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Houghton, BL,Johns, EJ;
2011
January
Rna-A Publication of The Rna Society
The pressor and renal sympathetic nerve responses to vascular and spinal V-1 receptor activation after manipulation of dietary sodium intake
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arginine vasopressin dietary sodium renal sympathetic nerves PARAVENTRICULAR NUCLEUS ACTIVATION HIGH-SALT DIET BLOOD-PRESSURE HYPERTENSIVE-RATS ANESTHETIZED RATS ANGIOTENSIN-II VASOPRESSIN NEURONS SYMPATHOEXCITATION VASOCONSTRICTION
29
915
921
Objective Excessive dietary Na+ intake can enhance the autonomic control of blood pressure, but the physiological mechanisms are unclear. This study examined how low (0.03%) and high (3.0%) dietary Na+ intake, from weaning (4 weeks) to adulthood (11 weeks), altered the pressor and renal sympathoexcitatory responses to peripheral and spinal V-1 receptor activation.Methods Mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were monitored in alpha-chloralose/urethane anaesthetized male Wistar rats.Results Dose-dependent increases in MAP were observed in all groups to intravenous (i.v.) vasopressin [arginine vasopressin (AVP); 1-10 ng 0.2 ml(-1)] and phenylephrine (1-10 mu g 0.2 ml(-1)), and in the high Na+ group, these responses were enhanced but to a greater extent for AVP than phenylephrine (P<0.001). A direct dose-dependent rise in RSNA to intrathecal (10 mu l) AVP (1-100 mu mol/l) and glutamate (10-100 mmol/l) was observed in the normal Na+ group. The RSNA responses were enhanced in the high Na+ group at lower doses of intrathecal AVP (1 mu mol/l, P<0.01; 5 mu mol/l, P<0.05) and all doses of glutamate (P<0.001) compared to the normal Na+ group. In the low Na+ group, the RSNA responses to intrathecal AVP were suppressed, but those to intrathecal glutamate were enhanced compared to normal Na+ (P<0.001) and similar to the high Na+ group.Conclusion These data demonstrated that high Na+ enhanced peripheral and spinal V-1-mediated responses. Interestingly, low Na+ intake blunted the spinal V-1-mediated RSNA responses, but sensitized those to spinal glutamate, which may be a compensatory mechanism to ensure adequate neural control of the kidney when dietary Na+ intake is reduced. J Hypertens 29: 915-921 (C) 2011 Wolters Kluwer Health vertical bar Lippincott Williams & Wilkins.
DOI 10.1097/HJH.0b013e328344b86b
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