Cardiac control of salt appetite

1987 ◽  
Vol 252 (5) ◽  
pp. R925-R929 ◽  
Author(s):  
E. Toth ◽  
J. Stelfox ◽  
S. Kaufman

Inflation of a balloon for 2 h at the superior vena caval-right atrial junction of the rat reduced the salt intake of animals that had been sodium and water depleted by peritoneal dialysis with hyperoncotic colloid. After the balloons were deflated, the experimental group drank more than the control group so that the total sodium intake of the two groups was the same. Thus stimulated increased venous return to the heart attenuates salt appetite. Since this phenomenon might be secondary to a reflex reduction in plasma renin activity, the experiment was repeated using a model of salt appetite in which the renin-angiotensin system is known to be suppressed, namely the deoxycorticosterone acetate-treated rat. Salt intake was again significantly reduced by inflation of the right atrial balloon. It is concluded that pathways exist, independent of the renin-angiotensin system, whereby information obtained from the cardiac volume receptors regarding the state of filling of the vasculature may be used to regulate salt intake.

Hypertension ◽  
2012 ◽  
Vol 60 (1) ◽  
pp. 98-105 ◽  
Author(s):  
Chris Tikellis ◽  
Raelene J. Pickering ◽  
Despina Tsorotes ◽  
Olivier Huet ◽  
Jaye Chin-Dusting ◽  
...  

1983 ◽  
Vol 244 (3) ◽  
pp. H351-H356 ◽  
Author(s):  
R. I. Kopelman ◽  
V. J. Dzau ◽  
S. Shimabukuro ◽  
A. C. Barger

The compensatory response to moderately severe hemorrhage (30 ml/kg) was studied in chronically catheterized conscious dogs maintained on normal and low salt intake. Although the fall in blood pressure and the increase in heart rate were similar in the two salt states, the salt-restricted animals had significantly greater rises in plasma renin activity and plasma catecholamines following hemorrhage than did the normal salt dogs. To compare further the relative roles of the alpha-adrenergic system and the renin-angiotensin system in the maintenance of blood pressure following hemorrhage, pharmacologic blockade with either phentolamine or converting enzyme inhibitor was performed 20 min after the completion of the hemorrhage. These latter experiments demonstrated that salt restriction resulted in a significantly greater role for the renin-angiotensin system. Moreover, interruption of the renin-angiotensin system blunted the anticipated rise in catecholamines and heart rate during the additional hypotension induced by converting enzyme blockade after hemorrhage.


2001 ◽  
Vol 281 (6) ◽  
pp. R1854-R1861 ◽  
Author(s):  
Raynald Bergeron ◽  
Michael Kjær ◽  
Lene Simonsen ◽  
Jens Bülow ◽  
Dorthe Skovgaard ◽  
...  

The study examined the implication of the renin-angiotensin system (RAS) in regulation of splanchnic blood flow and glucose production in exercising humans. Subjects cycled for 40 min at 50% maximal O2 consumption (V˙o 2 max) followed by 30 min at 70% V˙o 2 maxeither with [angiotensin-converting enzyme (ACE) blockade] or without (control) administration of the ACE inhibitor enalapril (10 mg iv). Splanchnic blood flow was estimated by indocyanine green, and splanchnic substrate exchange was determined by the arteriohepatic venous difference. Exercise led to an ∼20-fold increase ( P < 0.001) in ANG II levels in the control group (5.4 ± 1.0 to 102.0 ± 25.1 pg/ml), whereas this response was blunted during ACE blockade (8.1 ± 1.2 to 13.2 ± 2.4 pg/ml) and in response to an orthostatic challenge performed postexercise. Apart from lactate and cortisol, which were higher in the ACE-blockade group vs. the control group, hormones, metabolites, V˙o 2, and RER followed the same pattern of changes in ACE-blockade and control groups during exercise. Splanchnic blood flow (at rest: 1.67 ± 0.12, ACE blockade; 1.59 ± 0.18 l/min, control) decreased during moderate exercise (0.78 ± 0.07, ACE blockade; 0.74 ± 0.14 l/min, control), whereas splanchnic glucose production (at rest: 0.50 ± 0.06, ACE blockade; 0.68 ± 0.10 mmol/min, control) increased during moderate exercise (1.97 ± 0.29, ACE blockade; 1.91 ± 0.41 mmol/min, control). Refuting a major role of the RAS for these responses, no differences in the pattern of change of splanchnic blood flow and splanchnic glucose production were observed during ACE blockade compared with controls. This study demonstrates that the normal increase in ANG II levels observed during prolonged exercise in humans does not play a major role in the regulation of splanchnic blood flow and glucose production.


2001 ◽  
Vol 19 (1) ◽  
pp. 89-98 ◽  
Author(s):  
Xigeng Zhao ◽  
Roselyn White ◽  
Bing S. Huang ◽  
James Van Huysse ◽  
Frans H. H. Leenen

1981 ◽  
Vol 61 (s7) ◽  
pp. 385s-387s ◽  
Author(s):  
P. W. De Leeuw ◽  
G. A. W. Van Soest ◽  
R. Punt ◽  
R. P. L. M. Hoogma ◽  
A. J. P. M. Smout ◽  
...  

1. To investigate whether reduced activity of pressor systems could explain the spontaneous drop in pressure upon hospitalization, 51 subjects with uncomplicated essential hypertension were admitted to hospital. Sodium intake was fixed at 55 mmol/day. 2. Blood samples for noradrenaline, adrenaline, active renin, angiotensin II and aldosterone were drawn on each morning of the first 3 days of hospitalization; blood pressure was measured at 2 h intervals and values were averaged for each day. 3. Subjects were divided in two groups depending on whether they became normotensive (group 1; n = 12) or remained hypertensive (group 2; n = 39). This distinction was thought to reflect mild and more severe hypertensive groups respectively. 4. Although both groups showed a comparable fall in blood pressure during hospitalization, noradrenaline levels fell more consistently in group 1, whereas adrenaline levels fell only in group 2. The components of the renin—angiotensin—aldosterone system rose, but more conspicuously in group 1. 5. It is concluded that withdrawal of sympathetic activity can only partly explain the hypotensive response to hospitalization. The renin—angiotensin system behaves only passively and appears to be counterproductive to alterations in blood pressure.


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