The pressor and renal sympathetic nerve responses to vascular and spinal V1 receptor activation after manipulation of dietary sodium intake

Abstract

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 V1 receptor activation. Mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were monitored in α-chloralose/urethane anaesthetized male Wistar rats. Dose-dependent increases in MAP were observed in all groups to intravenous (i.v.) vasopressin [arginine vasopressin (AVP); 1-10 ng 0.2 ml] and phenylephrine (1-10 μg 0.2 ml), 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 μl) AVP (1-100 μmol/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 μmol/l, P<0.01; 5 μmol/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. These data demonstrated that high Na enhanced peripheral and spinal V1-mediated responses. Interestingly, low Na intake blunted the spinal V1-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.