Chronic salt loading and central adrenergic mechanisms in the spontaneously hypertensive rat.

The effects of chronic salt loading on central adrenergic mechanisms were evaluated in spontaneously hypertensive rats maintained on tap water or 1.2% sodium chloride drinking water for 4 weeks. Basal blood pressure was increased by 10% in the high salt group. Central catecholamines were measured spectrofluorimetrically after cation exchange chromatography. Endogenous levels of noradrenaline (NA) were not influenced by salt loading but the NA turnover (disappearance of NA following synthesis inhibition by alpha-methyltyrosine) was increased in the hemisperes. Central alpha 2-adrenoceptor sensitivity was assessed as the clonidine-induced reduction in blood pressure and as the clonidine-induced deceleration of NA turnover and locus coeruleus (LC) NA cell firing rate (single unit recording). The results were slightly disparate but the unchanged sensitivity of clonidine to reduce LC NA cell firing suggests that there were no alterations in central alpha 2-adrenoceptor sensitivity following a salt load. There were also no changes in alpha 1-adrenoceptor function, which was assessed semiquantitatively as the clonidine-induced increase in flexor reflex activity in spinalized rats. In salt loaded rats there was an enhanced blood pressure and heart rate reduction following ganglionic blockade which may be interpreted as an increased basal sympathetic tone. In the periphery the pressor responses to phenylephrine were increased whereas the chronotropic response to isoprenaline was unchanged. In conclusion, in the spontaneously hypertensive rat on a high salt intake the aggravated development of hypertension was not associated with major changes in central alpha 1 and alpha 2-adrenoceptor mediated functions or in neuronal activity of brain stem NA neurons. There were indications of an increased basal sympathetic tone and increased blood pressure response to pressor substances.