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EFFECT OF PERIPHERAL SYMPATHETIC NERVE DYSFUNCTION ON SALT SENSITIVITY OF ARTERIAL PRESSURE
Author(s) -
Osborn John W,
Collister John P,
Guzman Pilar
Publication year - 2008
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04827.x
Subject(s) - guanethidine , hexamethonium , ganglionic blocker , medicine , sympathetic nervous system , blood pressure , endocrinology , peripheral , mean arterial pressure , heart rate , blockade , prazosin , anesthesia , stimulation , receptor , antagonist
SUMMARY1 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) a‐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.