium Intake on the Pressor Response to Angiotensin II in the Unanaesthetized Rat

1976 ◽  
Vol 50 (4) ◽  
pp. 285-291
Author(s):  
Barbara L. Slack ◽  
J. M. Ledingham
Keyword(s):  
Angiotensin Ii ◽  
Dose Response ◽  
Response Curve ◽  
Dose Response Curve ◽  
Response Curves ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
High Sodium Diet

1. Dose—response curves for the pressor activity of angiotensin II have been determined in unanaesthetized rats receiving diets containing 2·5% (w/w) or 0·007% (w/w) sodium; the different diets were administered in various sequences. 2. In comparison with those from rats receiving a low sodium diet, the dose—response curves were displaced to the left on the high sodium diet, indicating a greater response to angiotensin, and this displacement persisted for a period of approximately 7 days after the diet was changed from high to low sodium. The dose—response curve subsequently shifted to the right when the low sodium diet was maintained for longer. 3. There was a negative correlation between the slope of the dose—response curve and the basal blood pressure in all groups; the correlation was significant in three out of the five different treatment groups. 4. Basal blood pressures were significantly raised in rats on the high sodium diet for 7 days. 5. A number of possible mechanisms have been considered to explain both the parallel shift of the dose—response curve and alteration in its slope. It is concluded that the observed findings are compatible with an action of sodium-loading on the sensitivity of the smooth muscle cell to angiotensin, on the resting of the renin—angiotensin system, on the rate of in-activation of angiotensin and on a change in initial length of the muscle fibre.

Cardiovascular responses to intrathecal vasopressin in conscious and anesthesized rats

1989 ◽  
Vol 256 (1) ◽  
pp. R193-R200 ◽  
Author(s):  
A. Martinez-Arizala ◽  
J. W. Holaday ◽  
J. B. Long
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressor Response ◽  
Cardiovascular Responses ◽  
Intrathecal Administration ◽  
Motor Dysfunction ◽  
Sprague Dawley ◽  
Cardiovascular Changes ◽  
Conscious Rats

Increases in mean arterial pressure and heart rate have been documented after the intrathecal administration of [Arg8]vasopressin (AVP) in rats. Prior studies in our laboratories with conscious rats indicated that these cardiovascular changes were associated with a marked hindlimb sensorimotor dysfunction. In this study, which represents the first systematic comparison of the effects of intrathecal AVP in conscious and anesthesized rats, we demonstrate that in conscious male Sprague-Dawley rats 1) the motor dysfunction induced by intrathecal AVP is accompanied by a rise in mean arterial pressure that is significantly greater than that produced by an equal intravenous dose of AVP, and 2) both paralytic and pressor effects of intrathecal but not intravenous AVP are blocked by the intrathecal administration of the V1-receptor antagonist d(CH2)5[Tyr(Me)2]AVP (V1-ANT) but are not blocked by intravenous phenoxybenzamine, hexamethonium, or [Sar1, Thr8]angiotensin II, an angiotensin II antagonist. In contrast, in anesthesized rats the arterial pressor response to intrathecal AVP was blocked by intrathecal V1-ANT, intravenous hexamethonium, and intravenous phenoxybenzamine. Furthermore, conscious but not anesthesized rats exhibited a tachyphylaxis to intrathecal AVP. These results indicate that intrathecal AVP produces both the cardiovascular changes and the sensorimotor deficits through interactions with centrally located V1-receptors. In addition, sympathetic catecholaminergic mechanisms mediate the rise in mean arterial pressure produced by intrathecal AVP in anesthesized rats, but they do not in conscious rats.

scholarly journals Dietary sodium modulates the interaction between efferent and afferent renal nerve activity by altering activation of α2-adrenoceptors on renal sensory nerves

2011 ◽  
Vol 300 (2) ◽  
pp. R298-R310 ◽  
Author(s):  
Ulla C. Kopp ◽  
Michael Z. Cicha ◽  
Lori A. Smith ◽  
Saku Ruohonen ◽  
Mika Scheinin ◽  
...  
Keyword(s):  
Substance P ◽  
Sodium Intake ◽  
Sensory Nerves ◽  
Nerve Activity ◽  
Renal Nerve ◽  
High Sodium ◽  
Sodium Diet ◽  
Low Sodium ◽  
Renal Nerve Activity ◽  
High Sodium Diet

Activation of efferent renal sympathetic nerve activity (ERSNA) increases afferent renal nerve activity (ARNA), which then reflexively decreases ERSNA via activation of the renorenal reflexes to maintain low ERSNA. The ERSNA-ARNA interaction is mediated by norepinephrine (NE) that increases and decreases ARNA by activation of renal α1-and α2-adrenoceptors (AR), respectively. The ERSNA-induced increases in ARNA are suppressed during a low-sodium (2,470 ± 770% s) and enhanced during a high-sodium diet (5,670 ± 1,260% s). We examined the role of α2-AR in modulating the responsiveness of renal sensory nerves during low- and high-sodium diets. Immunohistochemical analysis suggested the presence of α2A-AR and α2C-AR subtypes on renal sensory nerves. During the low-sodium diet, renal pelvic administration of the α2-AR antagonist rauwolscine or the AT1 receptor antagonist losartan alone failed to alter the ARNA responses to reflex increases in ERSNA. Likewise, renal pelvic release of substance P produced by 250 pM NE (from 8.0 ± 1.3 to 8.5 ± 1.6 pg/min) was not affected by rauwolscine or losartan alone. However, rauwolscine+losartan enhanced the ARNA responses to reflex increases in ERSNA (4,680 ± 1,240%·s), and renal pelvic release of substance P by 250 pM NE, from 8.3 ± 0.6 to 14.2 ± 0.8 pg/min. During a high-sodium diet, rauwolscine had no effect on the ARNA response to reflex increases in ERSNA or renal pelvic release of substance P produced by NE. Losartan was not examined because of low endogenous ANG II levels in renal pelvic tissue during a high-sodium diet. Increased activation of α2-AR contributes to the reduced interaction between ERSNA and ARNA during low-sodium intake, whereas no/minimal activation of α2-AR contributes to the enhanced ERSNA-ARNA interaction under conditions of high sodium intake.

scholarly journals Angiotensin II Sensitivity Is Associated With the Angiotensin II Type 1 Receptor A1166C Polymorphism in Essential Hypertensives on a High Sodium Diet

Hypertension ◽  
2000 ◽  
Vol 36 (3) ◽  
pp. 411-416 ◽  
Author(s):  
Wilko Spiering ◽  
Abraham A. Kroon ◽  
Monique M. J. J. Fuss-Lejeune ◽  
Mat J. A. P. Daemen ◽  
Peter W. de Leeuw
Keyword(s):  
Angiotensin Ii ◽  
High Sodium ◽  
Sodium Diet ◽  
A1166c Polymorphism ◽  
High Sodium Diet

Effect of endogenous angiotensin II on renal nerve activity and its arterial baroreflex regulation

1996 ◽  
Vol 271 (2) ◽  
pp. R361-R367 ◽  
Author(s):  
G. F. DiBona ◽  
S. Y. Jones ◽  
L. L. Sawin
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Renal Sympathetic Nerve Activity ◽  
High Sodium ◽  
Sodium Diet ◽  
Renal Sympathetic Nerve ◽  
High Sodium Diet ◽  
Renal Sympathetic

To determine the effects of physiological alterations in endogenous angiotensin II (ANG II) activity on basal renal sympathetic nerve activity and its arterial baroreflex regulation, the effect of ANG II receptor (AT1) blockade with losartan was examined in conscious rats consuming low, normal, or high sodium diet that were instrumented for the simultaneous measurement of arterial pressure and renal sympathetic nerve activity. Intravenous losartan decreased arterial pressure in low (-27 +/- 4 mmHg) and normal (-15 +/- 2 mmHg) but not in high sodium diet rats (-5 +/- 2 mmHg). When arterial pressure had been restored to the prelosartan value with methoxamine infusion, renal sympathetic nerve activity was decreased in low (-27 +/- 4%) and normal (-20 +/- 3%) but not in high sodium diet rats (-5 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-8 +/- 2 mmHg) and normal (-7 +/- 2 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). Intracerebroventricular losartan did not significantly decrease arterial pressure but decreased renal sympathetic nerve activity in low (-28 +/- 5%) and normal (-20 +/- 4%) but not in high sodium diet rats (-2 +/- 2%). Arterial baroreflex regulation of renal sympathetic nerve activity was shifted to a lower pressure (arterial pressure at midrange) in low (-7 +/- 2 mmHg) and normal (-5 +/- 1 mmHg) but not in high sodium diet rats (0 +/- 2 mmHg). These results indicate that physiological alterations in endogenous ANG II activity tonically influence basal levels of renal sympathetic nerve activity and its arterial baroreflex regulation.

Chronic activation of brain areas by high-sodium diet in Dahl salt-sensitive rats

1998 ◽  
Vol 274 (6) ◽  
pp. H2046-H2052 ◽  
Author(s):  
Adam S. Budzikowski ◽  
Faranak Vahid-Ansari ◽  
Frans H. H. Leenen
Keyword(s):  
Sodium Intake ◽  
Brain Areas ◽  
Hypothalamic Area ◽  
High Sodium ◽  
Sodium Diet ◽  
Transient Activation ◽  
Nucleus Of Solitary Tract ◽  
Central Gray ◽  
High Sodium Diet

To map changes in neuronal activity in the brains of Dahl salt-sensitive (Dahl S) vs. salt-resistant (Dahl R) rats by high-sodium diet, we used immunohistochemical detection of Fra-like proteins as a marker for long-term neuronal activation. Compared with Dahl R rats during regular sodium intake, Dahl S rats showed modestly higher expression of Fra-like immunoreactivity (Fra-LI) in the supraoptic nucleus, anterior hypothalamic area (AHA), central gray, and nucleus of solitary tract (NTS) at 5, 6, and 9 wk of age but clearly elevated Fra-LI in the magnocellular part of the paraventricular nucleus (PVN) at 6 wk of age (but not at 5 and 9 wk). In the median preoptic nucleus (MnPO) Fra-LI was lower at 9 wk of age and no differences were observed in the parvocellular PVN and subfornical organ in Dahl S vs. Dahl R rats on regular sodium intake. Compared with Dahl S rats on a regular-sodium diet, Dahl S rats on a high-sodium diet from 4 to 9 wk of age had significantly increased blood pressure and experienced transient activation of magnocellular PVN and MnPO and virtually no changes in the activity of the parvocellular PVN, AHA, and NTS. In contrast, Dahl R rats showed marked activation in the magnocellular PVN after 1 and 2 wk on a high-sodium diet compared with Dahl R rats on a regular-sodium diet. The present study demonstrates that Dahl S rats show differential activation of brain areas participating in regulation of osmotic and cardiovascular homeostasis during development of sodium-sensitive hypertension.

Impact of elevated dietary sodium intake on NAD(P)H oxidase and SOD in the cortex and medulla of the rat kidney

2010 ◽  
Vol 299 (1) ◽  
pp. R234-R240 ◽  
Author(s):  
Edward J. Johns ◽  
Barbara O'Shaughnessy ◽  
Susan O'Neill ◽  
Bríd Lane ◽  
Vincent Healy
Keyword(s):  
Oxidative Stress ◽  
Protein Expression ◽  
Oxidase Activity ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Renal Diseases ◽  
Water Excretion ◽  
High Sodium ◽  
Sodium Diet ◽  
High Sodium Diet

Pathophysiological states, including cardiovascular and renal diseases, are characterized by oxidative stress but what is less clear is whether physiological challenges incur a degree of altered oxidative metabolism. To this end, this study examined whether exposure to a high dietary sodium intake could cause an oxidative stress at the kidney. Animals, placed on either 0.3% or 3% sodium diets for 2 wk, were given a lethal dose of anesthetic, and kidneys were removed to analyze both NAD(P)H oxidase (NOX) and superoxide dismutase (SOD) expression and activities in the cortex and medulla. Placing animals on the high-sodium diet raised sodium and water excretion and caused an ∼14-fold increase in urinary excretion of 8-isoprostane, a marker of oxidative stress, which was attenuated by chronic treatment with apocynin to prevent NAD(P)H oxidase activity. The protein expression of the NAD(P)H oxidase subunits NOX2 and p47phox and overall NAD(P)H oxidase activity were approximately doubled in the cortex of the rats on the high-sodium diet compared with those on the normal sodium intake while both SOD activity and expression were unchanged. By contrast, neither NOX nor SOD protein expression or activity were altered in the medulla when the rats were placed on the high-sodium intake. These data suggest that an elevation in dietary sodium intake can lead to increased generation of reactive oxygen species and a state of oxidative stress in the cortex but not to such a degree that it extends to the medulla.

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