Catecholamines in Experimental and Essential Hypertension

Abstract

SummaryCatecholamines and catecholamine-synthesizing enzymes have been investigated in specific brain areas, plasma, and adrenal glands during the development of high blood pressure in spontaneously hypertensive rats (SHR) and rats made hypertensive by administration of deoxycorticosterone and sodium chloride (DOCA-salt hypertensive rats). Changes in catecholamine metabolism were localized to regions of the brain implicated in the regulation of blood pressure. In SHR noradrenaline (NA) levels and dopamines-β-hydroxylase (DBH) activities were decreased in specific nuclei of the hypothalamus and in the nucleus interstitialis striae terminalis ventralis, in both young and adult rats. The decrease in the formation of NA can result in a reduced activation of central α-adrenergic receptors in depressor areas, which may be related causally to the onset of hypertension. The activity of the adrenaline-forming enzyme, phenyl ethanoloamine-N-methy1 transferase (PNMT) was increased in brain stem areas of young SHR (A1, A2, area postrema), but it was normal in adult hypertensive animals. Adrenaline (A) levels in these areas were decreased in young SHR. In DOCA-salt hypertensive rats, enhanced PNMT activity occurred in A1 area postrema, and locus coeruleus and extended to A2 area with prolonged treatment and higher blood pressure. Plasma NA and DBH activity were increased in young SHR. In addition plasma A was increased in young stroke-prone SHR. In DOCA-salt hypertensive rats plasma NA was increased.In adrenal glands of young SHR activities of tyrosine hydroxylase (TH), DBH, and PNMT as well as A content were decreased. In adult SHR, only TH turned to an enhanced activity. Also in DOCA-salt hypertensive rats, TH activity and A content of adrenal glands were increased. Administration of PNMT inhibitors or depletion of adrenal catecholamines by an adrenergic neurone blocking drug result in a normalization of the blood pressure in both models studiedThe results suggest that central and peripheral catecholaminergic neurons may play a role during onset and maintenance of genetic and experimental hypertension.In patients with essential hypertension circulating NA levels were not significantly different from normotensive subjects. Also, no changes in resting plasma NA and A could be observed in patients with stabilized essential hypertension before or after acute or chronic administration of propranolol. However, during propranolol treatment exercise significantly increased circulating NA.3