1. Dysregulation of peripheral sympathetic pathways contributes to some forms of salt-dependent hypertension. However, at the present time it is not known whether salt-induced activation of sympathetic nerves or loss of normal sympathoinhibitory responses to salt-induced volume expansion contributes to neurogenic salt-dependent hypertension. The present study was performed to the test the hypothesis that loss of peripheral sympathetic nerve function results in salt-dependent hypertension. 2. The effect of three pharmacological interventions of sympathetic nerve function on the long-term salt-sensitivity of mean arterial pressure (MAP) were measured: (i) blockade of ganglionic transmission with hexamethonium (HEX; n = 5); (ii) destruction of sympathetic nerve terminals with guanethidine (GUAN; n = 7); and (iii) α-adrenoceptor blockade with two specific antagonists, namely prazosin (PRAZ; n = 7) and terazosin (TERAZ; n = 8). 3. Mean arterial pressure and heart rate were measured 24 h/day by radiotelemetry in conscious rats during 5 days of normal and 7 days of high (HNa) dietary sodium intake. Despite marked increases in both sodium and water intake during 7 days of the HNa diet, no statistically significant changes in MAP were observed in HEX, GUAN, PRAZ or TERAZ groups. 4. We conclude that loss of peripheral sympathetic neural pathways alone does not cause salt-dependent hypertension in the rat.
|Original language||English (US)|
|Number of pages||7|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|State||Published - Mar 2008|
- Ganglionic blockade
- α-adrenoceptor antagonists