Onset of hypertension in spontaneously hypertensive rats despite the depletion of spinal cord catecholamines

Functional Organization of Central Cardiovascular Pathways

“…According to their model, the A1 group of neurones in the caudal part of the ventrolateral medulla project to the IL cell column, where it mediates baroreceptor inhibition of sympathetic vasomotor tone. This model, however is not supported by recent evidence which indicates that the A1 group of cells makes no or only a small contribution to the CA innervation of the cord (Blessing et al, 1981;Loewy et al, 1980). Korner & Head (1980) have taken a different approach to this question by observing the cardiovascular effects of selective stimulation or destruction of central CA neurones in unanaesthetized rabbits.…”

“…Since the original finding by Dahlstrom & Fuxe (1965) that CA neurones within the caudal ventrolateral medulla (A1 group) and dorsomedial medulla (A2 group) showed increased fluorescence following spinal cord section, it has been widely assumed that these groups of cells supply the main CA innervation of the IL nucleus. There is now very good evidence, however, that the main origin of this innervation is the A5 group (Loewy et al, 1979b; Blessing et al, 1981), with only a very small contribution from the A1 group and none at all from the A2 group (Blessing et al 1981 ;Loewy, McKellar, Swensson & Panneton, 1980). The spinal routes of descending pathways to the IL nucleus have been studied mainly using stimulation and lesioning techniques.…”

Central Catecholaminergic Neurones and Spontaneously Hypertensive Rats

“…The suggestion that central catecholaminergic pathways are involved in the development of hypertension in SHR rats mainly arises from the observation that intracerebroventricular 6hydroxydopamine (6-OHDA), a catecholamine neurotoxin, prevents the development of hypertension in young SHR rats while having little effect on blood pressure in older rats when hypertension is established (Haeusler, Finch 8i Thoenen, 1972;Finch, Haeusler & Thoenen, 1972;Erinhoff, Heller & Oparil, 1975). The selective depletion of spinal catecholamines by intraspinal or intra-cisternal 6-OHDA injection (Kubo & Hashimoto, 1978;Loewy, McKellar, Swenson & Panneton, 1980) and from forebrain regions by injections of 6-OHDA into ascending noradrenergic pathways (van den Buuse, De Jonge & Versteeg, 1983) does not prevent the development of hypertension. This suggests that catecholaminergic neurones in the hypothalamus, mesencephalon or brainstem (pons-medulla) are necessary for the development but not the maintenance of hypertension in SHR rats, and that neither descending caecholaminergic pathways to the spinal preganglionic sympathetic neurones nor major ascending pathways are important in this respect.…”

Early Changes in Noradrenaline Content of Some Brain Nuclei in Spontaneously Hypertensive Rats

“…The early onset of hypertension in spontaneously hypertensive rats of the Okamoto strain (SH rats) may be central in origin (Haeusler, Finch & Thoenen, 1972;Loewy, McKellar, Swensson & Panneton, 1980). Such a trigger function of the central nervous system may be related to modifications of central adrenergic activity in the cardiovascular centres of young SH rats.…”